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Original Articles
Obesity and Metabolic Syndrome
Beneficial Effects of Aerobic Exercise Training Combined with Rosiglitazone on Glucose Metabolism in Otsuka Long Evans Tokushima Fatty Rats
Shan-Ji Piao, So Hun Kim, Young Ju Suh, Seong-Bin Hong, Seong Hee Ahn, Da Hae Seo, In-Sun Park, Moonsuk Nam
Diabetes Metab J. 2017;41(6):474-485.   Published online November 15, 2017
DOI: https://doi.org/10.4093/dmj.2017.41.6.474
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AbstractAbstract PDFPubReader   
Background

Regular aerobic exercise is essential for the prevention and management of type 2 diabetes mellitus and may be particularly beneficial for those treated with thiazolidinediones, since it may prevent associated weight gain. This study aimed to evaluate the effect of combined exercise and rosiglitazone treatment on body composition and glucose metabolism in obese diabetes-prone animals.

Methods

We analyzed metabolic parameters, body composition, and islet profiles in Otsuka Long Evans Tokushima Fatty rats after 28 weeks of aerobic exercise, rosiglitazone treatment, and combined exercise and rosiglitazone treatment.

Results

Combined exercise with rosiglitazone showed significantly less increase in weight and epididymal fat compared to rosiglitazone treatment. Aerobic exercise alone and combined rosiglitazone and exercise treatment led to similar retention of lean body mass. All experimental groups showed a decrease in fasting glucose. However, the combined exercise and rosiglitazone therapy group showed prominent improvement in glucose tolerance compared to the other groups. Rescue of islet destruction was observed in all experimental groups, but was most prominent in the combined therapy group.

Conclusion

Regular aerobic exercise combined with rosiglitazone treatment can compensate for the adverse effect of rosiglitazone treatment and has benefit for islet preservation.

Citations

Citations to this article as recorded by  
  • Impacts of an Exercise Intervention on the Health of Pancreatic Beta-Cells: A Review
    Shuang Zhang, Yaru Wei, Chunxiao Wang
    International Journal of Environmental Research and Public Health.2022; 19(12): 7229.     CrossRef
  • Molecular mechanisms by which aerobic exercise induces insulin sensitivity
    Habib Yaribeygi, Stephen L. Atkin, Luis E. Simental‐Mendía, Amirhossein Sahebkar
    Journal of Cellular Physiology.2019; 234(8): 12385.     CrossRef
Clinical Care/Education
Reduction of Sulfonylurea with the Initiation of Basal Insulin in Patients with Inadequately Controlled Type 2 Diabetes Mellitus Undergoing Long-Term Sulfonylurea-Based Treatment
Yeoree Yang, Jeong-Ah Shin, Hae Kyung Yang, Seung-Hwan Lee, Seung-Hyun Ko, Yu-Bae Ahn, Kun-Ho Yoon, Jae-Hyoung Cho
Diabetes Metab J. 2016;40(6):454-462.   Published online October 11, 2016
DOI: https://doi.org/10.4093/dmj.2016.40.6.454
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  • 45 Download
  • 4 Web of Science
  • 4 Crossref
AbstractAbstract PDFPubReader   
Background

There were a limited number of studies about β-cell function after insulin initiation in patients exposed to long durations of sulfonylurea treatment. In this study, we aimed to evaluate the recovery of β-cell function and the efficacy of concurrent sulfonylurea use after the start of long-acting insulin.

Methods

In this randomized controlled study, patients with type 2 diabetes mellitus (T2DM), receiving sulfonylurea for at least 2 years with glycosylated hemoglobin (HbA1c) >7%, were randomly assigned to two groups: sulfonylurea maintenance (SM) and sulfonylurea reduction (SR). Following a 75-g oral glucose tolerance test (OGTT), we administered long-acting basal insulin to the two groups. After a 6-month follow-up, we repeated the OGTT.

Results

Among 69 enrolled patients, 57 completed the study and were analyzed: 31 in the SM and 26 in the SR group. At baseline, there was no significant difference except for the longer duration of diabetes and lower triglycerides in the SR group. After 6 months, the HbA1c was similarly reduced in both groups, but there was little difference in the insulin dose. In addition, insulin secretion during OGTT was significantly increased by 20% to 30% in both groups. A significant weight gain was observed in the SM group only. The insulinogenic index was more significantly improved in the SR group.

Conclusion

Long-acting basal insulin replacement could improve the glycemic status and restore β-cell function in the T2DM patients undergoing sulfonylurea-based treatment, irrespective of the sulfonylurea dose reduction. The dose reduction of the concurrent sulfonylurea might be beneficial with regard to weight grain.

Citations

Citations to this article as recorded by  
  • Initiating or Switching to Insulin Degludec/Insulin Aspart in Adults with Type 2 Diabetes: A Real-World, Prospective, Non-interventional Study Across Six Countries
    Gregory R. Fulcher, Shahid Akhtar, Saleh J. Al-Jaser, Johan Medina, Mafauzy Mohamed, Nemencio A. Nicodemus, Anne Helene Olsen, Kiran P. Singh, Adri Kok
    Advances in Therapy.2022; 39(8): 3735.     CrossRef
  • Use of Insulin Glargine 100 U/mL for the Treatment of Type 2 Diabetes Mellitus in East Asians: A Review
    Takahisa Hirose, Ching-Chu Chen, Kyu Jeung Ahn, Jacek Kiljański
    Diabetes Therapy.2019; 10(3): 805.     CrossRef
  • Insulin Therapy for Adult Patients with Type 2 Diabetes Mellitus: A Position Statement of the Korean Diabetes Association, 2017
    Byung-Wan Lee, Jin Hwa Kim, Seung-Hyun Ko, Kyu-Yeon Hur, Nan-Hee Kim, Sang Youl Rhee, Hyun Jin Kim, Min Kyong Moon, Seok-O Park, Kyung Mook Choi
    Diabetes & Metabolism Journal.2017; 41(5): 367.     CrossRef
  • Insulin therapy for adult patients with type 2 diabetes mellitus: a position statement of the Korean Diabetes Association, 2017
    Byung-Wan Lee, Jin Hwa Kim, Seung-Hyun Ko, Kyu Yeon Hur, Nan-Hee Kim, Sang Youl Rhee, Hyun Jin Kim, Min Kyong Moon, Seok-O Park, Kyung Mook Choi
    The Korean Journal of Internal Medicine.2017; 32(6): 967.     CrossRef
Review
Fuel-Stimulated Insulin Secretion Depends upon Mitochondria Activation and the Integration of Mitochondrial and Cytosolic Substrate Cycles
Gary W. Cline
Diabetes Metab J. 2011;35(5):458-465.   Published online October 31, 2011
DOI: https://doi.org/10.4093/dmj.2011.35.5.458
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  • 9 Crossref
AbstractAbstract PDFPubReader   

