Diabetes & Metabolism Journal

Reviews

Basic Research
Roles of Histone Deacetylase 4 in the Inflammatory and Metabolic Processes: Hyunju Kang, Young-Ki Park, Ji-Young Lee, Minkyung Bae; Diabetes Metab J. 2024;48(3):340-353. Published online March 22, 2024; DOI: https://doi.org/10.4093/dmj.2023.0174

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Histone deacetylase 4 (HDAC4), a class IIa HDAC, has gained attention as a potential therapeutic target in treating inflammatory and metabolic processes based on its essential role in various biological pathways by deacetylating non-histone proteins, including transcription factors. The activity of HDAC4 is regulated at the transcriptional, post-transcriptional, and post-translational levels. The functions of HDAC4 are tissue-dependent in response to endogenous and exogenous factors and their substrates. In particular, the association of HDAC4 with non-histone targets, including transcription factors, such as myocyte enhancer factor 2, hypoxia-inducible factor, signal transducer and activator of transcription 1, and forkhead box proteins, play a crucial role in regulating inflammatory and metabolic processes. This review summarizes the regulatory modes of HDAC4 activity and its functions in inflammation, insulin signaling and glucose metabolism, and cardiac muscle development.

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Butyrate Supplementation Improves Intestinal Health and Growth Performance in Livestock: A Review
Wenting Chen, Qingshan Ma, Yan Li, Lin Wei, Zhenwei Zhang, Adnan Khan, Muhammad Zahoor Khan, Changfa Wang
Biomolecules.2025; 15(1): 85. CrossRef

Metabolic Risk/Epidemiology
Hepatic Fibrosis and Cancer: The Silent Threats of Metabolic Syndrome: Scott L. Friedman; Diabetes Metab J. 2024;48(2):161-169. Published online January 26, 2024; DOI: https://doi.org/10.4093/dmj.2023.0240

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Metabolic dysfunction-associated steatotic (fatty) liver disease (MASLD), previously termed non-alcoholic fatty liver disease, is a worldwide epidemic that can lead to hepatic inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). The disease is typically a component of the metabolic syndrome that accompanies obesity, and is often overlooked because the liver manifestations are clinically silent until late-stage disease is present (i.e., cirrhosis). Moreover, Asian populations, including Koreans, have a higher fraction of patients who are lean, yet their illness has the same prognosis or worse than those who are obese. Nonetheless, ongoing injury can lead to hepatic inflammation and ballooning of hepatocytes as classic features. Over time, fibrosis develops following activation of hepatic stellate cells, the liver’s main fibrogenic cell type. The disease is usually more advanced in patients with type 2 diabetes mellitus, indicating that all diabetic patients should be screened for liver disease. Although there has been substantial progress in clarifying pathways of injury and fibrosis, there no approved therapies yet, but current research seeks to uncover the pathways driving hepatic inflammation and fibrosis, in hopes of identifying new therapeutic targets. Emerging molecular methods, especially single cell sequencing technologies, are revolutionizing our ability to clarify mechanisms underlying MASLD-associated fibrosis and HCC.

