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Brief Report
- Technology/Device
- Effectiveness of the Stage 4 Smart Insulin Pen DIA:CONN P8 for Glycemic Control in a Real-World Setting
- So Yoon Kwon, Hyoseon Kwak, Jae Hyeon Kim
- Received February 11, 2025 Accepted March 23, 2025 Published online September 3, 2025
- DOI: https://doi.org/10.4093/dmj.2025.0112 [Epub ahead of print]
- 1,497 View
- 73 Download
-
Abstract
PDF
Supplementary Material
PubReader 
ePub - This study evaluated whether a stage 4 smart insulin pen (SIP) provides superior glycemic control compared with a traditional insulin pen (TIP) in individuals with intensively insulin-treated diabetes. Forty-two adults with continuous glucose monitoring (CGM), multiple daily insulin injections, and no prior SIP use were included. After diabetes self-management education (DSME), the SIP group (n=21) initiated SIP, whereas the TIP group (n=21) continued their usual regimens. Glycemic metrics were assessed using CGM before and 2 weeks after DSME. Both groups demonstrated significant improvements in glycemic outcomes. However, SIP users exhibited superior improvements in the percentage of time in range, percentage of time below range (%TBR) <70 mg/dL, %TBR <54 mg/dL, and glycemic risk index compared with TIP users (between-group difference [BD] 11.0%, P=0.046; BD –2.6%, P=0.024; BD –0.9%, P=0.027; BD –18.2, P=0.022, respectively). These findings suggest that SIP, with its bolus calculation and CGM integration, is associated with improved glycemic outcomes in adults with intensively insulin-treated diabetes.
Review
- Complications
- Diabetes Mellitus and Infectious Diseases: Current Evidence and Clinical Implications
- Taeeun Kim, Sang-Ho Choi
- Diabetes Metab J. 2025;49(5):915-933. Published online August 27, 2025
- DOI: https://doi.org/10.4093/dmj.2025.0508
- 5,298 View
- 357 Download
- 6 Web of Science
- 7 Crossref
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Abstract
PDFPubReader ePub
- Diabetes mellitus predisposes individuals to a broad spectrum of infections. People with diabetes face a 1.5- to 4-fold increased risk of both common and severe infections, and infections remain the leading cause of morbidity and mortality. Chronic hyperglycemia impairs neutrophil chemotaxis, oxidative burst, and complement activation, while vascular insufficiency and neuropathy compromise tissue perfusion and barrier integrity. These defects, together with altered skin, mucosal, and gut microbiota, influence the marked susceptibility to urinary tract infections (especially renal abscess and emphysematous pyelonephritis), osteomyelitis, diabetic foot infections, pneumonia (including influenza), tuberculosis, skin and soft tissue infections, and lifethreatening syndromes such as emphysematous cholecystitis and rhino-orbital mucormycosis that are almost exclusive to people with diabetes. Outcomes from infections are worse in diabetes. Although the core therapeutic principles align with those for patients without diabetes, management should be individualized. Glycemic control should balance infection risk and hypoglycemia; antimicrobial dosing should account for renal function and drug interactions; and strict antimicrobial stewardship is required. If needed, prompt debridement and multidisciplinary intervention are necessary to mitigate complications and reduce mortality. Preventive care relies on comprehensive vaccination (influenza, pneumococcus, severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2], hepatitis B, herpes zoster, and Tdap/Td) and regular foot surveillance with offloading to avert ulceration.
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Citations
Citations to this article as recorded by
- Review on the Gut‐Kidney Axis Mechanism and Therapeutic Strategies in Diabetic Nephropathy
Qing Li, Mingrong Cheng, Xiaoyan Zhang
Diabetes/Metabolism Research and Reviews.2026;[Epub] CrossRef - Prim-O-glucosylcimifugin targets Staphylococcus aureus caseinolytic protease P to inhibit α-hemolysin expression and promote healing of MRSA-induced diabetic skin infections
Yan Wang, Shanshan Luo, Xinping Guo, Mengli Jin, Xingye Wang, Mingran Li, Shuang Jiang, Lin Wei, Mingjun Liu, Wu Song
Microbial Pathogenesis.2026; 212: 108296. CrossRef - Preoperative triglyceride–glucose index as a metabolic predictor of surgical site infection after posterior lumbar fusion
Yu Hua, Shaoxing Li, Yuan Jiang, Jinwang Liu
Journal of Orthopaedic Surgery.2026;[Epub] CrossRef - Development and validation of a risk nomogram model for predicting superficial fungal infections in patients with type 2 diabetes mellitus : a cross-sectional study
Yu Li, Guozhong Zhou, Feifei Yang, Rong long, Wei Shi, Yan Dong, Yuanyuan Zhou, Nan Chen, Ying Yang
BMC Infectious Diseases.2026;[Epub] CrossRef - Immunometabolic reprogramming in diabetic osteomyelitis: from mechanisms to therapeutics
Hui Zhang, Zi-Shan Fu, Ying Zhou, Song-Nan Wang, Si-Ying Ye, An-Na Wang, Jun-Tong Liu
Frontiers in Cellular and Infection Microbiology.2025;[Epub] CrossRef - Risk of Acute Cholecystitis Based on Combination of Patient Age, Patient Sex, Leukocytosis, and Sonographic Murphy Sign
Hideaki Ishida, Hiroko Naganuma
Journal of Ultrasound in Medicine.2025;[Epub] CrossRef - Chronic Infections and Diabetes in Africa: A Narrative Review of Pathogen-Associated Metabolic Risk
Olabisi P Lawal, Fortune I Ebiala, Modinat Abayomi, Obiageri Ihuarulam Okeoma, Nana Ama Aduma Amankwah, John O Patrick, Queeneth Eguakun, Aliyu O Olaniyi
Cureus.2025;[Epub] CrossRef
- Review on the Gut‐Kidney Axis Mechanism and Therapeutic Strategies in Diabetic Nephropathy
Original Article
- Others
- Glycemic Benefit of Insulin Degludec/Insulin Aspart Compared to Basal Insulin in Type 2 Diabetes Mellitus Associated with Impaired Glucagon-Like Peptide-1 Response: A Randomized Crossover Trial
- Han Na Jang, Eun Shil Hong, Ye Seul Yang, Seong Ok Lee, Myoung-jin Jang, Andrea Mari, Soo Heon Kwak, Kyong Soo Park, Hak Chul Jang, Hye Seung Jung
- Received November 21, 2024 Accepted April 28, 2025 Published online August 14, 2025
- DOI: https://doi.org/10.4093/dmj.2024.0741 [Epub ahead of print]
- 1,750 View
- 66 Download
-
Abstract
PDFSupplementary MaterialPubReader ePub
- Background
We aimed to confirm that once-daily insulin degludec/insulin aspart (IDegAsp) is superior to basal insulin therapy in participants with type 2 diabetes mellitus (T2DM) exhibiting signs of overbasalization. Additionally, we analyzed incretin profiles in relation to the benefits of IDegAsp, providing insights into the underlying mechanisms.
Methods
A prospective study was conducted in participants receiving basal insulin therapy, with a fasting plasma glucose (FPG) level lower than predicted from their glycosylated hemoglobin (HbA1c). Participants were randomly assigned to either IDegAsp or insulin glargine (IGlar) in a 1:1 ratio. After 20 weeks of treatment, the insulins were switched in a crossover design. The primary endpoint was the change in HbA1c from baseline. Incretin profiles, hypoglycemic events, and continuous glucose monitoring (CGM) were also analyzed (Trial registration: www.cris.nih.go.kr; KCT0004597).
Results
The study included 55 participants (male 40%, mean age 65 years, FPG 103 mg/dL, and HbA1c 8.3%). HbA1c significantly decreased to 7.8%±0.8% with IDegAsp, compared to 8.0%±0.7% with IGlar. The mean estimated treatment difference of changes was –0.21% points (95% confidence interval, –0.39 to –0.02; P=0.031), favoring IDegAsp. Hypoglycemic events were comparable. CGM demonstrated significantly lower glucose measures during the daytime with IDegAsp compared to IGlar, and vice versa at dawn. The HbA1c benefit of IDegAsp over IGlar was associated with a low glucagon-like peptide-1 (GLP-1) ratio at 30 minutes relative to baseline (r=0.301, P=0.040), while not with glucose-dependent insulinotropic polypeptide.
Conclusion
The greater reduction in HbA1c achieved with IDegAsp compared to IGlar in individuals with T2DM was associated with an impaired GLP-1 response, facilitating personalized insulin therapy.
Sulwon Lecture 2024
- Basic and Translational Research
- Overcoming β-Cell Dysfunction in Type 2 Diabetes Mellitus: CD36 Inhibition and Antioxidant System
- Il Rae Park, Yong Geun Chung, Kyu Chang Won
- Diabetes Metab J. 2025;49(1):1-12. Published online January 1, 2025
- DOI: https://doi.org/10.4093/dmj.2024.0796
- 12,368 View
- 482 Download
- 10 Web of Science
- 11 Crossref
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Abstract
PDFPubReader ePub
- Type 2 diabetes mellitus (T2DM) is marked by chronic hyperglycemia, gradually worsening β-cell failure, and insulin resistance. Glucotoxicity and oxidative stress cause β-cell failure by increasing reactive oxygen species (ROS) production, impairing insulin secretion, and disrupting transcription factors such as pancreatic and duodenal homeobox 1 (PDX-1) and musculoaponeurotic fibrosarcoma oncogene family A (MafA). Cluster determinant 36 (CD36), an essential glycoprotein responsible for fatty acid uptake, exacerbates oxidative stress and induces the apoptosis of β-cells under hyperglycemic conditions through pathways involving ceramide, thioredoxin-interacting protein (TXNIP), and Rac1-nicotinamide adenine dinucleotide phosphate oxidase (NOX)-mediated redoxosome formation. Targeting CD36 pathways has emerged as a promising therapeutic strategy. Oral hypoglycemic agents, such as metformin, teneligliptin, and pioglitazone, have shown protective effects on β-cells by enhancing antioxidant defenses. These agents reduce glucotoxicity via mechanisms such as suppressing CD36 expression and stabilizing mitochondrial function. Additionally, novel insights into the glutathione antioxidant system and its role in β-cell survival underscore its therapeutic potential. This review focuses on the key contribution of oxidative stress and CD36 to β-cell impairment, the therapeutic promise of antioxidants, and the need for further research to apply these findings in clinical practice. Promising strategies targeting these mechanisms may help preserve β-cell function and slow T2DM progression.