The pancreatic islet β-cell is uniquely specialized to couple its metabolism and rates of insulin secretion with the levels of circulating nutrient fuels, with the mitochondrial playing a central regulatory role in this process. In the β-cell, mitochondrial activation generates an integrated signal reflecting rates of oxidativephosphorylation, Kreb's cycle flux, and anaplerosis that ultimately determines the rate of insulin exocytosis. Mitochondrial activation can be regulated by proton leak and mediated by UCP2, and by alkalinization to utilize the pH gradient to drive substrate and ion transport. Converging lines of evidence support the hypothesis that substrate cycles driven by rates of Kreb's cycle flux and by anaplerosis play an integral role in coupling responsive changes in mitochondrial metabolism with insulin secretion. The components and mechanisms that account for the integrated signal of ATP production, substrate cycling, the regulation of cellular redox state, and the production of other secondary signaling intermediates are operative in both rodent and human islet β-cells.

Citations

Citations to this article as recorded by  
  • Nicotinamide Adenine Dinucleotide: The Redox Sensor in Aging-Related Disorders
    Giovanna Schiuma, Djidjell Lara, James Clement, Marco Narducci, Roberta Rizzo
    Antioxidants & Redox Signaling.2024;[Epub]     CrossRef
  • ROCK1 regulates insulin secretion from β-cells
    Byung-Jun Sung, Sung-Bin Lim, Won-Mo Yang, Jae Hyeon Kim, Rohit N. Kulkarni, Young-Bum Kim, Moon-Kyu Lee
    Molecular Metabolism.2022; 66: 101625.     CrossRef
  • Hyperglycemic Stress and Carbon Stress in Diabetic Glucotoxicity
    Xiaoting Luo, Jinzi Wu, Siqun Jing, Liang-Jun Yan
    Aging and disease.2016; 7(1): 90.     CrossRef
  • Characterization of Phospholipids in Insulin Secretory Granules and Mitochondria in Pancreatic Beta Cells and Their Changes with Glucose Stimulation
    Michael J. MacDonald, Lacmbouh Ade, James M. Ntambi, Israr-Ul H. Ansari, Scott W. Stoker
    Journal of Biological Chemistry.2015; 290(17): 11075.     CrossRef
  • Roles of Pyruvate, NADH, and Mitochondrial Complex I in Redox Balance and Imbalance inβCell Function and Dysfunction
    Xiaoting Luo, Rongrong Li, Liang-Jun Yan
    Journal of Diabetes Research.2015; 2015: 1.     CrossRef
  • Peroxisome Proliferator-activated Receptor γ (PPARγ) and Its Target Genes Are Downstream Effectors of FoxO1 Protein in Islet β-Cells
    Dhananjay Gupta, Averi A. Leahy, Navjot Monga, Mina Peshavaria, Thomas L. Jetton, Jack L. Leahy
    Journal of Biological Chemistry.2013; 288(35): 25440.     CrossRef
  • Desnutrin/ATGL Activates PPARδ to Promote Mitochondrial Function for Insulin Secretion in Islet β Cells
    Tianyi Tang, Marcia J. Abbott, Maryam Ahmadian, Andressa B. Lopes, Yuhui Wang, Hei Sook Sul
    Cell Metabolism.2013; 18(6): 883.     CrossRef
  • Potent humanin analog increases glucose‐stimulated insulin secretion through enhanced metabolism in the β cell
    Regina Kuliawat, Laura Klein, Zhenwei Gong, Marianna Nicoletta‐Gentile, Anjana Nemkal, Lingguang Cui, Claire Bastie, Kai Su, Derek Huffman, Manju Surana, Nir Barzilai, Norman Fleischer, Radhika Muzumdar
    The FASEB Journal.2013; 27(12): 4890.     CrossRef
  • Proliferation and differentiation of osteoblasts from the mandible of osteoporotic rats
    Shu-Juan Yu, Hong-Chen Liu, Ling-Ling E, Dong-Sheng Wang, Guo-Xiong Zhu
    Experimental Biology and Medicine.2012; 237(4): 395.     CrossRef
Original Articles
Adenoviruses Expressing PDX-1, BETA2/NeuroD and MafA Induces the Transdifferentiation of Porcine Neonatal Pancreas Cell Clusters and Adult Pig Pancreatic Cells into Beta-Cells
Young-Hye You, Dong-Sik Ham, Heon-Seok Park, Marie Rhee, Ji-Won Kim, Kun-Ho Yoon
Diabetes Metab J. 2011;35(2):119-129.   Published online April 30, 2011
DOI: https://doi.org/10.4093/dmj.2011.35.2.119
  • 3,659 View
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  • 9 Crossref
AbstractAbstract PDFPubReader   
Background

A limitation in the number of insulin-producing pancreatic beta-cells is a special feature of diabetes. The identification of alternative sources for the induction of insulin-producing surrogate beta-cells is a matter of profound importance. PDX-1/VP16, BETA2/NeuroD, and MafA overexpression have been shown to influence the differentiation and proliferation of pancreatic stem cells. However, few studies have been conducted using adult animal pancreatic stem cells.