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The Triad of Risk: Linking MASLD, Cardiovascular Disease and Type 2 Diabetes; From Pathophysiology to Treatment
Eleni Michalopoulou, John Thymis, Stamatios Lampsas, George Pavlidis, Konstantinos Katogiannis, Dimitrios Vlachomitros, Eleni Katsanaki, Gavriella Kostelli, Sotirios Pililis, Loukia Pliouta, Aikaterini Kountouri, Ioannis S. Papanikolaou, Vaia Lambadiari,
Journal of Clinical Medicine.2025; 14(2): 428. CrossRef
Prognostic Impact of Metabolic Syndrome and Steatotic Liver Disease in Hepatocellular Carcinoma Using Machine Learning Techniques
Sergio Gil-Rojas, Miguel Suárez, Pablo Martínez-Blanco, Ana M. Torres, Natalia Martínez-García, Pilar Blasco, Miguel Torralba, Jorge Mateo
Metabolites.2024; 14(6): 305. CrossRef
Interplay between YAP/TAZ and metabolic dysfunction-associated steatotic liver disease progression
Na Young Lee, Myeung Gi Choi, Eui Jin Lee, Ja Hyun Koo
Archives of Pharmacal Research.2024; 47(6): 558. CrossRef
New Biomarkers in Liver Fibrosis: A Pass through the Quicksand?
Marzia Tagliaferro, Mariapaola Marino, Valerio Basile, Krizia Pocino, Gian Ludovico Rapaccini, Gabriele Ciasca, Umberto Basile, Valeria Carnazzo
Journal of Personalized Medicine.2024; 14(8): 798. CrossRef
AI Digital Pathology Using qFibrosis Shows Heterogeneity of Fibrosis Regression in Patients with Chronic Hepatitis B and C with Viral Response
Feng Liu, Yameng Sun, Dean Tai, Yayun Ren, Elaine L. K. Chng, Aileen Wee, Pierre Bedossa, Rui Huang, Jian Wang, Lai Wei, Hong You, Huiying Rao
Diagnostics.2024; 14(16): 1837. CrossRef
Conditional deletion of CEACAM1 in hepatic stellate cells causes their activation
Harrison T. Muturi, Hilda E. Ghadieh, Suman Asalla, Sumona G. Lester, Getachew D. Belew, Sobia Zaidi, Raziyeh Abdolahipour, Abhishek P. Shrestha, Agnes O. Portuphy, Hannah L. Stankus, Raghd Abu Helal, Stefaan Verhulst, Sergio Duarte, Ali Zarrinpar, Leo A.
Molecular Metabolism.2024; 88: 102010. CrossRef
The impact of traditional Chinese medicine and dietary compounds on modulating gut microbiota in hepatic fibrosis: A review
Xingting Xue, Hongbing Zhou, Jiaxing Gao, Xinghua Li, Jia Wang, Wanfu Bai, Yingchun Bai, Liya Fan, Hong Chang, Songli Shi
Heliyon.2024; 10(19): e38339. CrossRef
Beneficial Effects of Tyrosol and Oleocanthal from Extra Virgin Olive Oil on Liver Health: Insights into Their Mechanisms of Action
Daniela Gabbia
Biology.2024; 13(10): 760. CrossRef
Kisspeptin Alleviates Human Hepatic Fibrogenesis by Inhibiting TGFβ Signaling in Hepatic Stellate Cells
Kavita Prasad, Dipankar Bhattacharya, Shams Gamal Eldin Shams, Kimberly Izarraras, Tia Hart, Brent Mayfield, Maryjka B. Blaszczyk, Zhongren Zhou, Utpal B. Pajvani, Scott L. Friedman, Moshmi Bhattacharya
Cells.2024; 13(19): 1651. CrossRef
Novel Strategies Enhancing Bioavailability and Therapeutical Potential of Silibinin for Treatment of Liver Disorders
Michal Selc, Radka Macova, Andrea Babelova
Drug Design, Development and Therapy.2024; Volume 18: 4629. CrossRef
Valorizing Agro‐Food Waste for Nutraceutical Development: Sustainable Approaches for Managing Metabolic Dysfunction‐Associated Steatotic Liver Disease and Related Co‐Morbidities
Laura Comi, Claudia Giglione, Fationa Tolaj Klinaku, Federico Pialorsi, Valentina Tollemeto, Maria Zurlo, Antonio Seneci, Paolo Magni
Food Frontiers.2024;[Epub] CrossRef

Original Articles

Basic Research
CycloZ Improves Hyperglycemia and Lipid Metabolism by Modulating Lysine Acetylation in KK-Ay Mice: Jongsu Jeon, Dohyun Lee, Bobae Kim, Bo-Yoon Park, Chang Joo Oh, Min-Ji Kim, Jae-Han Jeon, In-Kyu Lee, Onyu Park, Seoyeong Baek, Chae Won Lim, Dongryeol Ryu, Sungsoon Fang, Johan Auwerx, Kyong-Tai Kim, Hoe-Yune Jung; Diabetes Metab J. 2023;47(5):653-667. Published online April 26, 2023; DOI: https://doi.org/10.4093/dmj.2022.0244

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Background
CycloZ, a combination of cyclo-His-Pro and zinc, has anti-diabetic activity. However, its exact mode of action remains to be elucidated.
Methods
KK-Ay mice, a type 2 diabetes mellitus (T2DM) model, were administered CycloZ either as a preventive intervention, or as a therapy. Glycemic control was evaluated using the oral glucose tolerance test (OGTT), and glycosylated hemoglobin (HbA1c) levels. Liver and visceral adipose tissues (VATs) were used for histological evaluation, gene expression analysis, and protein expression analysis.
Results
CycloZ administration improved glycemic control in KK-Ay mice in both prophylactic and therapeutic studies. Lysine acetylation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha, liver kinase B1, and nuclear factor-κB p65 was decreased in the liver and VATs in CycloZ-treated mice. In addition, CycloZ treatment improved mitochondrial function, lipid oxidation, and inflammation in the liver and VATs of mice. CycloZ treatment also increased the level of β-nicotinamide adenine dinucleotide (NAD⁺), which affected the activity of deacetylases, such as sirtuin 1 (Sirt1).
Conclusion
Our findings suggest that the beneficial effects of CycloZ on diabetes and obesity occur through increased NAD⁺ synthesis, which modulates Sirt1 deacetylase activity in the liver and VATs. Given that the mode of action of an NAD+ booster or Sirt1 deacetylase activator is different from that of traditional T2DM drugs, CycloZ would be considered a novel therapeutic option for the treatment of T2DM.