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Citations
Citations to this article as recorded by- Small‐Molecule Sarco/Endoplasmic Reticulum Ca2+‐ATPase Activators Reverse Methylglyoxal‐Induced Inhibition through Nonantioxidant Mechanisms
Carlos Cruz‐Cortés, Silvia Micháliková, Petronela Rezbáriková, L. Michel Espinoza‐Fonseca, Jana Viskupičová
ChemMedChem.2026;[Epub] CrossRef - Bone Marrow Mesenchymal Stromal Cells and Their Derived Extracellular Vesicles Protect Pancreatic Beta‐TC‐6 Cells From Hypoxia‐Induced Injury via miR‐539‐3p‐Mediated Downregulation of CD36 Expression
Na Lin, Yaoyao Liang, Minying Tang, Fei Liu, Liuyan Chen, Lvying Wu, Yunfeng Fu, Zhuoyu Li, Lingfeng Zhu, Jin Chen, Yuelin Zhang
Stem Cells International.2026;[Epub] CrossRef - Potential Involvement of PI3K/AKT Signaling Pathway in the Protective Effects of Rhinacanthus nasutus Against Diabetic Nephropathy-Induced Oxidative Stress
Junyu Liu, Yehao Lin, Xudong Yi, Min Zhang, Pharkphoom Panichayupakaranant, Joseph Buhagiar, Haixia Chen
Antioxidants.2026; 15(2): 252. CrossRef - Amylin and parameters of carbohydrate and lipid metabolism in patients with type 2 diabetes mellitus in the Azerbaijani population
Z.G. Akhmedova, D.I. Kagramanova
INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine).2026; 22(1): 35. CrossRef - Polygonatum sibiricum polysaccharides enhance pancreatic β-cell function in diabetic zebrafish by mitigating mitochondrial oxidative damage via the AMPK-SIRT1 pathway
Fan Lin, Wenjing Yu, Ping Li, Shuyao Tang, Yitong Ouyang, Liya Huang, Di Wu, Shaowu Cheng, Zhenyan Song
Frontiers in Nutrition.2025;[Epub] CrossRef - Melatonin Improves Lipid Homeostasis, Mitochondrial Biogenesis, and Antioxidant Defenses in the Liver of Prediabetic Rats
Milena Cremer de Souza, Maria Luisa Gonçalves Agneis, Karoliny Alves das Neves, Matheus Ribas de Almeida, Geórgia da Silva Feltran, Ellen Mayara Souza Cruz, João Paulo Ferreira Schoffen, Luiz Gustavo de Almeida Chuffa, Fábio Rodrigues Ferreira Seiva
International Journal of Molecular Sciences.2025; 26(10): 4652. CrossRef - From Glucotoxicity to Lung Injury: Emerging Perspectives on Diabetes-Associated Respiratory Complications
Hongmei Yu, Jie Liu, Xiaojuan He
Lung.2025;[Epub] CrossRef - Quercetin as an Anti-Diabetic Agent in Rodents—Is It Worth Testing in Humans?
Tomasz Szkudelski, Katarzyna Szkudelska, Aleksandra Łangowska
International Journal of Molecular Sciences.2025; 26(15): 7391. CrossRef - Preclinical Evaluation of 2-Aminobenzothiazole Derivatives: In Silico, In Vitro, and Preliminary In Vivo Studies as Diabetic Treatments and Their Complications
Natalia Reyes-Vallejo, Miguel Valdes, Adelfo Reyes-Ramírez, Juan Andres Alvarado-Salazar, Alejandro Cruz, Erik Andrade-Jorge, Jessica Elena Mendieta-Wejebe
Molecules.2025; 30(16): 3427. CrossRef - Metal organic frameworks (MOFs) synthesis and their use as a loading agent in oxidative stress-based diseases
Muhammad Saqib Saif, Sana Batool, Yusra Majeed, Asadullah, Tuba Tariq, Li Haitao, Yanjun Duan, Ghazala Mustafa, Murtaza Hasan
Journal of Environmental Chemical Engineering.2025; 13(5): 118725. CrossRef - Synergism of Synthetic Sulfonamides and Natural Antioxidants for the Management of Diabetes Mellitus Associated with Oxidative Stress
Ancuța Dinu (Iacob), Luminita-Georgeta Confederat, Ionut Dragostin, Ionela Daniela Morariu, Dana Tutunaru, Oana-Maria Dragostin
Current Issues in Molecular Biology.2025; 47(9): 709. CrossRef
- Small‐Molecule Sarco/Endoplasmic Reticulum Ca2+‐ATPase Activators Reverse Methylglyoxal‐Induced Inhibition through Nonantioxidant Mechanisms
Original Articles
- Complications
- Impact of Hyperglycemia on Complication and Mortality after Transarterial Chemoembolization for Hepatocellular Carcinoma
- Sun Joon Moon, Chang Ho Ahn, Yun Bin Lee, Young Min Cho
- Diabetes Metab J. 2024;48(2):302-311. Published online January 3, 2024
- DOI: https://doi.org/10.4093/dmj.2022.0255
- 5,241 View
- 233 Download
- 4 Web of Science
- 3 Crossref
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Abstract
PDFSupplementary MaterialPubReader ePub
- Background
Current guidelines regarding periprocedural glycemic control to prevent complications after nonsurgical invasive procedures are insufficient. Transarterial chemoembolization (TACE) is a widely used treatment for unresectable hepatocellular carcinoma. We aimed to investigate the association between diabetes mellitus (DM) per se and the degree of hyperglycemia with postprocedural complications after TACE.
Methods
A total of 22,159 TACE procedures performed at Seoul National University Hospital from 2005 to 2018 were retrospectively analyzed. The associations between DM, preprocedural glycosylated hemoglobin (HbA1c), and periprocedural average glucose with postprocedural adverse outcomes were evaluated. The primary outcome was occurrence of postprocedural bacteremia. Secondary outcomes were acute kidney injury (AKI), delayed discharge and death within 14 days. Periprocedural glucose was averaged over 3 days: the day of, before, and after the TACE procedures. Propensity score matching was applied for procedures between patients with or without DM.
Results
Periprocedural average glucose was significantly associated with bacteremia (adjusted odds ratio per 50 mg/dL of glucose, 1.233; 95% confidence interval, 1.071 to 1.420; P=0.004), AKI, delayed discharge, and death within 14 days. DM per se was only associated with bacteremia and AKI. Preprocedural HbA1c was associated with delayed discharge. Average glucose levels above 202 and 181 mg/dL were associated with a significantly higher risk of bacteremia and AKI, respectively, than glucose levels of 126 mg/dL or lower.
Conclusion
Periprocedural average glucose, but not HbA1c, was associated with adverse outcomes after TACE, which is a nonsurgical invasive procedure. This suggests the importance of periprocedural glycemic control to reduce postprocedural complications. -
Citations
Citations to this article as recorded by- Serum CYFRA 21-1 and CK19-2G2 as Predictive Biomarkers of Response to Transarterial Chemoembolization in Hepatitis C–related Hepatocellular Carcinoma Among Egyptians: A Prospective Study
Mohamed Y. Taher, Ehab Hassouna, Abeer El Hadidi, Omar El-aassar, Mohamed Fathy Bakosh, Mohamed Said Shater
Journal of Clinical and Experimental Hepatology.2025; 15(1): 102405. CrossRef - A Machine Learning Model for Predicting Prognosis in HCC Patients With Diabetes After TACE
Linxia Wu, Lei Chen, Lijie Zhang, Yiming Liu, Die Ouyang, Wenlong Wu, Yu Lei, Ping Han, Huangxuan Zhao, Chuansheng Zheng
Journal of Hepatocellular Carcinoma.2025; Volume 12: 77. CrossRef - Use of an insulin titration protocol based on continuous glucose monitoring in postoperative cardiac surgery patients with type 2 diabetes and prediabetes: a randomized controlled trial
Sun-Joon Moon, Min-Su Kim, Yun Tae Kim, Ha-Eun Lee, Young-Woo Lee, Su-Ji Lee, Euy-Suk Chung, Cheol-Young Park
Cardiovascular Diabetology.2025;[Epub] CrossRef
- Serum CYFRA 21-1 and CK19-2G2 as Predictive Biomarkers of Response to Transarterial Chemoembolization in Hepatitis C–related Hepatocellular Carcinoma Among Egyptians: A Prospective Study
- Basic Research
- Hyperglycemia-Suppressed SMARCA5 Disrupts Transcriptional Homeostasis to Facilitate Endothelial Dysfunction in Diabetes
- Ju Wang, Hui Zhou, Jinhua Shao, Shu Zhang, Jing Jin
- Diabetes Metab J. 2023;47(3):366-381. Published online March 6, 2023
- DOI: https://doi.org/10.4093/dmj.2022.0179
- 5,972 View
- 129 Download
- 4 Web of Science
- 4 Crossref
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Abstract
PDFSupplementary MaterialPubReader ePub
- Background
Dysfunction of vascular endothelial cells (ECs) plays a central role in the pathogenesis of cardiovascular complications in diabetes. SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 5 (SMARCA5) is a key regulator of chromatin structure and DNA repair, but its role in ECs remains surprisingly unexplored. The current study was designed to elucidate the regulated expression and function of SMARCA5 in diabetic ECs.