Methods

Adult pig pancreatic cells were prepared from the non-endocrine fraction of adult pig pancreata. Porcine neonatal pancreas cell clusters (NPCCs) were prepared from neonatal pigs aged 1-2 days. The dispersed pancreatic cells were infected with PDX-1/VP16, BETA2/NeuroD, and MafA adenoviruses. After infection, these cells were transplanted under the kidney capsules of normoglycemic nude mice.

Results

The adenovirus-mediated overexpression of PDX-1, BETA2/NeuroD and MafA induced insulin gene expression in NPCCs, but not in adult pig pancreatic cells. Immunocytochemistry revealed that the number of insulin-positive cells in NPCCs and adult pig pancreatic cells was approximately 2.6- and 1.1-fold greater than those in the green fluorescent protein control group, respectively. At four weeks after transplantation, the relative volume of insulin-positive cells in the grafts increased in the NPCCs, but not in the adult porcine pancreatic cells.

Conclusion

These data indicate that PDX-1, BETA2/NeuroD, and MafA facilitate the beta-cell differentiation of NPCCs, but not adult pig pancreatic cells. Therefore PDX-1, BETA2/NeuroD, and MafA-induced NPCCs can be considered good sources for the induction of pancreatic beta-cells, and may also have some utility in the treatment of diabetes.

Citations

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  • The pig pangenome provides insights into the roles of coding structural variations in genetic diversity and adaptation
    Zhengcao Li, Xiaohong Liu, Chen Wang, Zhenyang Li, Bo Jiang, Ruifeng Zhang, Lu Tong, Youping Qu, Sheng He, Haifan Chen, Yafei Mao, Qingnan Li, Torsten Pook, Yu Wu, Yanjun Zan, Hui Zhang, Lu Li, Keying Wen, Yaosheng Chen
    Genome Research.2023; 33(10): 1833.     CrossRef
  • Improvement of the therapeutic capacity of insulin-producing cells trans-differentiated from human liver cells using engineered cell sheet
    Yu Na Lee, Hye-Jin Yi, Eun Hye Seo, Jooyun Oh, Song Lee, Sarah Ferber, Teruo Okano, In Kyong Shim, Song Cheol Kim
    Stem Cell Research & Therapy.2021;[Epub]     CrossRef
  • Generation of iPSC-derived insulin-producing cells from patients with type 1 and type 2 diabetes compared with healthy control
    Min Jung Kim, Eun Young Lee, Young-Hye You, Hae Kyung Yang, Kun-Ho Yoon, Ji-Won Kim
    Stem Cell Research.2020; 48: 101958.     CrossRef
  • Effect of FIGF overexpression on liver cells transforming to insulin-producing cells
    Yaqin He, Xiaoliang Xie, Xiaoyan Li, Shikuo Rong, Yukui Li, Zhenhui Lu
    Journal of Biosciences.2019;[Epub]     CrossRef
  • Generation of Insulin-Expressing Cells in Mouse Small Intestine by Pdx1, MafA, and BETA2/NeuroD
    So-Hyun Lee, Marie Rhee, Ji-Won Kim, Kun-Ho Yoon
    Diabetes & Metabolism Journal.2017; 41(5): 405.     CrossRef
  • Quantitative Raman spectral changes of the differentiation of mesenchymal stem cells into islet-like cells by biochemical component analysis and multiple peak fitting
    Xin Su, Shaoyin Fang, Daosen Zhang, Qinnan Zhang, Yingtian He, Xiaoxu Lu, Shengde Liu, Liyun Zhong
    Journal of Biomedical Optics.2015; 20(12): 125002.     CrossRef
  • Generation of Functional Insulin-Producing Cells from Neonatal Porcine Liver-Derived Cells by PDX1/VP16, BETA2/NeuroD and MafA
    Dong-Sik Ham, Juyoung Shin, Ji-Won Kim, Heon-Seok Park, Jae-Hyoung Cho, Kun-Ho Yoon, Kathrin Maedler
    PLoS ONE.2013; 8(11): e79076.     CrossRef
  • PPARγ Activation Attenuates Glycated-Serum Induced Pancreatic Beta-Cell Dysfunction through Enhancing Pdx1 and Mafa Protein Stability
    Yunxia Zhu, Ai Ma, Hongxiu Zhang, Chaojun Li, Rebecca Berdeaux
    PLoS ONE.2013; 8(2): e56386.     CrossRef
  • β‐Cell differentiation and regeneration in type 1 diabetes
    L. Ding, C. Gysemans, C. Mathieu
    Diabetes, Obesity and Metabolism.2013; 15(s3): 98.     CrossRef
Transdifferentiation of Enteroendocrine K-cells into Insulin-expressing Cells.
Esder Lee, Jun Mo Yu, Min Kyung Lee, Gyeong Ryul Ryu, Seung Hyun Ko, Yu Bae Ahn, Sung Dae Moon, Ki Ho Song
Korean Diabetes J. 2009;33(6):475-484.   Published online December 1, 2009
DOI: https://doi.org/10.4093/kdj.2009.33.6.475
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AbstractAbstract PDF
BACKGROUND
Despite a recent breakthough in human islet transplantation for treating type 1 diabetes mellitus, the limited availability of donor pancreases remains a major obstacle. Endocrine cells within the gut epithelium (enteroendocrine cells) and pancreatic beta cells share similar pathways of differentiation during embryonic development. In particular, K-cells that secrete glucose-dependent insulinotropic polypeptide (GIP) have been shown to express many of the key proteins found in beta cells. Therefore, we hypothesize that K-cells can be transdifferentiated into beta cells because both cells have remarkable similarities in their embryonic development and cellular phenotypes. METHODS: K-cells were purified from heterogeneous STC-1 cells originating from an endocrine tumor of a mouse intestine. In addition, a K-cell subclone expressing stable Nkx6.1, called "Kn4-cells," was successfully obtained. In vitro differentiation of K-cells or Kn4-cells into beta cells was completed after exendin-4 treatment and serum deprivation. The expressions of insulin mRNA and protein were examined by RT-PCR and immunocytochemistry. The interacellular insulin content was also measured. RESULTS: K-cells were found to express glucokinase and GIP as assessed by RT-PCR and Western blot analysis. RT-PCR showed that K-cells also expressed Pdx-1, NeuroD1/Beta2, and MafA, but not Nkx6.1. After exendin-4 treatment and serum deprivation, insulin mRNA and insulin or C-peptide were clearly detected in Kn4-cells. The intracellular insulin content was also increased significantly in these cells. CONCLUSION: K-cells are an attractive potential source of insulin-producing cells for treatment of type 1 diabetes mellitus. However, more experiments are necessary to optimize a strategy for converting K-cells into beta cells.