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Cyclo His‐Pro Attenuates Muscle Degeneration in Murine Myopathy Models
Alessia De Masi, Nadège Zanou, Keno Strotjohann, Dohyun Lee, Tanes I. Lima, Xiaoxu Li, Jongsu Jeon, Nicolas Place, Hoe‐Yune Jung, Johan Auwerx
Advanced Science.2024;[Epub] CrossRef
CycloZ Suppresses TLR4-Driven Inflammation to Reduce Asthma-Like Responses in HDM-Exposed Mouse Models
Dohyun Lee, Jongsu Jeon, Seoyeong Baek, Onyu Park, Ah-Ram Kim, Myoung-Sool Do, Hoe-Yune Jung
Cells.2024; 13(23): 2034. CrossRef
Cyclic Peptides as Protein Kinase Modulators and Their Involvement in the Treatment of Diverse Human Diseases
Lorena Martínez-Alcantar, Laura Hernández-Padilla, Alma Laura Díaz-Pérez, Lizbeth Guadalupe Villalón-Magallán, Mayra Xóchitl Durán-Maldonado, César Díaz-Pérez, Marlene E. Campos-Morales, Citlali Figueroa-Guzmán, Jesús Campos-García
Kinases and Phosphatases.2024; 2(4): 346. CrossRef

Basic Research
Pharmacologic Activation of Angiotensin-Converting Enzyme II Alleviates Diabetic Cardiomyopathy in db/db Mice by Reducing Reactive Oxidative Stress: Donghyun Kim, Wooju Jeong, Yumin Kim, Jibeom Lee, Sung Woo Cho, Chang-Myung Oh, Raekil Park; Diabetes Metab J. 2023;47(4):487-499. Published online April 25, 2023; DOI: https://doi.org/10.4093/dmj.2022.0125

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Background
Diabetes mellitus is one of the most common chronic diseases worldwide, and cardiovascular disease is the leading cause of morbidity and mortality in diabetic patients. Diabetic cardiomyopathy (DCM) is a phenomenon characterized by a deterioration in cardiac function and structure, independent of vascular complications. Among many possible causes, the renin-angiotensin-aldosterone system and angiotensin II have been proposed as major drivers of DCM development. In the current study, we aimed to investigate the effects of pharmacological activation of angiotensin-converting enzyme 2 (ACE2) on DCM.
Methods
The ACE2 activator diminazene aceturate (DIZE) was administered intraperitoneally to male db/db mice (8 weeks old) for 8 weeks. Transthoracic echocardiography was used to assess cardiac mass and function in mice. Cardiac structure and fibrotic changes were examined using histology and immunohistochemistry. Gene and protein expression levels were examined using quantitative reverse transcription polymerase chain reaction and Western blotting, respectively. Additionally, RNA sequencing was performed to investigate the underlying mechanisms of the effects of DIZE and identify novel potential therapeutic targets for DCM.
Results
Echocardiography revealed that in DCM, the administration of DIZE significantly improved cardiac function as well as reduced cardiac hypertrophy and fibrosis. Transcriptome analysis revealed that DIZE treatment suppresses oxidative stress and several pathways related to cardiac hypertrophy.
Conclusion
DIZE prevented the diabetes mellitus-mediated structural and functional deterioration of mouse hearts. Our findings suggest that the pharmacological activation of ACE2 could be a novel treatment strategy for DCM.

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Update on clinical and experimental management of diabetic cardiomyopathy: addressing current and future therapy
Peter Galis, Linda Bartosova, Veronika Farkasova, Monika Bartekova, Kristina Ferenczyova, Tomas Rajtik
Frontiers in Endocrinology.2024;[Epub] CrossRef
Vascular remodelling in cardiovascular diseases: hypertension, oxidation, and inflammation
Justyna Totoń-Żurańska, Tomasz P. Mikolajczyk, Blessy Saju, Tomasz J. Guzik
Clinical Science.2024; 138(13): 817. CrossRef

Review

Basic Research
Mitochondrial-Encoded Peptide MOTS-c, Diabetes, and Aging-Related Diseases: Byung Soo Kong, Changhan Lee, Young Min Cho; Diabetes Metab J. 2023;47(3):315-324. Published online February 24, 2023; DOI: https://doi.org/10.4093/dmj.2022.0333