Methods
SMARCA5 expression was evaluated in ECs from diabetic mouse and human circulating CD34+ cells using quantitative reverse transcription polymerase chain reaction and Western blot. Effects of SMARCA5 manipulation on ECs function were evaluated using cell migration, in vitro tube formation and in vivo wound healing assays. Interaction among oxidative stress, SMARCA5 and transcriptional reprogramming was elucidated using luciferase reporter assay, electrophoretic mobility shift assay and chromatin immunoprecipitation.
Results
Endothelial SMARCA5 expression was significantly decreased in diabetic rodents and humans. Hyperglycemia-suppressed SMARCA5 impaired EC migration and tube formation in vitro, and blunted vasculogenesis in vivo. Contrarily, overexpression of SMARCA5 in situ by a SMARCA5 adenovirus-incorporated hydrogel effectively promoted the rate of wound healing in a dorsal skin punch injury model of diabetic mice. Mechanistically, hyperglycemia-elicited oxidative stress suppressed SMARCA5 transactivation in a signal transducer and activator of transcription 3 (STAT3)-dependent manner. Moreover, SMARCA5 maintained transcriptional homeostasis of several pro-angiogenic factors through both direct and indirect chromatin-remodeling mechanisms. In contrast, depletion of SMARCA5 disrupted transcriptional homeostasis to render ECs unresponsive to established angiogenic factors, which ultimately resulted in endothelial dysfunction in diabetes.
Conclusion
Suppression of endothelial SMARCA5 contributes to, at least in part, multiple aspects of endothelial dysfunction, which may thereby exacerbate cardiovascular complications in diabetes. -
Citations
Citations to this article as recorded by- From waste to wonder: exploring the hypoglycemic and anti-oxidant properties of corn processing by−products
Xiaoqian Yang, Yuelong Wang, Jingfeng Li, Yuxing Tai, Kunping Yang, Jingwei Lv, Jiaming Sun, Hui Zhang
Frontiers in Chemistry.2024;[Epub] CrossRef - E3 ubiquitin ligase RNF180 mediates the ALKBH5/SMARCA5 axis to promote colon inflammation and Th17/Treg imbalance in ulcerative colitis mice
Kailing Wang, Fan Liu, Budumu Muchu, Jiawen Deng, Jing Peng, Yan Xu, Fujun Li, Miao Ouyang
Archives of Pharmacal Research.2024; 47(7): 645. CrossRef - USP3 promotes DNA damage response and chemotherapy resistance through stabilizing and deubiquitinating SMARCA5 in prostate cancer
Sheng Li, Situ Xiong, Zhongqi Li, Lin Yang, Hailang Yang, Jing Xiong, Wang Pan, Ju Guo, Songhui Xu, Bin Fu
Cell Death & Disease.2024;[Epub] CrossRef - Overexpression of Chromatin Remodeling Factor SRG3 Down-Regulates IL1β-Expressing M1 Macrophages and IL17-Producing T Cells in Adipose Tissues
Jungmin Jeon, Sung Won Lee, Hyun Jung Park, Yun Hoo Park, Tae-Cheol Kim, Sujin Lee, Seyeong Lee, Luc Van Kaer, Seokmann Hong
International Journal of Molecular Sciences.2024; 25(21): 11681. CrossRef
- From waste to wonder: exploring the hypoglycemic and anti-oxidant properties of corn processing by−products
- Genetics
- Genome-Wide Association Study on Longitudinal Change in Fasting Plasma Glucose in Korean Population
- Heejin Jin, Soo Heon Kwak, Ji Won Yoon, Sanghun Lee, Kyong Soo Park, Sungho Won, Nam H. Cho
- Diabetes Metab J. 2023;47(2):255-266. Published online January 19, 2023
- DOI: https://doi.org/10.4093/dmj.2021.0375
- 7,735 View
- 237 Download
- 3 Web of Science
- 3 Crossref
-
Abstract
PDFSupplementary MaterialPubReader ePub
- Background
Genome-wide association studies (GWAS) on type 2 diabetes mellitus (T2DM) have identified more than 400 distinct genetic loci associated with diabetes and nearly 120 loci for fasting plasma glucose (FPG) and fasting insulin level to date. However, genetic risk factors for the longitudinal deterioration of FPG have not been thoroughly evaluated. We aimed to identify genetic variants associated with longitudinal change of FPG over time.
Methods
We used two prospective cohorts in Korean population, which included a total of 10,528 individuals without T2DM. GWAS of repeated measure of FPG using linear mixed model was performed to investigate the interaction of genetic variants and time, and meta-analysis was conducted. Genome-wide complex trait analysis was used for heritability calculation. In addition, expression quantitative trait loci (eQTL) analysis was performed using the Genotype-Tissue Expression project.
Results
A small portion (4%) of the genome-wide single nucleotide polymorphism (SNP) interaction with time explained the total phenotypic variance of longitudinal change in FPG. A total of four known genetic variants of FPG were associated with repeated measure of FPG levels. One SNP (rs11187850) showed a genome-wide significant association for genetic interaction with time. The variant is an eQTL for NOC3 like DNA replication regulator (NOC3L) gene in pancreas and adipose tissue. Furthermore, NOC3L is also differentially expressed in pancreatic β-cells between subjects with or without T2DM. However, this variant was not associated with increased risk of T2DM nor elevated FPG level.
Conclusion
We identified rs11187850, which is an eQTL of NOC3L, to be associated with longitudinal change of FPG in Korean population. -
Citations
Citations to this article as recorded by- Investigation of the degree of family history of diabetes in different clusters of newly diagnosed type 2 diabetes in Thailand
Watip Tangjittipokin, Tassanee Narkdontri, Nipaporn Teerawattanapong, Sarocha Suthon, Vorthunju Nakhonsri, Rujipat Wasitthankasem, Nirinya Sudtachat, Lukana Preechasuk, Varisara Lapinee, Nuntakorn Thongtang, Sissades Tongsima, Nattachet Plengvidhya
Annals of Medicine.2025;[Epub] CrossRef - Unraveling the understudied influence of a lead variant in the 9p21 locus on the atherogenic index among type 2 diabetes patients with coronary artery disease
Mahsa Naserian, Ahad Alizadeh, Mani Nosrati, Abdolkarim Mahrooz
Journal of Diabetes & Metabolic Disorders.2024; 23(2): 1879. CrossRef - Abdominal aortic aneurysm and cardiometabolic traits share strong genetic susceptibility to lipid metabolism and inflammation
Shufen Zheng, Philip S. Tsao, Cuiping Pan
Nature Communications.2024;[Epub] CrossRef
- Investigation of the degree of family history of diabetes in different clusters of newly diagnosed type 2 diabetes in Thailand
Brief Report
- Complications
- Acute Hyperglycemic Crises with Coronavirus Disease-19: Case Reports
- Na-young Kim, Eunyeong Ha, Jun Sung Moon, Yong-Hoon Lee, Eun Young Choi
- Diabetes Metab J. 2020;44(2):349-353. Published online April 23, 2020
- DOI: https://doi.org/10.4093/dmj.2020.0091
- 13,961 View
- 217 Download
- 72 Web of Science
- 76 Crossref
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Abstract
PDFPubReader ePub
Since the first case was contracted by coronavirus disease-19 (COVID-19) in Daegu, Korea in February 2020, about 6,800 cases and 130 deaths have been reported on April 9, 2020. Recent studies have reported that patients with diabetes showed higher mortality and they had a worse prognosis than the group without diabetes. In poorly controlled patients with diabetes, acute hyperglycemic crises such as diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic state (HHS) also might be precipitated by COVID-19. Thus, intensive monitoring and aggressive supportive care should be needed to inadequately controlled patients with diabetes and COVID-19 infection. Here, we report two cases of severe COVID-19 patients with acute hyperglycemic crises in Korea.