Citations

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  • Reprogramming of enteroendocrine K cells to pancreatic β-cells through the combined expression of Nkx6.1 and Neurogenin3, and reaggregation in suspension culture
    Esder Lee, Gyeong Ryul Ryu, Sung-Dae Moon, Seung-Hyun Ko, Yu-Bae Ahn, Ki-Ho Song
    Biochemical and Biophysical Research Communications.2014; 443(3): 1021.     CrossRef
Insulin Sensitivity and Insulin Secretion Determined by Homeostasis Model Assessment and Future Risk of Diabetes Mellitus in Korean Men.
Eun Suk Choi, Eun Jung Rhee, Ji Hoon Kim, Jong Chul Won, Cheol Young Park, Won Young Lee, Ki Won Oh, Sung Woo Park, Sun Woo Kim
Korean Diabetes J. 2008;32(6):498-505.   Published online December 1, 2008
DOI: https://doi.org/10.4093/kdj.2008.32.6.498
  • 2,701 View
  • 34 Download
  • 17 Crossref
AbstractAbstract PDF
BACKGROUND
Insulin resistance and progressive pancreatic beta cell dysfunction have been identified as the two fundamental features in the type 2 diabetes. Homeostasis model assessment (HOMA), based on plasma levels of fasting glucose and insulin, has been widely validated and applied for quantifying insulin resistance and secretion. This study was performed to assess the predictive value of HOMA indices for future diabetes risk. METHODS: In 14,976 Korean men, in which medical check-up was performed both in 2002 and 2006 in a university hospital health promotion center in Seoul, Korea, prospective assessment for diabetes risk was assessed. At baseline, anthropometric measurements were done and fasting glucose, insulin, lipid profiles were measured. HOMA-insulin resistance (HOMA-IR) and beta cell function (HOMA beta-cell) were calculated from fasting glucose and insulin levels. RESULTS: After 4 years, 286 subjects (1.9%) were newly diagnosed as diabetes mellitus. These patients (mean age 40.3 years) were age-matched with 632 control subjects (mean age 39.8 years) and diabetes risk was assessed with HOMA indices. Among the parameters, body mass index, fasting glucose and HOMA beta-cell were the significant determinants for future diabetes risk. When the subjects were divided into two groups according to the baseline median values of HOMA-IR and HOMA beta-cell, and assessed jointly, those with the low HOMA beta-cell and high HOMA-IR showed the highest risk for future diabetes (RR 39.065, 95% CI 11.736~130.035, P < 0.01). The subjects with low baseline HOMA beta-cell showed higher RR for diabetes than those with high baseline HOMA-IR (4.413 vs. 3.379, P = 0.018, P = 0.051). CONCLUSION: High HOMA-IR and low HOMA beta-cell were associated with the highest risk for future diabetes in this prospective study of Korean male subjects. These data suggest the value of HOMA indices for diabetes risk in epidemiologic studies in Asian subjects.