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Mitochondria are complex metabolic organelles with manifold pathophysiological implications in diabetes. Currently published mitochondrial-encoded peptides, which are expressed from the mitochondrial open reading frame of the 12S ribosomal RNA type-c (MOTS-c), 16S rRNA (humanin and short humanin like peptide 1-6 [SHLP1-6]), or small human mitochondrial open reading frame over serine tRNA (SHMOOSE) are associated with regulation of cellular metabolism and insulin action in age-related diseases, such as type 2 diabetes mellitus. This review focuses mainly on recent advances in MOTS-c research with regards to diabetes, including both type 1 and type 2. The emerging understanding of MOTS-c in diabetes may provide insight into the development of new therapies for diabetes and other age or senescence-related diseases.

Citations

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Mitochondrial-derived peptides: Antidiabetic functions and evolutionary perspectives
Satadeepa Kal, Sumana Mahata, Suborno Jati, Sushil K. Mahata
Peptides.2024; 172: 171147. CrossRef
Mitochondrial Stress and Mitokines: Therapeutic Perspectives for the Treatment of Metabolic Diseases
Benyuan Zhang, Joon Young Chang, Min Hee Lee, Sang-Hyeon Ju, Hyon-Seung Yi, Minho Shong
Diabetes & Metabolism Journal.2024; 48(1): 1. CrossRef
Mitochondrial bioenergetics, metabolism, and beyond in pancreatic β-cells and diabetes
Alejandra María Rivera Nieves, Brian Michael Wauford, Accalia Fu
Frontiers in Molecular Biosciences.2024;[Epub] CrossRef
Haplotype variability in mitochondrial rRNA predisposes to metabolic syndrome
Petr Pecina, Kristýna Čunátová, Vilma Kaplanová, Guillermo Puertas-Frias, Jan Šilhavý, Kateřina Tauchmannová, Marek Vrbacký, Tomáš Čajka, Ondřej Gahura, Markéta Hlaváčková, Viktor Stránecký, Stanislav Kmoch, Michal Pravenec, Josef Houštěk, Tomáš Mráček, A
Communications Biology.2024;[Epub] CrossRef
Pyrroloquinoline Quinone Alleviates Mitochondria Damage in Radiation-Induced Lung Injury in a MOTS-c-Dependent Manner
Yanli Zhang, Jianfeng Huang, Shengpeng Li, Junlin Jiang, Jiaojiao Sun, Dan Chen, Qingfeng Pang, Yaxian Wu
Journal of Agricultural and Food Chemistry.2024; 72(38): 20944. CrossRef

Original Article

Basic Research
Long Non-Coding RNA TUG1 Attenuates Insulin Resistance in Mice with Gestational Diabetes Mellitus via Regulation of the MicroRNA-328-3p/SREBP-2/ERK Axis: Xuwen Tang, Qingxin Qin, Wenjing Xu, Xuezhen Zhang; Diabetes Metab J. 2023;47(2):267-286. Published online January 19, 2023; DOI: https://doi.org/10.4093/dmj.2021.0216

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Background
Long non-coding RNAs (lncRNAs) have been illustrated to contribute to the development of gestational diabetes mellitus (GDM). In the present study, we aimed to elucidate how lncRNA taurine upregulated gene 1 (TUG1) influences insulin resistance (IR) in a high-fat diet (HFD)-induced mouse model of GDM.
Methods
We initially developed a mouse model of HFD-induced GDM, from which islet tissues were collected for RNA and protein extraction. Interactions among lncRNA TUG1/microRNA (miR)-328-3p/sterol regulatory element binding protein 2 (SREBP-2) were assessed by dual-luciferase reporter assay. Fasting blood glucose (FBG), fasting insulin (FINS), homeostasis model assessment of insulin resistance (HOMA-IR), HOMA pancreatic β-cell function (HOMA-β), insulin sensitivity index for oral glucose tolerance tests (ISOGTT) and insulinogenic index (IGI) levels in mouse serum were measured through conducting gain- and loss-of-function experiments.
Results
Abundant expression of miR-328 and deficient expression of lncRNA TUG1 and SREBP-2 were characterized in the islet tissues of mice with HFD-induced GDM. LncRNA TUG1 competitively bound to miR-328-3p, which specifically targeted SREBP-2. Either depletion of miR-328-3p or restoration of lncRNA TUG1 and SREBP-2 reduced the FBG, FINS, HOMA-β, and HOMA-IR levels while increasing ISOGTT and IGI levels, promoting the expression of the extracellular signal-regulated kinase (ERK) signaling pathway-related genes, and inhibiting apoptosis of islet cells in GDM mice. Upregulation miR-328-3p reversed the alleviative effects of SREBP-2 and lncRNA TUG1 on IR.
Conclusion
Our study provides evidence that the lncRNA TUG1 may prevent IR following GDM through competitively binding to miR-328-3p and promoting the SREBP-2-mediated ERK signaling pathway inactivation.