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Citations
Citations to this article as recorded by- Unraveling A‐β+ ketosis‐prone diabetes: An evolving diagnosis with an elusive pathogenesis
Nina Suda, Gabrielle Page‐Wilson, Jacqueline Lonier, Utpal B. Pajvani
Journal of Diabetes Investigation.2026;[Epub] CrossRef - Continuous Glucose Monitoring for Inpatients on Intravenous Insulin
Karen Good, Renu Joshi, Vanessa Snell
Clinical Nurse Specialist.2025; 39(2): 99. CrossRef - Potential Effects of Hyperglycemia on SARS-CoV-2 Entry Mechanisms in Pancreatic Beta Cells
Tara M. Michaels, M. Faadiel Essop, Danzil E. Joseph
Viruses.2024; 16(8): 1243. CrossRef - Diagnosis of acute hyperglycemia based on data-driven prediction models
Xinxin Dong, Wenping Dong, Xueshan Guo
SLAS Technology.2024; 29(5): 100182. CrossRef - COVID-19 and diabetes research: Where are we now and what does the future hold? A bibliometric visualization analysis
Xunlan Zhang, Ru Wen, Hengzhi Chen, Jian Liu, Yu Wu, Min Xu, Rongpin Wang, Xianchun Zeng
Heliyon.2024; 10(18): e37615. CrossRef - Clinical Characteristics and Predictors of Mortality in Obese African-Americans with COVID-19: a Single-Center Retrospective Study
Pavani Reddy Garlapati, Suneet Kumar, Meet Patel, Bidyut Sarker, Benjamin Tiongson, Sreedhar Adapa, Sohail Abdul Salim, Mark K. Adler, Vijay Reddy Gayam
Journal of Racial and Ethnic Health Disparities.2023; 10(1): 160. CrossRef - Diabetes and the COVID-19 pandemic
Kamlesh Khunti, Jonathan Valabhji, Shivani Misra
Diabetologia.2023; 66(2): 255. CrossRef - Adult-Onset Type 1 Diabetes Development Following COVID-19 mRNA Vaccination
Hyeyeon Moon, Sunghwan Suh, Mi Kyoung Park
Journal of Korean Medical Science.2023;[Epub] CrossRef - COVID‐19 associated ketosis and diabetic ketoacidosis: A rapid review
Tharun T. Alamuri, Sandhya Mahesh, Kevin Dell'Aquila, Taylor Jan Leong, Rebecca Jennings, Tim Q. Duong
Diabetes, Obesity and Metabolism.2023; 25(7): 1785. CrossRef - Risks associated with acute pancreatitis (AP) with diabetic ketoacidosis (DKA) in COVID-19 patients: a literature review
Sundru Manjulata Devi, Annapurna Pamreddy, Venkata Ramana Narendra
Journal of Diabetes & Metabolic Disorders.2023; 22(1): 135. CrossRef - A Review of Hyperglycemia in COVID-19
Maryam Zahedi, Saba Kordrostami, Mohammadreza Kalantarhormozi, Marziyeh Bagheri
Cureus.2023;[Epub] CrossRef - A UK nationwide study of adults admitted to hospital with diabetic ketoacidosis or hyperosmolar hyperglycaemic state and COVID‐19
Benjamin C. T. Field, Yue Ruan, Kinga A. Várnai, Jim Davies, Robert E. J. Ryder, Rajiv Gandhi, Sophie Harris, Dinesh Nagi, Dipesh Patel, Punith Kempegowda, Sarah H. Wild, Emma G. Wilmot, Kamlesh Khunti, Rustam Rea, Parth Narendran
Diabetes, Obesity and Metabolism.2023; 25(7): 2012. CrossRef - Diabetic Ketoacidosis in COVID-19 Patients: Clinical Characteristics and Outcomes – A Retrospective Study in a Single Tertiary Care Hospital, Dubai, United Arab Emirates
Hana AL Sughaiyer, Abeer AL Haj, Samia Murad Ibrahim Abdulrahman
Dubai Diabetes and Endocrinology Journal.2023; 29(2): 107. CrossRef - COVID-19 and diabetes
Artur Furga
Probacja.2023; 3: 235. CrossRef - COVID-19 SALGININDA DİYABET YÖNETİMİ VE HEMŞİRENİN ROLÜ
Dilek BÜYÜKKAYA BESEN, Merve DERVİŞOĞLU
Gazi Sağlık Bilimleri Dergisi.2022; 7(2): 78. CrossRef - Diabetic ketoacidosis and COVID-19: what have we learned so far?
Caio Oliveira de Sá-Ferreira, Camila Helena Macedo da Costa, João Campos Wiltgen Guimarães, Nathasha Souza Sampaio, Leticia de Moraes Lopes Silva, Larissa Paula de Mascarenhas, Nicollas Garcia Rodrigues, Talita Labonia dos Santos, Solange Campos, Esther C
American Journal of Physiology-Endocrinology and Metabolism.2022; 322(1): E44. CrossRef - COVID-19 and hyperglycaemic emergencies: perspectives from a developing country
Raisa Bhikoo, Marli Conradie-Smit, Gerhard Van Wyk, Sa’ad Lahri, Elizabeth Du Plessis, Jaco Cilliers, Susan Hugo, Ankia Coetzee
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Amr Shaaban Hanafy, Waseem M. Seleem, Hany A. Elkattawy
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Review
- Basic Research
- The Role of CD36 in Type 2 Diabetes Mellitus: β-Cell Dysfunction and Beyond
- Jun Sung Moon, Udayakumar Karunakaran, Elumalai Suma, Seung Min Chung, Kyu Chang Won
- Diabetes Metab J. 2020;44(2):222-233. Published online April 23, 2020
- DOI: https://doi.org/10.4093/dmj.2020.0053
- 14,632 View
- 226 Download
- 31 Web of Science
- 31 Crossref
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Abstract
PDFPubReader ePub
Impaired β-cell function is the key pathophysiology of type 2 diabetes mellitus, and chronic exposure of nutrient excess could lead to this tragedy. For preserving β-cell function, it is essential to understand the cause and mechanisms about the progression of β-cells failure. Glucotoxicity, lipotoxicity, and glucolipotoxicity have been suggested to be a major cause of β-cell dysfunction for decades, but not yet fully understood. Fatty acid translocase cluster determinant 36 (CD36), which is part of the free fatty acid (FFA) transporter system, has been identified in several tissues such as muscle, liver, and insulin-producing cells. Several studies have reported that induction of CD36 increases uptake of FFA in several cells, suggesting the functional interplay between glucose and FFA in terms of insulin secretion and oxidative metabolism. However, we do not currently know the regulating mechanism and physiological role of CD36 on glucolipotoxicity in pancreatic β-cells. Also, the downstream and upstream targets of CD36 related signaling have not been defined. In the present review, we will focus on the expression and function of CD36 related signaling in the pancreatic β-cells in response to hyperglycemia and hyperlipidemia (ceramide) along with the clinical studies on the association between CD36 and metabolic disorders.
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Brief Report
- Cardiovascular risk/Epidemiology
- Clinical Impact of Dysglycemia in Patients with an Acute Myocardial Infarction
- Jae-Wook Chung, Yeong-Seon Park, Jeong-Eon Seo, Yeseul Son, Cheol-Woo Oh, Chan-Hee Lee, Jong-Ho Nam, Jung-Hee Lee, Jang-Won Son, Ung Kim, Jong-Seon Park, Kyu-Chang Won, Dong-Gu Shin
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- DOI: https://doi.org/10.4093/dmj.2019.0164
- 9,233 View
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Graphical Abstract
Abstract
PDFPubReader ePub This study aimed to determine the impact of dysglycemia on myocardial injury and cardiac dysfunction in acute myocardial infarctions (AMIs). From 2005 to 2016, a total of 1,593 patients with AMIs who underwent percutaneous coronary intervention were enrolled. The patients were classified into five groups according to the admission glucose level: ≤80, 81 to 140, 141 to 200, 201 to 260, and ≥261 mg/dL. The clinical and echocardiographic parameters and 30-day mortality were analyzed. The peak troponin I and white blood cell levels had a positive linear relationship to the admission glucose level. The left ventricular ejection fraction had an inverted
U -shape trend, and the E/E' ratio wasU -shaped based on euglycemia. The 30-day mortality also increased as the admission glucose increased, and the cut-off value for predicting the mortality was 202.5 mg/dL. Dysglycemia, especially hyperglycemia, appears to be associated with myocardial injury and could be another adjunctive parameter for predicting mortality in patients with AMIs.-
Citations
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Review
- Others
- Continuous Glucose Monitoring Sensors for Diabetes Management: A Review of Technologies and Applications
- Giacomo Cappon, Martina Vettoretti, Giovanni Sparacino, Andrea Facchinetti
- Diabetes Metab J. 2019;43(4):383-397. Published online July 25, 2019
- DOI: https://doi.org/10.4093/dmj.2019.0121
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Abstract
PDFPubReader ePub
By providing blood glucose (BG) concentration measurements in an almost continuous-time fashion for several consecutive days, wearable minimally-invasive continuous glucose monitoring (CGM) sensors are revolutionizing diabetes management, and are becoming an increasingly adopted technology especially for diabetic individuals requiring insulin administrations. Indeed, by providing glucose real-time insights of BG dynamics and trend, and being equipped with visual and acoustic alarms for hypo- and hyperglycemia, CGM devices have been proved to improve safety and effectiveness of diabetes therapy, reduce hypoglycemia incidence and duration, and decrease glycemic variability. Furthermore, the real-time availability of BG values has been stimulating the realization of new tools to provide patients with decision support to improve insulin dosage tuning and infusion. The aim of this paper is to offer an overview of current literature and future possible developments regarding CGM technologies and applications. In particular, first, we outline the technological evolution of CGM devices through the last 20 years. Then, we discuss about the current use of CGM sensors from patients affected by diabetes, and, we report some works proving the beneficial impact provided by the adoption of CGM. Finally, we review some recent advanced applications for diabetes treatment based on CGM sensors.
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Original Articles
- Epidemiology
- Insulin Resistance and the Risk of Diabetes and Dysglycemia in Korean General Adult Population
- Jong Ha Baek, Hosu Kim, Kyong Young Kim, Jaehoon Jung
- Diabetes Metab J. 2018;42(4):296-307. Published online April 24, 2018
- DOI: https://doi.org/10.4093/dmj.2017.0106
- 14,825 View
- 227 Download
- 28 Web of Science
- 32 Crossref
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Abstract
PDFSupplementary MaterialPubReader ePub
Background Insulin resistance is a major pathogenic hallmark of impaired glucose metabolism. We assessed the accuracy of insulin resistance and cut-off values using homeostasis model assessment of insulin resistance (HOMA-IR) to classify type 2 diabetes mellitus (T2DM) and dysglycemia according to age and sex.