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  • Effects of a 2-Week Kinect-Based Mixed-Reality Exercise Program on Prediabetes: A Pilot Trial during COVID-19
    So Young Ahn, Si Woo Lee, Hye Jung Shin, Won Jae Lee, Jun Hyeok Kim, Hyun-Jun Kim, Wook Song
    Journal of Obesity & Metabolic Syndrome.2024; 33(1): 54.     CrossRef
  • Case Report of Impaired Fasting Glucose Improved with Korean Medicine Treatment and Dietetic Therapy
    Eun-mi Kim, Ki-tae Kim
    The Journal of Internal Korean Medicine.2021; 42(2): 175.     CrossRef
  • Insulin Resistance Is Associated with Early Gastric Cancer: A Prospective Multicenter Case Control Study
    Hye Jung Kwon, Moo In Park, Seun Ja Park, Won Moon, Sung Eun Kim, Jae Hyun Kim, Youn Jung Choi, Sang Kil Lee
    Gut and Liver.2019; 13(2): 154.     CrossRef
  • Effect of Coenzyme Q10 on Insulin Resistance in Korean Patients with Prediabetes: A Pilot Single-Center, Randomized, Double-Blind, Placebo-Controlled Study
    Ja-Young Yoo, Keun-Sang Yum
    BioMed Research International.2018; 2018: 1.     CrossRef
  • Insulin resistance increases the risk of incident type 2 diabetes mellitus in patients with non‐alcoholic fatty liver disease
    Yuya Seko, Yoshio Sumida, Saiyu Tanaka, Kojiroh Mori, Hiroyoshi Taketani, Hiroshi Ishiba, Tasuku Hara, Akira Okajima, Atsushi Umemura, Taichiro Nishikawa, Kanji Yamaguchi, Michihisa Moriguchi, Kazuyuki Kanemasa, Kohichiroh Yasui, Shunsuke Imai, Keiji Shim
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    Seyoung Kwon, Youngak Na
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    Kiook Baek, Namhoon Lee, Insung Chung
    Annals of Occupational and Environmental Medicine.2017;[Epub]     CrossRef
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    Rimkyo Yeo, So Ra Yoon, Oh Yoen Kim
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    Young Seok Song, You-Cheol Hwang, Hong-Yup Ahn, Cheol-Young Park
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    Dae Hoon Lee, Jae Min Han, Woong Mo Yang
    Journal of Korean Medicine.2015; 36(1): 75.     CrossRef
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    Tae Jung Oh, Se Hee Min, Chang Ho Ahn, Eun Ky Kim, Soo Heon Kwak, Hye Seung Jung, Kyong Soo Park, Young Min Cho
    Diabetes & Metabolism Journal.2015; 39(2): 147.     CrossRef
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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
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    You Mi Lee, Hye Kyung Chung, Heejin Kimm, Sun Ha Jee
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    Dong Pil Kim, Kang Seo Park, Dong Sun Kim, Bong Suk Ko, Ji Hae Lee, Jae Hyuk Lee, Jong Ho Shin, Byung Jun Kim, Hyun Jin Kim
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    Sang Yong Kim
    Korean Diabetes Journal.2009; 33(1): 73.     CrossRef
  • Insulin Sensitivity and Insulin Secretion Determined by Homeostasis Model Assessment and Future Risk of Diabetes Mellitus in Korean Men (Korean Diabetes J 32(6):498-505, 2008)
    Eun-Suk Choi, Eun-Jung Rhee
    Korean Diabetes Journal.2009; 33(1): 75.     CrossRef
Effects of Islet Transplantation on Endogenous beta-cell Regeneration after Partial Pancreatectomy in Rodents.
Hye Seung Jung, You Ran Ahn, Seung Hoon Oh, Jung Hwa Jung, Tae Hyun Kim, You Cheol Hwang, Mira Kang, Yongsuk Bae, Young seok Kim, Jae Hoon Chung, Yong Ki Min, Myung Shik Lee, Moon Kyu Lee, Kwang Won Kim
Korean Diabetes J. 2007;31(2):113-122.   Published online March 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.2.113
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AbstractAbstract PDF
BACKGROUND
Islet transplantation is one of regimens supplying the deficient insulin in diabetes patients, but the effects of islet grafts on the changes of endogenous beta-cells are not clear. In the present study, we examined the changes of endogenous beta-cell mass after islet transplantation in partially pancreatectomized mice. METHODS: Balb/c mice were 70% pancreatectomized, transplanted with syngeneic islets (group IV), and were compared with pancreatectomized mice treated with insulin (group III) or no insulin (group II). Blood glucose levels and body weight were monitored. Remnant pancreas was obtained at 6 or 10 days after pancreatectomy, and immunohistochemical staining was done for the evaluation of beta-cell mass changes. RESULTS: Hyperglycemia and weight loss were induced after pancreatectomy. After islet transplantation or insulin treatment, blood glucose levels recovered to normal, and body weight started to increase. Plasma insulin levels were higher and beta-cell mass was larger in group IV than in group II (P < 0.05). Especially, the difference of beta-cell mass between them was more evident at 7 days as compared to at 3 day after transplantation. When compared to group III, group IV showed larger individual beta-cell area after 7 days and larger beta-cell mass after 3 days of islet transplantation (P < 0.05). CONCLUSION: These observations indicate that islet transplantation plays a role in enhancing remnant beta-cell regeneration after partial pancreatectomy in rodents.
Mechanism of 2-Deoxy-D-ribose-induced Damage in Pancreatic beta-cells.
Gwanpyo Koh, Jeong taek Woo, Dae Ho Lee, Seungjoon Oh, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Deok Bae Park
Korean Diabetes J. 2007;31(2):105-112.   Published online March 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.2.105
  • 2,215 View
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  • 2 Crossref
AbstractAbstract PDF
BACKGROUND
Mechanism for glucose toxicity is known to be an increased oxidative stress produced by multiple pathways. In our previous report, 2-deoxy-d-ribose (dRib) promoted apoptosis by increasing oxidative stress in a pancreatic beta-cell line. We performed this study to investigate the mechanism of dRib-induced damage of beta-cells. METHODS: HIT-T15 cells were cultured in RPMI-1640 medium with 40 mM dRib for 24 hours after pretreatment with various concentrations of a metal chelator (DTPA) and inhibitors of protein glycation (aminoguanidine and pyridoxamine). Cell viability was determined by MTT assay. Apoptosis was analyzed by flow cytometry with annexin V/PI double staining. RESULTS: DTPA, which inhibits the monosaccharide autoxidation, partially reversed dRib-induced cytotoxicity in a dose-dependent manner (P < 0.01). The cytotoxicity was also suppressed dose-dependently by aminoguanidine (AG) and pyridoxamine (PM) (P < 0.05 and P < 0.01, repectively). Flow cytometric analysis showed that pretreatment of DTPA and AG also reversed the dRib-triggered apoptosis in a dose-dependent manner. We assessed the additional protective effects of inhibitors of protein glycation from dRib-induced cytotoxiciy in the presence of a metal chelator. The additions of AG (P < 0.05) and PM (P < 0.01) significantly reduced the cytotoxicity compared with DTPA alone group. CONCLUSION: This results suggest that dRib produce cytotoxicity and apoptosis through the mechanisms of advanced glycation endproducts (AGEs) formation including the monsaccharide autoxidation and protein glycation in pancreatic beta-cell. Thus, dRib could be a surrogate for glucose in the study of glucose toxicity and chronic diabetic complications.