Citations

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Research Progress of Risk Factors Associated with Gestational Diabetes Mellitus
Zi-Jun Lin, Lian-Ping He, Cui-Ping Li
Endocrine, Metabolic & Immune Disorders - Drug Targets.2025; 25(2): 99. CrossRef
Diabetes and diabetic associative diseases: An overview of epigenetic regulations of TUG1
Mohammed Ageeli Hakami
Saudi Journal of Biological Sciences.2024; 31(5): 103976. CrossRef
Expression and Regulatory Ability of Long Non-Coding RNADLX6 Antisense RNA 1 in Gestational Diabetes Mellitus
Qiuhong Huang, Lichun Tang, Xiaohui Meng, Meiling Wen, Yin Qin, Jingjing Liu, Xuanxuan Luo, Rong Liang, Xia Dai
Clinical and Experimental Obstetrics & Gynecology.2024;[Epub] CrossRef
Chemerin alleviates the placental oxidative stress and improves fetal overgrowth of gestational diabetes mellitus mice induced by high fat diet
Xuan Zhou, Yi Jiang, Zizhuo Wang, Lijie Wei, Huiting Zhang, Chenyun Fang, Shenglan Zhu, Yuanyuan Du, Rui Su, Weikun Li, Zhenzhen He, Liangnan Zhang, Weidong Tan, Mengzhou He, Jun Yu, Shaoshuai Wang, Wencheng Ding, Ling Feng
Molecular Medicine.2024;[Epub] CrossRef
Effect of Tinospora cordifolia on gestational diabetes mellitus and its complications
Ritu Rani, Havagiray Chitme, Avinash Kumar Sharma
Women & Health.2023; 63(5): 359. CrossRef
Therapeutic Effect of Tinospora cordifolia (Willd) Extracts on Letrozole-Induced Polycystic Ovarian Syndrome and its Complications in Murine Model
Ritu Rani, Avinash Kumar Sharma, Havagiray R Chitme
Clinical Medicine Insights: Endocrinology and Diabetes.2023;[Epub] CrossRef
The role of ncRNA regulatory mechanisms in diseases—case on gestational diabetes
Dong Gao, Liping Ren, Yu-Duo Hao, Nalini Schaduangrat, Xiao-Wei Liu, Shi-Shi Yuan, Yu-He Yang, Yan Wang, Watshara Shoombuatong, Hui Ding
Briefings in Bioinformatics.2023;[Epub] CrossRef
lncRNA TUG1 as Potential Novel Biomarker for Prognosis of Cardiovascular Diseases
Habib Haybar, Narjes Sadat Sadati, Daryush Purrahman, Mohammad Reza Mahmoudian-Sani, Najmaldin Saki
Epigenomics.2023; 15(23): 1273. CrossRef

Review

Basic Research
The Link between Mitochondrial Dysfunction and Sarcopenia: An Update Focusing on the Role of Pyruvate Dehydrogenase Kinase 4: Min-Ji Kim, Ibotombi Singh Sinam, Zerwa Siddique, Jae-Han Jeon, In-Kyu Lee; Diabetes Metab J. 2023;47(2):153-163. Published online January 12, 2023; DOI: https://doi.org/10.4093/dmj.2022.0305

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Sarcopenia, defined as a progressive loss of muscle mass and function, is typified by mitochondrial dysfunction and loss of mitochondrial resilience. Sarcopenia is associated not only with aging, but also with various metabolic diseases characterized by mitochondrial dyshomeostasis. Pyruvate dehydrogenase kinases (PDKs) are mitochondrial enzymes that inhibit the pyruvate dehydrogenase complex, which controls pyruvate entry into the tricarboxylic acid cycle and the subsequent adenosine triphosphate production required for normal cellular activities. PDK4 is upregulated in mitochondrial dysfunction-related metabolic diseases, especially pathologic muscle conditions associated with enhanced muscle proteolysis and aberrant myogenesis. Increases in PDK4 are associated with perturbation of mitochondria-associated membranes and mitochondrial quality control, which are emerging as a central mechanism in the pathogenesis of metabolic disease-associated muscle atrophy. Here, we review how mitochondrial dysfunction affects sarcopenia, focusing on the role of PDK4 in mitochondrial homeostasis. We discuss the molecular mechanisms underlying the effects of PDK4 on mitochondrial dysfunction in sarcopenia and show that targeting mitochondria could be a therapeutic target for treating sarcopenia.