Methods In this cross-sectional study, we analyzed 4,291 anti-diabetic drug-naïve adults (≥20 years) from the 6th Korea National Health and Nutrition Examination Survey in 2015. Metabolic syndrome (MetS) was defined by the modified National Cholesterol Education Program III guideline. Diagnosis of dysglycemia and T2DM were based on fasting glucose and glycosylated hemoglobin levels. The receiver operating characteristic curve and optimal cut-off values of HOMA-IR were assessed to identify T2DM/dysglycemia according to sex and were further analyzed by age.
Results Sex differences were found in the association of MetS and the different MetS components with T2DM/dysglycemia. The overall optimal cut-off value of HOMA-IR for identifying dysglycemia was 1.6 in both sex. The cut-off values for T2DM were 2.87 in men and 2.36 in women. However, there are differences in diagnostic range of HOMA-IR to distinguish T2DM according to sex and age, and the accuracy of HOMA-IR in identifying T2DM gradually decreased with age especially in women.
Conclusion Insulin resistance is closely associated with the risk for T2DM/dysglycemia. The accuracy of HOMA-IR levels is characterized by sex- and age-specific differences in identifying T2DM. In addition to insulin resistance index, insulin secretory function, and different MetS components should be considered in the detection of early T2DM, especially in elderly.
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- Comparison of Glucose Area Under the Curve Measured Using Minimally Invasive Interstitial Fluid Extraction Technology with Continuous Glucose Monitoring System in Diabetic Patients
- Mei Uemura, Yutaka Yano, Toshinari Suzuki, Taro Yasuma, Toshiyuki Sato, Aya Morimoto, Samiko Hosoya, Chihiro Suminaka, Hiromu Nakajima, Esteban C. Gabazza, Yoshiyuki Takei
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Abstract
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Background Continuous glucose monitoring (CGM) is reported to be a useful technique, but difficult or inconvenient for some patients and institutions. We are developing a glucose area under the curve (AUC) monitoring system without blood sampling using a minimally invasive interstitial fluid extraction technology (MIET). Here we evaluated the accuracy of interstitial fluid glucose (IG) AUC measured by MIET in patients with diabetes for an extended time interval and the potency of detecting hyperglycemia using CGM data as a reference.
Methods Thirty-eight inpatients with diabetes undergoing CGM were enrolled. MIET comprised a pretreatment step using a plastic microneedle array and glucose accumulation step with a hydrogel patch, which was placed on two sites from 9:00 AM to 5:00 PM or from 10:00 PM to 6:00 AM. IG AUC was calculated by accumulated glucose extracted by hydrogel patches using sodium ion as standard.
Results A significant correlation was observed between the predicted AUC by MIET and CGM in daytime (
r =0.76) and nighttime (r =0.82). The optimal cutoff for the IG AUC value of MIET to predict hyperglycemia over 200 mg/dL measured by CGM for 8 hours was 1,067.3 mg·hr/dL with 88.2% sensitivity and 81.5% specificity.Conclusion We showed that 8-hour IG AUC levels using MIET were valuable in estimating the blood glucose AUC without blood sampling. The results also supported the concept of using this technique for evaluating glucose excursion and for screening hyperglycemia during 8 hours in patients with diabetes at any time of day.
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Reviews
- The Role of Glucagon-Like Peptide-1 Receptor Agonists in Type 2 Diabetes: Understanding How Data Can Inform Clinical Practice in Korea
- Seungjoon Oh, Suk Chon, Kyu Jeong Ahn, In-Kyung Jeong, Byung-Joon Kim, Jun Goo Kang
- Diabetes Metab J. 2015;39(3):177-187. Published online June 15, 2015
- DOI: https://doi.org/10.4093/dmj.2015.39.3.177
- 8,369 View
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Abstract
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Glucagon-like peptide-1 receptor agonists (GLP-1RAs) reduce glycosylated hemoglobin (HbA1c, 0.5% to 1.0%), and are associated with moderate weight loss and a relatively low risk of hypoglycemia. There are differences between Asian and non-Asian populations. We reviewed available data on GLP-1RAs, focusing on Korean patients, to better understand their risk/benefit profile and help inform local clinical practice. Control of postprandial hyperglycemia is important in Asians in whom the prevalence of post-challenge hyperglycemia is higher (vs. non-Asians). The weight lowering effects of GLP-1RAs are becoming more salient as the prevalence of overweight and obesity among Korean patients increases. The higher rate of gastrointestinal adverse events amongst Asian patients in clinical trials may be caused by higher drug exposure due to the lower body mass index of the participants (vs. non-Asian studies). Data on the durability of weight loss, clinically important health outcomes, safety and optimal dosing in Korean patients are lacking. Use of GLP-1RAs is appropriate in several patient groups, including patients whose HbA1c is uncontrolled, especially if this is due to postprandial glucose excursions and patients who are overweight or obese due to dietary problems (e.g., appetite control). The potential for gastrointestinal adverse events should be explained to patients at treatment initiation to facilitate the promotion of better compliance.
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Jeonghee Han, Woo Je Lee, Kyu Yeon Hur, Jae Hyoung Cho, Byung Wan Lee, Cheol-Young Park
Diabetes & Metabolism Journal.2024; 48(3): 418. CrossRef - Tolerability and Effectiveness of Switching to Dulaglutide in Patients With Type 2 Diabetes Inadequately Controlled With Insulin Therapy
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Frontiers in Endocrinology.2022;[Epub] CrossRef - Antihyperglycemic Agent Therapy for Adult Patients with Type 2 Diabetes Mellitus 2017: A Position Statement of the Korean Diabetes Association
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- Diabetes Metab J. 2014;38(5):330-336. Published online October 17, 2014
- DOI: https://doi.org/10.4093/dmj.2014.38.5.330
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Abstract
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As the prevalence of diabetes mellitus is substantially increasing worldwide, associated diseases such as renal failure, cardiovascular diseases, fatty liver, and cancers have also increased. A number of cancers such as pancreatic, liver, breast, and female reproductive cancers have shown an increased prevalence and a higher mortality rate in diabetic patients compared to healthy subjects. Thus, this suggests an association between diabetes, especially type 2 diabetes and cancer incidence and progression. Recent studies have suggested that hyperinsulinemia, chronic inflammation and hyperglycemia, all frequently seen in diabetics, may lead to increased tumor growth; the underlying molecular mechanisms of this association are not fully understood. In particular, chronic hyperglycemic episodes could serve as a direct or indirect mediator of the increase in tumor cell growth. Here, we will discuss our current understanding how hyperglycemia and cancer risk may be linked, and what the implications are for the treatment of diabetic cancer patients.
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- DOI: https://doi.org/10.4093/dmj.2011.35.1.8
- 9,285 View
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- 26 Crossref
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Abstract
PDFPubReader ePub
Diabetic vascular complications are among the leading causes of morbidity and mortality in diabetic patients. In the past, many studies have focused on the mechanisms of hyperglycemia-induced chronic vascular complications via the formation of toxic metabolites such as oxidative stress, advanced glycosylated end products, persistent activation of protein kinase C, and increased sorbitol concentrations. However, vascular complications result from imbalances caused by increases in systemic toxic metabolites, such as those that occur under conditions of hyperglycemia and dyslipidemia, and by reductions in endogenous protective factors such as insulin, vascular endothelial growth factor, and platelet derived growth factor. This review outlines some of the evidence supporting the importance of enhancing endogenous regenerative factors.
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Original Articles
- The Association of Brachial-Ankle Pulse Wave Velocity with 30-Minute Post-Challenge Plasma Glucose Levels in Korean Adults with No History of Type 2 Diabetes
- Eun-Suk Choi, Eun-Jung Rhee, Ji-Hoon Choi, Ji-Cheol Bae, Seung-Hyun Yoo, Won-Jun Kim, Se-Eun Park, Cheol-Young Park, Won-Young Lee, Yong-Kyun Cho, Ki-Won Oh, Sung-Woo Park, Sun-Woo Kim
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- DOI: https://doi.org/10.4093/kdj.2010.34.5.287
- 6,939 View
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Abstract
PDFPubReader ePub
Background Acute postprandial hyperglycemia is an important affector for atherosclerosis in subjects with glucose intolerance. We analyzed the relationship of brachial-ankle pulse wave velocity (baPWV) with fasting and post-challenge plasma glucose levels according to different time points during oral glucose tolerance test (OGTT).
Methods In 663 subjects with fasting hyperglycemia, 75 g OGTT were performed to confirm the glucose tolerant status, and fasting, post-challenge 30-minute and 120-minute glucose levels were measured. Anthropometric measurements were done, and fasting lipid profiles were measured. baPWV were measured in all subjects and the relationship between fasting, 30- and 120-minute post-challenge glucose levels and baPWV were analyzed.
Results Among the participants, 62.9% were prediabetes and 31.7% were diabetes. Mean baPWV value was significantly higher in subjects with diabetes compared with prediabetes group. In bivariate correlation analyses, age, blood pressure, total cholesterol, low density lipoprotein cholesterol, 30-minute and 120-minute post-challenge glucose levels showed significant positive correlation with baPWV value. In multiple regression analysis, 30-minute post-challenge glucose level was a weak but significant determinant for mean baPWV value even after adjustment for other confounding variables.
Conclusions Postprandial hyperglycemia, especially 30-minute glucose levels showed significant correlation with baPWV in subjects with fasting hyperglycemia. These results can imply the deleterious effect of acute hyperglycemic excursion on arterial stiffness in subjects with glucose intolerance.