Citations

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  • Isolation of Citrus Peel Flavonoid Bioconversion Microorganism and Inhibitory Effect on the Oxidative Damage in Pancreatic Beta Cells
    Chi-Deok Park, Hee-Kyung Jung, Chang-Ho Park, Yoo-Seok Jung, Joo-Heon Hong, Hee-Sun Ko, Dong-Hee Kang, Hyun-Soo Kim
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    Yun Jung Lee, Kwang Sik Suh, Moon Chan Choi, Suk Chon, Seungjoon Oh, Jeong‐Taek Woo, Sung‐Woon Kim, Jin‐Woo Kim, Young Seol Kim
    Phytotherapy Research.2010; 24(3): 419.     CrossRef
PDX-1/VP16 Overexpression Induce the Transdifferentiation of Canine Adult Pancreatic Cells into Beta-cells.
Young Hye You, Sun Cheol Park, Seung Hwan Lee, Heon Seok Park, Dong Sik Ham, Marie Rhee, Ji Won Kim, Ki Ho Song, Kun Ho Yoon
Korean Diabetes J. 2007;31(1):51-62.   Published online January 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.1.51
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AbstractAbstract PDF
BACKGROUND
A major obstacle of islet transplantation is an inadequate supply of insulin-producing tissue. Ad-PDX-1/VP16 overexpression and Exendin-4 treatment have been proved the effects on differentiation and proliferation of pancreatic stem cells. But, the study is insufficient using adult animal pancreatic stem cells. METHODS: Pancreatic cells were prepared from the non-endocrine fraction of canine pancreases. This cells were cultivated free floating state and monolayer culture after dispersion. The floating pancreatic cells were transplanted under the kidney capsule of normoglycaemic nude mice. The dispersed pancreatic cells were infected with Ad-PDX-1/VP16 or Ad-GFP. After infection, those cells were transplanted of nude mice. After transplantation, mice were treated with either 1 nmol/kg exendin-4 or saline solution by intraperitoneal injection for 10 days. RESULTS: The relative volume of the beta-cells in the grafts of the free floating cultured pancreatic cells were 23.4 +/- 13.1% at two weeks and 5.2 +/- 2.0% at eight weeks. At two weeks after transplantation, the relative volume of insulin-positive cells in the grafts of dispersed pancreatic cells were 28 +/- 5.7%, 20.5 +/- 0.7% and 31 +/- 1.4% in control, GFP and PDX-1/VP16 treated groups respectively. At eight weeks after transplantation, the relative volume of insulin-positive cells in the grafts were 11.8 +/- 5.9%, 8 +/- 7.3% and 16.6 +/- 7.4% in control, GFP and PDX-1/VP16 treated groups respectively. Exendin-4 treatment didn't show any additive effects on transdifferentiation of pancreas stem cell into beta-cells. CONCLUSION: The expansion and transdifferentiation were not observed after the transplantation of the free floating cultured pancreatic cells. PDX-1/VP16 overexpression induces the transdifferentiation of adult pancreatic cells into beta-cells. However Exendin-4 treatment hasn't any effects on the expansion and transdifferentiation of the cells in the grafts.