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Thomas Lilley, Donny M. Camera, Faith A.A. Kwa
Drug Discovery Today.2025; 30(1): 104283. CrossRef
Synthesis, activatory effects, molecular docking and ADME studies as rabbit muscle pyruvate kinase activators of ureido phenyl substituted 1,4-dihydropyridine derivatives
Mustafa Oğuzhan Kaya, Tuna Demirci, Ümit Çalışır, Oğuzhan Özdemir, Yeşim Kaya, Mustafa Arslan
Research on Chemical Intermediates.2024; 50(1): 437. CrossRef
Unraveling the causes of sarcopenia: Roles of neuromuscular junction impairment and mitochondrial dysfunction
Yanmei Miao, Leiyu Xie, Jiamei Song, Xing Cai, Jinghe Yang, Xinglong Ma, Shaolin Chen, Peng Xie
Physiological Reports.2024;[Epub] CrossRef
Metabolic clues to aging: exploring the role of circulating metabolites in frailty, sarcopenia and vascular aging related traits and diseases
Zonghao Qian, Yuzhen Huang, Yucong Zhang, Ni Yang, Ziwei Fang, Cuntai Zhang, Le Zhang
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Inhibition of Pyruvate Dehydrogenase Kinase 4 Protects Cardiomyocytes from lipopolysaccharide-Induced Mitochondrial Damage by Reducing Lactate Accumulation
Tangtian Chen, Qiumin Xie, Bin Tan, Qin Yi, Han Xiang, Rui Wang, Qin Zhou, Bolin He, Jie Tian, Jing Zhu, Hao Xu
Inflammation.2024; 47(4): 1356. CrossRef
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Hirotaka Takayama, Takuya Yoshimura, Hajime Suzuki, Yuka Hirano, Masahiro Tezuka, Takayuki Ishida, Kiyohide Ishihata, Marie Amitani, Haruka Amitani, Yasunori Nakamura, Yasushi Imamura, Akio Inui, Norifumi Nakamura
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Songling Jiang, Han Sol Kim, Ji Hyun Ryu, Yong-Soo Lee, Dong-Ik Kim, Eun-Jung Jin
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Inflammation.2024;[Epub] CrossRef
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Liang Pei, Zhuo Yao, Dong Liang, Keda Yang, Lin Tao
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Sodium Phenylbutyrate Attenuates Cisplatin-Induced Acute Kidney Injury Through Inhibition of Pyruvate Dehydrogenase Kinase 4
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International Journal of Nanomedicine.2023; Volume 18: 7559. CrossRef

Original Articles

Metabolic Risk/Epidemiology
Reproductive Life Span and Severe Hypoglycemia Risk in Postmenopausal Women with Type 2 Diabetes Mellitus: Soyeon Kang, Yong-Moon Park, Dong Jin Kwon, Youn-Jee Chung, Jeong Namkung, Kyungdo Han, Seung-Hyun Ko; Diabetes Metab J. 2022;46(4):578-591. Published online January 24, 2022; DOI: https://doi.org/10.4093/dmj.2021.0135

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Background
Estrogen promotes glucose homeostasis, enhances insulin sensitivity, and maintains counterregulatory responses in recurrent hypoglycemia in women of reproductive age. Postmenopausal women with type 2 diabetes mellitus (T2DM) might be more vulnerable to severe hypoglycemia (SH) events. However, the relationship between reproductive factors and SH occurrence in T2DM remains unelucidated.
Methods
This study included data on 181,263 women with postmenopausal T2DM who participated in a national health screening program from January 1 to December 31, 2009, obtained using the Korean National Health Insurance System database. Outcome data were obtained until December 31, 2018. Associations between reproductive factors and SH incidence were assessed using Cox proportional hazards models.
Results
During the mean follow-up of 7.9 years, 11,279 (6.22%) postmenopausal women with T2DM experienced SH episodes. A longer reproductive life span (RLS) (≥40 years) was associated with a lower SH risk compared to a shorter RLS (<30 years) (adjusted hazard ratio [HR], 0.74; 95% confidence interval [CI], 0.69 to 0.80; P for trend <0.001) after multivariable adjustment. SH risk decreased with every 5-year increment of RLS (with <30 years as a reference [adjusted HR, 0.91; 95% CI, 0.86 to 0.95; P=0.0001 for 30−34 years], [adjusted HR, 0.80; 95% CI, 0.76 to 0.84; P<0.001 for 35−39 years], [adjusted HR, 0.74; 95% CI, 0.68 to 0.81; P<0.001 for ≥40 years]). The use of hormone replacement therapy (HRT) was associated with a lower SH risk than HRT nonuse.
Conclusion
Extended exposure to endogenous ovarian hormone during lifetime may decrease the number of SH events in women with T2DM after menopause.