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Atsuko Tsuboi, Chikako Ito, Rumi Fujikawa, Hideya Yamamoto, Yasuki Kihara
Internal Medicine.2015; 54(16): 1961. CrossRef - Insulin Sensitivity and Beta-Cell Function Are Associated with Arterial Stiffness in Individuals without Hypertension
Chuchen Meng, Min Sun, Zhixiao Wang, Qi Fu, Mengdie Cao, Zhenxin Zhu, Jia Mao, Yun Shi, Wei Tang, Xiaoping Huang, Yu Duan, Tao Yang
Journal of Diabetes Research.2013; 2013: 1. CrossRef - Urinary adiponectin concentration is positively associated with micro- and macro-vascular complications
Won Seon Jeon, Ji Woo Park, Namseok Lee, Se Eun Park, Eun Jung Rhee, Won Young Lee, Ki Won Oh, Sung Woo Park, Cheol-Young Park, Byung-Soo Youn
Cardiovascular Diabetology.2013;[Epub] CrossRef
- One-Hour Post-Load Plasma Glucose Levels are Associated with Early Arterial Stiffness in Subjects with Different Glucose Tolerance
- The Changes in Early Phase Insulin Secretion in Newly Diagnosed, Drug Naive Korean Prediabetes Subjects
- Sang Youl Rhee, Joo Young Kim, Suk Chon, You Cheol Hwang, In Kyung Jeong, Seungjoon Oh, Kyu Jeung Ahn, Ho Yeon Chung, Jeong-taek Woo, Sung Woon Kim, Jin-Woo Kim, Young Seol Kim
- Korean Diabetes J. 2010;34(3):157-165. Published online June 30, 2010
- DOI: https://doi.org/10.4093/kdj.2010.34.3.157
- 7,871 View
- 36 Download
- 15 Crossref
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Abstract
PDFPubReader ePub
Background There have been no systematic observations regarding changes in early phase insulin secretion among Korean prediabetes and early stage type 2 diabetes mellitus (T2DM) patients.
Methods We conducted 75-g oral glucose tolerance tests (OGTT) in 873 subjects with suspected abnormal glucose tolerance. All subjects were diagnosed as having normal glucose tolerance (NGT), prediabetes (preDM), or T2DM according to the OGTT results and the insulin secretory and insulin resistance indices of each subject were calculated. Additionally, we analyzed the changes in early phase insulin secretion according to changes in fasting (Glc0), post-prandial (Glc120) glucose and HbA1c (A1c) levels.
Results As compared to subjects with NGT, the insulin secretory indices of the preDM and T2DM subjects progressively declined, and the insulin resistance indices were progressively aggravated. Early phase insulin secretion decreased rapidly according to the increments of Glc0, Glc120 and A1c, and these changes were most prominent in the NGT stage. Compared to the control group, the early phase insulin secretion levels of the preDM or T2DM subjects were less than 50% when Glc0 was over 100 mg/dL, Glc120 was over 145 mg/dL, and A1c was over 5.8%.
Conclusion This study suggests that progressive beta cell dysfunction in Koreans may be initiated and rapidly aggravated during the period generally designated as 'normal.'
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Citations
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C.‐H. Kim, H.‐K. Kim, E. H. Kim, S. J. Bae, J.‐Y. Park
Diabetic Medicine.2013; 30(9): 1075. CrossRef - Associations among Body Mass Index, Insulin Resistance, and Pancreatic β-Cell Function in Korean Patients with New-Onset Type 2 Diabetes
Jin Ook Chung, Dong Hyeok Cho, Dong Jin Chung, Min Young Chung
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Y. Heianza, Y. Arase, K. Fujihara, H. Tsuji, K. Saito, S. D. Hsieh, S. Kodama, H. Shimano, N. Yamada, S. Hara, H. Sone
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Sang Youl Rhee, Jeong-Taek Woo
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Chul-Hee Kim
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Review
- Glycemic Index Revisited.
- In Joo Kim
- Korean Diabetes J. 2009;33(4):261-266. Published online August 1, 2009
- DOI: https://doi.org/10.4093/kdj.2009.33.4.261
- 4,237 View
- 61 Download
- 14 Crossref
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Abstract
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- The implementation of effective dietary strategies is important for diabetes management. Dietary carbohydrate is the main factor determining blood sugar level, especially in the postprandial period. Carbohydrate-rich diets can have deleterious effects on glycemic control in diabetic patients and may play an important role in the development of cardiovascular diseases. Low glycemic diets have been reported to have beneficial effects for diabetes control and cardiovascular risk factors. However, according to the American Diabetes Association recommendations for medical nutrition therapy, monitoring carbohydrate intake, whether by carbohydrate counting, exchange, or experience-based estimation, remains a key strategy for achieving glycemic control, with the use of the glycemic index and glycemic load recommended only as an auxiliary method that may provide a modest additional benefit for glycemic control over the effects observed when total carbohydrate is considered alone. Recently, an increasing amount of clinical evidence supports the efficacy of low glycemic diets for the management of diabetes. The development of practical methods to apply the glycemic index and glycemic load to the management of diabetes in clinical settings is warranted.
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Do Yeon Kim, Hansongyi Lee, Eun Young Choi, Hyunjung Lim
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Jeong-a Yoo
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Kyung Won Paek, Ki Hong Chun, Soo Jin Lee
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Original Article
- The Effect of Chronic High Glucose Concentration on Endoplasmic Reticulum Stress in INS-1 Cells.
- Mi Kyung Kim, Hye Young Seo, Tae Sung Yun, Nam Kyung Kim, Yu Jin Hah, Yun Jung Kim, Ho Chan Cho, Young Yun Jang, Hye Soon Kim, Seong Yeol Ryu, In Kyu Lee, Keun Gyu Park
- Korean Diabetes J. 2008;32(2):112-120. Published online April 1, 2008
- DOI: https://doi.org/10.4093/kdj.2008.32.2.112
- 4,002 View
- 49 Download
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Abstract
PDF
- BACKGROUND
The highly developed endoplasmic reticulum (ER) structure is one of the characteristic features of pancreatic beta-cells. Recent study showed that ER stress causes beta-cell dysfunction. However, little is known about the effects of high glucose concentration on induction of ER stress in pancreatic beta-cells. Therefore, this study was designed to evaluate whether exposure of high glucose concentration in rat insulinoma cell line, INS-1 cell induces ER stress and whether ER stress decreases insulin gene expression. METHODS: The effect of 30 mM glucose on insulin expression and secretion in INS-1 cells was evaluated by Northern blot analysis and glucose-stimulated insulin secretion (GSIS). Cell viability was evaluated by XTT assay. The effect of 30 mM glucose on phosphorylation of eIF2alpha and CHOP expression, which are markers of ER stress were evaluated by Western blot analysis. RT-PCR analysis was performed to determine whether high glucose concentration induces XBP-1 splicing. To investigate whether ER stress decreases insulin gene expression, the effect of tunicamycin on insulin mRNA expression was evaluated by Northern blot analysis. RESULTS: The prolonged exposure of INS-1 cells with the 30 mM glucose concentration decreased insulin mRNA expression in a time dependent manner and impaired GSIS while did not influence on cell viability. 30 mM glucose increased phosphorylation of eIF2alpha, XBP-1 splicing and CHOP expression in INS-1 cells. Tunicamycin-treated INS-1 increased XBP-1 splicing and decreased insulin mRNA expression in a dose dependent manner. CONCLUSION: This study showed that prolonged exposure of INS-1 with high glucose concentration induces ER stress and ER stress decreases insulin gene expression. Further studies about underlying molecular mechanism by which ER stress induces beta-cell dysfunction are needed.
Case Report
- A Case of Cured Diabetes Mellitus after Occult Malignant Pheochromocytoma Removal.
- Ho Chan Cho, Hye Soon Kim, Yoon Jung Kim, Yu Jin Hah, Nam Keong Kim, Mi Kyung Kim, Keun Gyu Park, Yong Hoon Kim, Sun Young Kwon
- Korean Diabetes J. 2007;31(6):520-524. Published online November 1, 2007
- DOI: https://doi.org/10.4093/jkda.2007.31.6.520
- 3,864 View
- 23 Download
- 1 Crossref
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Abstract
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- Pheochromocytoma is characterized by a combination of various clinical manifestations that include the classic triad of severe headache, palpitations and diaphoresis. In addition, hyperglycemia can be caused by overproduction of catecholamines, which are secreted by a catecholamine-secreting neoplasm of adrenal or extra-adrenal chromaffin tissue. We encountered a case of diabetes with an occult malignant adrenal pheochromocytoma, who did not have any classic manifestations. A 37-year-old male was admitted because of polydipsia, polyuria, and weight loss. Fasting blood glucose level was 497 mg/dL, hemoglobin A1c level was 15%, and diabetic retinopathy and peripheral polyneuropathy were also accompanied. Incidentally, right adrenal mass was detected by ultrasonography of abdomen. Urinary excretion of total metanephrine and epinephrine were elevated. Adrenal CT showed a 7.1 cm sized right adrenal cystic mass with enhancing solid portion and hemorrhagic content. The scan with 123I-MIBG revealed the cystic mass with increased rim uptake in the region of right adrenal gland. After removal of the tumor, the increased levels of catecholamine were normalized. Moreover, blood glucose level was normalized without administration of insulin or oral hypoglycemic agents. The pathologic examination showed that the neoplasm was a malignant adrenal pheochromocytoma. We report this case that diabetes was cured after removal of malignant tumor with literature review at first in Korea.