Citations

Citations to this article as recorded by  
  • Generation of Functional Insulin-Producing Cells from Neonatal Porcine Liver-Derived Cells by PDX1/VP16, BETA2/NeuroD and MafA
    Dong-Sik Ham, Juyoung Shin, Ji-Won Kim, Heon-Seok Park, Jae-Hyoung Cho, Kun-Ho Yoon, Kathrin Maedler
    PLoS ONE.2013; 8(11): e79076.     CrossRef
  • Adenoviruses Expressing PDX-1, BETA2/NeuroD and MafA Induces the Transdifferentiation of Porcine Neonatal Pancreas Cell Clusters and Adult Pig Pancreatic Cells into Beta-Cells
    Young-Hye You, Dong-Sik Ham, Heon-Seok Park, Marie Rhee, Ji-Won Kim, Kun-Ho Yoon
    Diabetes & Metabolism Journal.2011; 35(2): 119.     CrossRef
  • Transdifferentiation of Enteroendocrine K-cells into Insulin-expressing Cells
    Esder Lee, Jun Mo Yu, Min Kyung Lee, Gyeong Ryul Ryu, Seung-Hyun Ko, Yu-Bae Ahn, Sung-Dae Moon, Ki-Ho Song
    Korean Diabetes Journal.2009; 33(6): 475.     CrossRef
Clinical Meaning of Postprandial Insulin Secretory Function in Korean Type 2 Diabetes Mellitus.
Wan Sub Shim, Soo Kyung Kim, Hae Jin Kim, Se Eun Park, Eun Seok Kang, Yu Mie Rhee, Chul Woo Ahn, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee, Bong Soo Cha
Korean Diabetes J. 2005;29(4):367-377.   Published online July 1, 2005
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AbstractAbstract PDF
BACKGROUND
Impaired pancreatic beta-cell responsiveness is associated with type 2 diabetes mellitus. Postprandial insulin deficiency is closely related with fasting plasma glucose, HbA1c and insulin responses to meals, but most studies examining postprandial beta-cell responsiveness have been limited by the small number of type 2 diabetic patients examined. The aim of this study was to evaluate fasting and postprandial insulin secretions in relation to the duration of diabetes, BMI and glycemic control in a large number of patients with variable disease durations. METHODS: We evaluated the fasting plasma glucose, insulin, C-peptide, HbA1c, BMI, postprandial 2 hour glucose, insulin and C-peptide in 1,170(male 662, female 508, age 54.6+/-1.6 years, duration of diabetes 5.2+/-6.3 years, BMI 25.4+/-3.3kg/m(2)) type 2 diabetic patients. The delta C-peptide, delta insulin, fasting(M0) and postprandial(M1) pancreatic beta-cell responsiveness were also calculated. The subjects were divided into three groups according to their duration of diabetes, BMI, and fasting and postprandial C-peptide levels. After adjusting for age, sex and BMI, the correlation of diabetes and HbA1c were correlated parameters. RESULTS: In the group of patients whose duration of diabetes was longer than 10 years, the BMI, fasting, postprandial and delta C-peptide, and M0 and M1 were significantly lower, but age, fasting and postprandial glucose, as well as HbA1c were significantly higher than those in the other groups. There were no significant differences in the fasting and postprandial glucose and HbA1c according to their fasting C-peptide tertiles. However, in the group of patients with the highest postprandial C-peptide tertile, the fasting and postprandial glucose and HbA1c were significantly lower than those in the other groups. The duration of diabetes, after adjustment of age, sex and BMI, was negatively correlated with the fasting, postprandial and delta C-peptide, M0 and M1, but was positively correlated with the fasting and postprandial 2 hour glucose and HbA1c. The HbA1c after adjustment of age, sex and BMI, was positively correlated with duration of diabetes, and fasting and postprandial glucose, but was negatively correlated with fasting postprandial and delta C-peptide, M0 and M1. CONCLUSION: Although the fasting and postprandial insulin secretions were decreased with duration of diabetes, the decrease in the postprandial insulin secretion was more prominent. The postprandial pancreatic responsiveness may be a more important factor in predicting glycemic control in Korean type 2 diabetic patients than the fasting pancreatic responsiveness.
The Effect of cAMP-Elevating Agents on High Glucose-Induced Apoptosis of Isolated Islets of Rat Pancreas.
Gwan Pyo Koh, Kwang Sik Suh, Suk Chon, Seung Joon Oh, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Sun Hee Kwon
Korean Diabetes J. 2004;28(6):490-500.   Published online December 1, 2004
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AbstractAbstract PDF
BACKGROUND
High glucose-induced apoptosis has been implicated in the loss of beta-cells of the pancreatic islets in animal models of type 2 diabetes. GLP-1 has been shown to reduce apoptosis by the cAMP-dependent mechanism in beta-cells. Other studies have also shown that elevated levels of intracellular cyclic AMP delayed apoptosis in other types of cells. We investigated whether cAMP-elevating agents could suppress the high glucose-induced apoptosis of isolated rat islets. METHODS: Pancreatic islets were isolated from Sprague-Dawley (SD) rats. The expression of phosphodiesterase (PDE) 3 subtypes was investigated by using extracts of freshly isolated islets and analyzing them by RT-PCR. After 2 days of isolation, the islets were cultured in RPMI-1640 media containing 5% FBS with various glucose concentrations (11.1, 16.7 and 27.8 mM), 5x10-6 M forskolin, 2x10-4 M 3-isobutyl-1-methylxanthine (IBMX), 10-5 M cilostazol, and 10-6, 5x10-6 and 10-5 M H-89 for 5 days. The islet apoptosis was measured by a sandwich enzyme-immunoassay using antihistone antibody. RESULTS: Apoptosis was lowest at 11.1 mM glucose concentration, and increased at higher glucose concentrations (1.00 +/- 0.04 A.U. (arbitrary unit) at 11.1 mM, 1.17 +/- 0.12 A.U. at 16.7 mM, and 1.65 +/-0.13 A.U. at 27.8 mM (P <0.05 for 11.1 mM). Both PDE 3A and 3B mRNA were expressed in the islet extracts. In 16.7 and 27.8 mM glucose concentrations, forskolin (P <0.01), IBMX (P <0.05) and cilostazol (P < 0.05) suppressed apoptosis of the islet cells. Protein kinase A (PKA) nhibitor, H-89, did not prevent the inhibition of apoptosis by forskolin. CONCLUSION: These results show that high glucose-induced apoptosis of the cells in rat islet is attenuated by such cAMP-elevating agents as cilostazol. However, cyclic AMP regulation of islet apoptosis may occur via a PKA-independent signaling pathway.
The Effects of Dexamethasone on the Expansion and Transdifferentiation of Transplanted Porcine Neonatal Pancreas Cell Clusters into beta-cells in Normal Nude Mice.
Ji Hun Yang, Sun Hee Suh, Sung Yoon Jeon, Oak Kee Hong, Kun Ho Yoon
Korean Diabetes J. 2004;28(5):356-366.   Published online October 1, 2004
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BACKGROUND
Several studies have suggested that glucocorticoid has an influence on the development and function of the -cells. Thus, we undertook this study to determine whether exposure to dexamethasone (Dx) has an influence on the expansion or transdifferentiation of transplanted porcine NPCCs. METHODS: After transplantation (Tx) of 4,000 islet equivalents (IEQs) of porcine NPCCs into normal nude mice, Dx (1mg/kg) or the control vehicle were injected daily for 10 weeks. To clarify the effects of timing and duration of the Dx, one group was treated by Dx at the first 2 weeks (n=10) and the other group was treated later 8 weeks (n=10) during the 10 weeks treatment period. Thr total graft and beta-cell masses were determined by morphometric analysis. We preformed semi-quantitative RT-PCR for evaluating the pancreas transcription factors. RESULTS: The relative volume and absolute mass of the beta-cells and the total graft were significantly decreased by 10 weeks Dx treatment. Moreover, Dx treatment at thr first 2 weeks (n=10) also significantly decreased the total graft mass and absolute mass of the beta-cells. The relative volume of the beta-cells was negatively correlated and the area of the duct cysts was positively correlated with the duration of the Dx treatment. Pancreas transcription factors including PDX1, Ngn 3, ISL1 and NKx6.1 were decreased in the graft by 2 days treatment of Dx. CONCLUSION: These results suggest that Dx treatment suppresses the expansion and transdifferentiation of transplanted pancreas precursor cells into beta-cell.