Citations

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Association between serum copper level and reproductive health of Women in the United States: a cross-sectional study
Yi Yuan, Tong-Yu Peng, Guang-Yuan Yu, Zhao Zou, Meng-Ze Wu, Ruofei Zhu, Shuang Wu, Zi Lv, Su-Xin Luo
International Journal of Environmental Health Research.2024; 34(6): 2441. CrossRef
Defining Continuous Glucose Monitor Time in Range in a Large, Community-Based Cohort Without Diabetes
Nicole L Spartano, Naznin Sultana, Honghuang Lin, Huimin Cheng, Sophia Lu, David Fei, Joanne M Murabito, Maura E Walker, Howard A Wolpert, Devin W Steenkamp
The Journal of Clinical Endocrinology & Metabolism.2024;[Epub] CrossRef
Reproductive Lifespan and Motor Progression of Parkinson’s Disease
Ruwei Ou, Qianqian Wei, Yanbing Hou, Lingyu Zhang, Kuncheng Liu, Junyu Lin, Tianmi Yang, Jing Yang, Zheng Jiang, Wei Song, Bei Cao, Huifang Shang
Journal of Clinical Medicine.2022; 11(20): 6163. CrossRef
Menopause and development of Alzheimer’s disease: Roles of neural glucose metabolism and Wnt signaling
Paulina Villaseca, Pedro Cisternas, Nibaldo C. Inestrosa
Frontiers in Endocrinology.2022;[Epub] CrossRef

Basic Research
Carnitine Orotate Complex Ameliorates Insulin Resistance and Hepatic Steatosis Through Carnitine Acetyltransferase Pathway: Jung-Hee Hong, Moon-Kyu Lee; Diabetes Metab J. 2021;45(6):933-947. Published online August 19, 2021; DOI: https://doi.org/10.4093/dmj.2020.0223

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Background
Carnitine orotate complex (Godex) has been shown to decrease glycated hemoglobin levels and improve steatosis in patients with type 2 diabetes mellitus with non-alcoholic fatty liver disease. However, the mechanisms of Godex in glucose metabolism remain unclear.
Methods
Male C57BL/6J mice were divided into four groups: normal-fat diet, high-fat diet, a high-fat diet supplemented with intraperitoneal injection of (500 mg or 2,000 mg/kg/day) Godex for 8 weeks. Computed tomography, indirect calorimetry, and histological analyses including electron microscopy of the liver were performed, and biochemical profiles and oral glucose tolerance test and insulin tolerance test were undertaken. Expressions of genes in the lipid and glucose metabolism, activities of oxidative phosphorylation enzymes, carnitine acetyltransferase, pyruvate dehydrogenase, and acetyl-coenzyme A (CoA)/CoA ratio were evaluated.
Results
Godex improved insulin sensitivity and significantly decreased fasting plasma glucose, homeostatic model assessment for insulin resistance, steatosis, and gluconeogenesis, with a marked increase in fatty acid oxidation as well as better use of glucose in high-fat diet-fed mice. It preserved mitochondrial function and ultrastructure, restored oxidative phosphorylation enzyme activities, decreased acetyl-CoA/CoA ratio, and increased carnitine acetyltransferase content and pyruvate dehydrogenase activity. Carnitine acetyltransferase knockdown partially reversed the effects of Godex in liver and in vitro.
Conclusion
Godex improved insulin resistance and steatosis by regulating carnitine acetyltransferase in liver in high-fat diet-fed mice.

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Impact of l-Carnitine Supplementation on Liver Enzyme Normalization in Patients with Chronic Liver Disease: A Meta-Analysis of Randomized Trials
Hyunwoo Oh, Chan Hyuk Park, Dae Won Jun
Journal of Personalized Medicine.2022; 12(7): 1053. CrossRef
Prolonged Use of Carnitine-Orotate Complex (Godex®) Is Associated with Improved Mortality: A Nationwide Cohort Study
Kye-Yeung Park, Sangmo Hong, Kyung-Soo Kim, Kyungdo Han, Cheol-Young Park
Journal of Personalized Medicine.2022; 12(12): 1970. CrossRef
The Role of Carnitine Orotate Complex in Fatty Liver
Hyon-Seung Yi
Diabetes & Metabolism Journal.2021; 45(6): 866. CrossRef