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Citations
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Chai Ryoung Eun, Jae Hee Ahn, Ji A Seo, Nan Hee Kim
Endocrinology and Metabolism.2014; 29(1): 83. CrossRef
- Pheochromocytoma with Markedly Abnormal Liver Function Tests and Severe Leukocytosis
Original Articles
- Alteration of Hypertonic Responses in Hyperglycemic Human Retinal Pigment Epithelial and Placental Cells.
- Won Kun Park
- Korean Diabetes J. 2004;28(3):164-176. Published online June 1, 2004
- 1,301 View
- 21 Download
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Abstract
PDF
- BACKGROUND
In mammals, cellular protection from hypertonic damage is achieved by increasing the expression of genes, such as aldose reductase(AR) and Na+/myo-inositol transporter(SMIT). Recent studies have revealed that tonicityresponsive enhancer binding protein(TonEBP) regulates the increased transcription of these genes. Increased AR gene expression leads to hyperglycemiainduced cellular impairment, and the degree of basal aldose reductase gene expression influences the development of diabetic complication. The alteration of cellular protection genes, such as AR, SMIT, HSP(Heat Shock Protein) 70 and TonEBP, from hypertonic stress in the presence of sustained hyperglycemia was examined in human retinal pigment epithelial(hRPE) and placental cells. METHODS: After the cultures became confluent, the hRPE cells were exposed to 25mM glucose, 100mM NaCl or both for 1, 2 and 3 days. The expressions of AR, SMIT and HSP70 were determined by northern blot analysis. Decreased inductions of the hypertonicity in AR and SMIT mRNA were first evident after exposure to 25mM glucose after 1 day, achieving near maximal level after 3 days; however, no significant alteration in the HSP70 mRNA was noted at any time. For these reasons, the alteration of cellular protection genes, such as AR, SMIT and TonEBP, in hRPE and placental cells were examined after 3-days exposure to the various experimental conditions. The cells were incubated in serum-free media, containing 5.5 or 25mM glucose, 100mM NaCl(in hRPE cells) or 75mM NaCl(in placental cells) and 25mM glucose+100mM NaCl(in hRPE cells) or 75mM NaCl(in placental cells), with or without 20muM tolrestat for 72hrs, at which time the expressions of AR, SMIT and TonEBP were determined. To examine the role of cellular ionic strength in hyperglycemic hRPE cells, excess(5mM) betaine was added to the medium to accelerate the accumulation of the compatible osmolyte, which should lead to a strength reduction. RESULTS: In the hRPE and placental cells, incubated in media with 25mM glucose+100mM(in hRPE cells) or 75mM(in placental cells) NaCl, the AR and SMIT mRNA levels were decreased compared to those cells incubated in media with 100mM(in hRPE cells) or 75mM(in placental cells) NaCl alone. Significant prevention of these decreased AR and SMIT mRNA levels were also observed in those cells incubated with tolrestat. The addition of betaine reduced the abundance of AR and SMIT mRNA in hypertonic stress, similar to in hypertonic and hyperglycemic cells. The inhibition of aldose reductase due to tolrestat in hyperglycemic and hypertonic media was complete in the media not containing betaine. CONCLUSION: Under conditions where sorbitol rapidly increases in hypertonic and hyperglycemic medium should be an important new system for exploring the mechanism of cellular impairment to the effects of hyperglycemia. The expressions of AR and SMIT genes that may influence the development of diabetic complication were down-regulated by the intracellular accumulation of sorbitol in sustained hyperglycemia, and the reliable effect of AR inhibitors on the biological improvements were verified in hyperglycemic cells.
- The Effects of High Glucose, Insulin and TGF-beta 1 on Proliferation and Differentiation of the Pancreatic Stellate Cells.
- Oak Kee Hong, Hyuk Sang Kwon, Kyu Hyun Yeom, Marie Lee, Ji Hun Yang, Seung Hyeon Ko, Soon Jib Yoo, Hyun Sik Son, Kun Ho Yoon, Bong Yeon Cha, Kwang Woo Lee, Ho Yong Son, Sung Koo Kang
- Korean Diabetes J. 2003;27(3):228-240. Published online June 1, 2003
- 1,816 View
- 34 Download
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Abstract
PDF
- BACKGROUND
Although chronic pancreatitis gives rise to fibrosis of pancreatic exocrine tissue, and type 2 diabetes is accompanied by pancreatic fibrosis, the mechanisms of fibrogenesis in the pancreas have been insufficiently studied. The activated Pancreatic stellate cells (PSC) have recently been identified in human and experimental fibrotic areas from chronic panceatitis tissues. As PSC are similar in their morphology and biochemistry to hepatic stellate cells, they are suspected to play the same role in pancreatic fibrogenesis as the hepatic stellate cells in liver fibrosis. The PSC were isolated from the rat pancreata, and mediators stimulating the proliferation and differentiation identified. METHODS: The pancreatic stellate shaped cells were isolated by a minor modification to the method described by Apte et al (ref), using a Nycodenz gradient. The isolated PSCs were confirmed by phase-contrast and by the immunofluorescence of vimentin, desmin and smooth muscle a-actin (a-SMA). The level of alpha-SMA was quantified by Western blot in the PSCs in the culture, over time, and the cell proliferation was measured by 3[H]-Thymidine incorporation. The effect of the proliferation and differentiation of the PSC were assessed in relation to D-glucose (500 mg/dL), Insulin (10 IU/mL) and TGF-beta (10 ng/mL) treatment of the culture medium. RESULTS: The stellate shaped cells from the rat pancreata grew readily in the culture. Unactivated PSCs, cultured for 3 days, had an angular appearance, contained lipid droplets, manifesting positive vitamin A autofliuorescence, and stained positively for vimentin and desmin, but negatively for alpha-SMA. Within 4~8 days of primary culturing, the PSCs were activated, the sizes and numbers of the fat droplets decreased, the cells flattened, developed long cytoplasmic extensions and expressed alpha-SMA. After 3 passages, almost 100% of the cells were positive for alpha-SMA expression, indicating a myofibroblast type of differentiation in vitro. The addition of high-glucose concentrations and insulin to the activated PSCs significantly stimulated cell proliferation (194.4+/-8.3, 175.0+/-31.0 vs. control), and when the combination of high- glucose and insulin was applied, the cell proliferation was increased to an even greater extent (247.0+/-21.8 vs. control). CONCLUSIONS: Pancreata stellate cells can be isolated, and cultured in vitro, from normal SD rats. High concentrations of glucose and insulin in culture medium activated the PSC proliferation.
- Effect of Nerve Growth Factor on Cultured Mouse Dorsal Root Ganglion Cells in Hyperglycemic Condition.
- Byoung Hyun Park, Chung Gu Cho, Geun Young Jang, Ki Hun Kim, Seung Taeck Park
- Korean Diabetes J. 2001;25(4):286-296. Published online August 1, 2001
- 1,640 View
- 24 Download
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Abstract
PDF
- BACKGROUND
Multiple etiology of diabetic neuropathy has been proposed, including altered polyol metabolism, superoxide radical formation, protein glycation, vascular insufficiency, blunted nitric oxide production and neurotrophic factor (NTF) deficiency. Nerve growth factor (NGF) is a member and family of neurotrophic factors. NGF is produced in tissues innervated by its responsive neurons. In the peripheral nervous system, NGF messenger RNA (mRNA) is produced in target fields of small pain and temperature-mediating dorsal root ganglia (DRG) sensory neurons and sympathetic neurons. NGF has been shown to promote their survival, differentiation, and maintenance. However, the mechanism of neuronal damage in diabetes and the effect of NGF on diabetic neuropathy are not clear. METHODS: In order to clarify the effect of NGF, the changes of cell viability were evaluated by MTT assay on mouse cultured dorsal root ganglion cells which were grown with media containing concentrations of high glucose for inducing hyperglycemic condition. Furthermore, the neuroprotective effect of nerve growth factor (NGF) against hyperglycemia-induced dorsal root ganglion cell changes were also examined. RESULTS: 1. Cell viability of cultured mouse dorsal root ganglion cells treated with hyperglycemic media made with 15, 25 mM glucose was markedly decreased in a dose-dependent manner when compared with control medium (normoglycemic medium) containing concentration of 5.5 mM glucose (p<0.05). 2. Cultured dorsal root ganglion cells exposed to hyperglycemic medium made with 25 mM glucose for 72 hours showed morphological changes such as dissociations, loss of neurites and decrease of cell viability (p<0.05). 3. Pretreatment of 150 ng/mL NGF for 2 hours significantly increased the cell viability of cultured dorsal root ganglion cells which exposed to hyperglycemic medium (25 mM glucose for 72 hours). CONCLUSION: Findings from this study suggested that hyperglycemic condition induces the decrease of cell viability and morphological changes (loss of neurites, dissociation) on cultured dorsal root ganglion cells of mouse. Furthermore, selective neurotrophic factors such as NGF are very effective in preventing dysfunction and morphological changes of DRG cells induced by hyperglycemic condition.
- Study on the Mechanism of Neutrophil Adhesion to Retinal Capillary Endothelial Cells under High Glucose Condition.