3-Dimensional Long Term Culture of Monolayer Cultured Dispersed Neonatal Porcine Pancreas Cells (NPCC).
Sun Hee Suh, Kun Ho Yoon, Hyuk Sang Kwon, Ok Ki Hong, Jung Min Lee, Ki Ho Song, Soon Jib Yoo, Hyun Sik Son, Moo Il Kang, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Koo Kang
Korean Diabetes J. 2002;26(5):383-395.   Published online October 1, 2002
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BACKGROUND
We have reported porcine neonatal pancreas cell clusters (NPCCs) to be useful clinical alternative due to their growth potential and convenience. However, to apply the porcine NPCCs in human islet transplantation, there is a need to achieve in vitro maturation of porcine pancreas duct cells for the immediate cure of diabetes, and to escape hyperacute rejection. We have established a long-term 3D culture system of porcine pancreas duct cells for their in vitro induction in differentiated beta-cells. METHOD: For making NPCCs, pancreata from 1~3 days old pigs were minced, digested and cultured for 8 days. After 8 days, the cells were layered with Matrigel. After 50 days, the 3 dimensional cultures, the components of the reconstructed cell clusters were confirmed by three approaches: immunofluorescent staining, mea-surement of glucose stimulated insulin secretion and semiquantitative RT-PCR. RESULT: The monolayers of epithelial cells formed three-dimensional structures of cysts from which 50~200 micro meter diameter islet-like clusters of pancreas cells budded. The insulin and DNA contents, and the ratio of insulin/DNA, did not change significantly, even after 50 days of culturinge. The levels of insulin and galactosyl transferase mRNA showed a tendency to increase in the monolayer culture of the duct cells until day 8, after which the levels significantly decreased. However, the level of glucagon mRNA was maintained until day 50. Compared with their basal secretion at 5mM glucose, the cysts/cultivated porcine islet buds exposed to stimulatory 20mM glucose did not show difference in insulin secretion. CONCLUSION: We have shown the expansion of dispersed porcine neonatal pancreas cells in vitro, and the reconstruction of a three-dimensional structure, following Matrigel overlaying, but were unable to observe the transition of duct cells to beta cells, as observed in human duct cells. Further studies will be required to elucidate this difference.
Pancreatic beta-cell Function and Development in Male Offspring of Protein-Malnourished Rats.
Hyeong Kyu Park, Cheng Ji Jin, Do Joon Park, Chan Soo Shin, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee
Korean Diabetes J. 2002;26(1):21-30.   Published online February 1, 2002
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AbstractAbstract PDF
BACKGROUND
Nutritional deprivation of the fetus and infant may be associated with susceptibility to impaired glucose tolerance or type 2 diabetes in adult life. This association has been interpreted as a long-term effects of nutritional factors that reduce fetal growth and impair the development of tissues that regulate glucose metabolism. This study aimed to investigate the effect of protein malnutrition in a fetus and early life on the pancreatic beta-cell function and development. METHODS: Sprague-Dawley rats were fed a low-protein (8% casein) diet during pregnancy and lactation. Their male offspring were weaned onto either a control (18% casein) diet (recuperated group, R) or a low-protein diet (low-protein group, LP). The offspring of the rats fed control diet were weaned onto control diet (control group, C). Glucose tolerance tests and morphometry of the pancreas were performed to evaluate the pancreatic beta-cell function and development at the 25th week of age. RESULTS: Offspring of the protein-malnourished rats had a significantly lower body weights than the controls. The R and LP showed no major impairment in glucose tolerance, but the plasma insulin concentrations in the R (0.24+/-.03 nmol/L) and LP (0.28+/-.02 nmol/L) groups were lower at 20 min during IVGTT than the C (0.43+/-.05 nmol/L) groups. The areas under the curve for insulin (AUC insulin) during IVGTT were significantly lower in R and LP (0.39+/-.03 nmol/L/min, 0.43+/-.02 nmol/L/min) groups than the C (0.54+/-.03 nmol/L/min) group. In particular, the rats with fetal protein malnutrition showed severe impairment in late-phase insulin secretion to a glucose load. Both the pancreas weight and the proportion of the pancreas weight to the body weight were significantly lower in the R and LP groups than the C group. The proportion of beta-cells to pancreatic cells was lower in the LP (0.91+/-.14%) group than the C (2.19+/-.23%) and R (1.79+/-.25%) group. The relative beta-cell mass was significantly lower in the LP (by 62%) group that the C group. CONCLUSION: Rats with fetal protein malnutrition showed persistently impaired pancreatic beta-cell development and reduced insulin secretion capacity. These findings suggest that in utero protein malnutrition can contribute to the development of type 2 diabetes in adult life along with other deleterious environmental or genetic conditions.
The Role of beta-cell Dysfunction and Insulin Resistance in the Development of Post-renal Transplantation Diabetes Mellitus.
Jae Hyun Nam, Hyun Chul Lee, Churl Woo Ahn, Jang Il Mun, Soon Il Kim, Kiil Park, Young Duk Song, Sung Kil Lim, Kyung Rae Kim, Kap Bum Huh
Korean Diabetes J. 2000;24(4):485-514.   Published online January 1, 2001
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BACKGROUND
Our study was undertaken to investigate the pathogenesis and possible risk factors for post-renal transplantation diabetes mellitus (PTDM). METHODS: we recruited 114 patients with normal glucose tolerance, and performed the 75 g oral glucose tolerance tests (OGTT) and the short insulin tolerance tests 1 week before and 9~12 months after transplantation, respectively. RESULTS: The subjects were classified into three groups on the basis of OGTT after transplantation by WHO criteria: 1) 36 (31.6%) subjects with normal glucose tolerance; 2) 51 (45.7%) subjects with impaired glucose tolerance; and 3) 27 (23.7%) subjects with post-renal transplantation diabetes mellitus. Dosages of steroid and cyclosporin-A (CsA) were equivalent among the 3 groups. Before transplantation, the fasting and 2-h plasma glucose, and proinsulin/insulin (PI/I) ratios were significantly higher in the IGT and PTDM groups than in the NGT group, but insulin sensitivity index (ISI) was not different among 3 groups. In addition, the area under the curve (AUC)-insulin on OGTT was significantly lower in the PTDM group than in the NGT group. After transplantation, however, ISI was increased in all groups. Furthermore, the ISI and PI/I ratios revealed significantly higher values in the PTDM group than in the NGT group after transplantation. CONCLUSION: These results revealed that fasting and 2-h plasma glucose levels, as well as proinsulin/insulin ratio before transplantation, which may all be indicators of beta-cell dysfunction, could be the predictors for the development of PTDM and beta-cell dysfunction rather than insulin resistance was proved to be the main factor for the pathogenesis of PTDM.

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