- Seok Man Son, Young Sil Lee, Chang Won Lee, Seok Dong Yoo, In Ju Kim, Yong Ki Kim
- Korean Diabetes J. 2001;25(1):35-49. Published online February 1, 2001
- 1,459 View
- 19 Download
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Abstract
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- BACKGROUND
Diabetic retinopathy is a leading cause of adult vision loss and blindness. Much of the retinal damage that characterizes the disease results from retinal vascular leakage and occlusion. Capillary occlusion is the result of microvascular thrombi in which erythrocytes, platelets and leukocytes each may play a major role. Thus, we investigated the pathogenesis of leukocyte stasis by exposing bovine retinal capillary endothelial cells (BRCECs) for high glucose concentration. METHODS: We examined the adhesion of neutrophils to BRCECs incubated in media containing 5.5-30 mmol/L D-glucose for 24 hours. We also measured the expression of E-selectin on endothelial cells and the activation of NF(nuclear transcription factor)-kappaB in nuclear fractions of endothelial cells by using electrophoretic mobility shift assay. RESULTS: We observed that 30 mmol/L D-glucose significantly increased the adhesion of neutrophils to BRCECs (12.5% vs. 3.0%, p<0.01) and migration of neutrophil across cultured BRCEC monolayers (41.0% vs. 21.0%, p<0.05) in respect to 5.5 mmol/L D-glucose. The expression of E-selectin was increased incubated with 30 mmol/L D-glucose compared with 5.5 mmol/L D-glucose (1.45 OD vs. 0.54 OD, p<0.01). Electrophoretic mobility shift assay of nuclear extracts of BRCECs exposed for 24 h to 30 mmol/L D-glucose revealed an intense NF-kappaB activation compared with cells cultured in 5.5 mmol/L D-glucose (8.72x104 countsxmm2 vs.1.88x104 countsxmm2, p<0.01). CONCLUSION: These results suggest that high glucose concentration promote neutrophil adhesion to the BRCECs through upregulation of cell surface expression of E-selectin, possibly depending on NF-kappaB activation and may have implications for the induction of microvasculopathy of diabetic retinopathy.
- Mechanism of the lnsulin Secretory Defect by Chronically Elevated Glucose Leveis in Pancreatic lslets: Depletion of lnsulin Content due to Hyperstimulation by Glucose.
- Yeon Ah Sung, Young Sun Hong
- Korean Diabetes J. 2000;24(1):1-9. Published online January 1, 2001
- 1,286 View
- 19 Download
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Abstract
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- BACKGROUND
Type 2 diabetes is characterized by impaired insulin secretion and decreased insulin sensitivity, although the exact relationship between these two derangements during the development of the disease has not been fully established. Hyperglycemia per se impairs insulin secretion in pancreatic B-cell and the mechanism of impaired insulin by chronic hyperglycemia could be the clue to clarify pathogenesis of type 2 diabetes, and possibly identify the treatments. This study was performed to elucidate the mechanism of impairment of glucose induced insulin secretion by chronic hyperglycemia in pancreatic islets. METHODS: Pancreatic islets were isolated from Sprague-Dawley rats. After incubation of islets in high glucose (20mM) and low glucose (5mM) media for 10 days, glucose (16.7 mM) induced insulin secretion and insulin and DNA content in the islets were measured. Then subcellular distribution of low molecular and heterotrimeric G-proteins were assessed by ADP-ribosylation and radiolabeled GTP binding. RESULTS: 1) Glucose-induced insulin secretion of the islets cultured for 10 days in high glucose media was significantly lower when compared with that in islets cultured in low glucose media (p<0,05) 2) Subcellular distributions of low and heterotrimeric G-protein was not different in the islets cultured in low glucose when compared to those cultured in high glucose. 3) lnsulin content was significantly lower in the islets cultured in high glucose media compared with that in islets cultured in low glucose media (p<0.05) 4) DNA content was not significantly different between the islets cultured in low and high glucose media, and insulin content to DNA ratio was significantly lower in the islets cultured in high glucose media compared with that in islets cultured in low glucose media (p<0.05). CONCLUSION: Impaired insulin secretion to glucose in pancreatic islets exposed to high glucose is caused by depletion of insulin stores affer hyperstimulation.
- Effect of Hyperglycemia on Internalization of Insulin-receptor Complexes in Human Umbilical Vein Endothelial Cells.
- Ki Ho Song, Yu Bae Ahn, Je Ho Han, Soon Jip Yoo, Kun Ho Yoon, Moo Il Kang, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Koo Kang
- Korean Diabetes J. 1999;23(2):131-141. Published online January 1, 2001
- 1,700 View
- 28 Download
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Abstract
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- BACKGROUND
It is well known that hyperglycemia activates protein kinase C (PKC) in vascular endothelial cells. However, the effect of hyperglycemia on internalization and recycling of insulin receptors by insulin in endothelial cells has not been examined thus far. METHODS: Human umbilical vein endothelial cells (HUVECs) were isolated from healthy, pregnant women. Confluent HUVECs were incubated in a culture media containing either 5 (NG group) or 25 mM glucose (HG group) for 4 days. Then, we measured the insulin binding, internalization and recycling of the insulin receptor and release of internalized insulin into the media. RESULTS: There was no difference in binding of 0.17 nM 125I-insulin between the two groups. However, the amount of internalized 125I-insulin, determined by the aeid washing method, was significantly greater in the HG group compared to the NG group. The addition of 10 pM 1-(5-isoquino-linesulfonyl)-2-methyl-piperazine (H7), a PKC inhibitor, to the HG group prevented the increase of internalization in 125I-insulin. In addition, preincubation with unlabeled insulin resulted in a decrease of 125I-insulin binding to a greater extent in the HG group compared with the NG group, indicating that high glucose levels increased internalizntion of insulin receptors. The high glucose-induced increase in internalization of insulin receptors was prevented by an addition of H7. Recycling of insulin receptors to the cell surface was not affected by high glucose. Internalized 125I-insulin released into media with time. The released amount of I-insulin in the HC group tended to be greater compared to the NG group. CONCLUSION: These results suggest that hyperglycemia may increase internalization of the insulin-receptor complexes in vascular endothelial cells through PKC activation.
- The Effect of Acute Hyperglycemia on Endothelial Function in Type 2 Diabetes.
- Sang Jun Lee, Dong Wook Lee, In Kyu Lee
- Korean Diabetes J. 2000;24(5):574-586. Published online January 1, 2001
- 1,733 View
- 16 Download
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Abstract
- BACKGROUND
Multiple studies in patients with diabetes demonstrate impaired endothelial-dependent vasodilation. But the mechanisms of vascular dysfunction in type 2 diabetes are still controversial. Some risk factors, such as dyslipidemia, hypertension and obesity, are commonly associated with type 2 diabetes. These risk factor may cause endothelial dysfunction. And hyperglycemia may have a specific role in the increased risk of vascular complications in diabetes but it remains unclear. The purpose of this study was to examine whether endothelial dysfunction occurs when acute hyperglycemia is induced by oral glucose loading. METHOD: Using the high-resolution ultrasound, we measured flow-mediated vasodilation (endothelial dependent vasodilation: FMD) during oral glucose tolerance test in 11 men (mean age: 59+/-5 years) with type 2 diabetes without chronic diabetic complications. For statistical analysis, we used paired t-test, generalized linear method (GLM) to compare FMD before and after glucose loading. RESULT: Flow-mediated vasodilation was diminished after glucose loading (13.2+/- 6.4%, 7.3+/-3.3*%, 12.8+/-5.6%, in fasting, at 1- and 2-h, respectively; *p<0.001 vs fasting). Superoxide anion formation by neutrophils was increased after glucose loading (4.65+/-2.8, 6.17+/-2.2, in fasting, at 1-h respectively: p<0.05 vs fasting)( 10-7nmol/106cells/30min). Endothelial independent vasodilation was not significantly affected by glucose loading. The concentration of triglyceride were not changed after glucose loading. CONCLUSION: This study shows that acute hyperglycemia induced by 75 gm oral glucose intake results in endothelial dysfunction. These results suggest that prolonged and repeated hyperglycemia may play an important role in the developement and progression of vascular complication in diabetes.
- The Changes in Insulin Secretion and GTPase Activity after the Exposure to High Glucose in Rat Pancreatic Islets.
- Young Sun Hong, Yeon Ah Sung, Nan Ho Kyung
- Korean Diabetes J. 2000;24(5):515-523. Published online January 1, 2001
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Abstract
- BACKGROUND
Type 2 diabetes mellitus is characterized by defective glucose- induced and glucose-potentiated insulin secretion. Chronic elevation of glucose levels are considered to be a cause of impaired insulin secretion. It has been suggested that such defects in insulin secretion can be related to the alteration in stimulus-secretion coupling. Recent studies have provided evidences for the existence of guanine nucleotide-binding protein (G protein), and the regulatory role of G protein and GTPase activity in stimulus-secretion coupling in pancreatic islets. This study was performed to determine whether the exposure to high glucose concentration alters GTPase activity with decreased insulin secretion in pancreatic islets isolated from normal rats. METHODS: Pancreatic islets isolated from normal Sprague-Dawley rats were incubated in high (20 mM) and low (5 mM) glucose concentration for 48 hours. After incubation, glucose (20 mM) induced insulin secretion was measured. Then subcellular fractions of islets by homogenization and differential centrifugation were obtained and glucose induced inhibition of GTPase activities in each fraction was measured. RESULTS: 1) After 48 hour exposure to 5 mM and 20 mM glucose, insulin secretion in response to 20 mM glucose were 134.4+/-16.8 fmol/10 islets/hr and 90.0+/-10.2 fmol/10 islets/hr, respectively. After the exposure to high glucose, glucose-induced insulin secretion significantly decreased (p<0.05). 2) In each subcellular fraction, there was no significant difference between the islets exposed to 5 mM and 20 mM glucose in the degree of inhibition of GTPase activities by high glucose. CONCLUSION: The exposure to high glucose for 48 hours decreased insulin secretion without any significant differences in the degree of inhibition of GTPase activities. This results suggest that impaired insulin secretion by high glucose is not associated with the change in GTPase activity.
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