Complications
Renal Tubular Damage Marker, Urinary N-acetyl-β-D-Glucosaminidase, as a Predictive Marker of Hepatic Fibrosis in Type 2 Diabetes Mellitus: Hae Kyung Kim, Minyoung Lee, Yong-ho Lee, Eun Seok Kang, Bong-Soo Cha, Byung-Wan Lee; Diabetes Metab J. 2022;46(1):104-116. Published online July 13, 2021; DOI: https://doi.org/10.4093/dmj.2020.0273

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Background
Non-alcoholic steatohepatitis is closely associated with the progression of diabetic kidney disease (DKD) in type 2 diabetes mellitus (T2DM). We investigated whether urinary N-acetyl-β-D-glucosaminidase (u-NAG), an early renal tubular damage biomarker in DKD, could be related to the degree of hepatic fibrosis in patients with T2DM.
Methods
A total of 300 patients with T2DM were enrolled in this study. Hepatic steatosis and fibrosis were determined using transient elastography. The levels of urinary biomarkers, including u-NAG, albumin, protein, and creatinine, and glucometabolic parameters were measured.
Results
Based on the median value of the u-NAG to creatinine ratio (u-NCR), subjects were divided into low and high u-NCR groups. The high u-NCR group showed a significantly longer duration of diabetes, worsened hyperglycemia, and a more enhanced hepatic fibrosis index. A higher u-NCR was associated with a greater odds ratio for the risk of higher hepatic fibrosis stage (F2: odds ratio, 1.99; 95% confidence interval [CI], 1.04 to 3.82). Also, u-NCR was an independent predictive marker for more advanced hepatic fibrosis, even after adjusting for several confounding factors (β=1.58, P<0.01).
Conclusion
The elevation of u-NAG was independently associated with a higher degree of hepatic fibrosis in patients with T2DM. Considering the common metabolic milieu of renal and hepatic fibrosis in T2DM, the potential use of u-NAG as an effective urinary biomarker reflecting hepatic fibrosis in T2DM needs to be validated in the future.

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High Glycated Hemoglobin Instead of High Body Mass Index Might Increase the Urine N-Acetyl-β-D-glucosaminidase Con-Centration in Children and Adolescents with Diabetes Mellitus
Jin-Soon Suh, Kyoung Soon Cho, Seul Ki Kim, Shin-Hee Kim, Won Kyoung Cho, Min Ho Jung, Moon Bae Ahn
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Basic Research
Sulforaphane Ameliorates Diabetes-Induced Renal Fibrosis through Epigenetic Up-Regulation of BMP-7: Lili Kong, Hongyue Wang, Chenhao Li, Huiyan Cheng, Yan Cui, Li Liu, Ying Zhao; Diabetes Metab J. 2021;45(6):909-920. Published online June 4, 2021; DOI: https://doi.org/10.4093/dmj.2020.0168

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Background
The dietary agent sulforaphane (SFN) has been reported to reduce diabetes-induced renal fibrosis, as well as inhibit histone deacetylase (HDAC) activity. Bone morphologic protein 7 (BMP-7) has been shown to reduce renal fibrosis induced by transforming growth factor-beta1. The aim of this study was to investigate the epigenetic effect of SFN on BMP-7 expression in diabetes-induced renal fibrosis.
Methods
Streptozotocin (STZ)-induced diabetic mice and age-matched controls were subcutaneously injected with SFN or vehicle for 4 months to measure the in vivo effects of SFN on the kidneys. The human renal proximal tubular (HK11) cell line was used to mimic diabetic conditions in vitro. HK11 cells were transfected to over-express HDAC2 and treated with high glucose/palmitate (HG/Pal) to explore the epigenetic modulation of BMP-7 in SFN-mediated protection against HG/Pal-induced renal fibrosis.
Results
SFN significantly attenuated diabetes-induced renal fibrosis in vivo. Among all of the HDACs we detected, HDAC2 activity was markedly elevated in the STZ-induced diabetic kidneys and HG/Pal-treated HK11 cells. SFN inhibited the diabetes-induced increase in HDAC2 activity which was associated with histone acetylation and transcriptional activation of the BMP-7 promoter. HDAC2 over-expression reduced BMP-7 expression and abolished the SFN-mediated protection against HG/Pal-induced fibrosis in vitro.
Conclusion
Our study demonstrates that the HDAC inhibitor SFN protects against diabetes-induced renal fibrosis through epigenetic up-regulation of BMP-7.

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Review

Basic Research
Histone Deacetylase 9: Its Role in the Pathogenesis of Diabetes and Other Chronic Diseases: Siqi Hu, Eun-Hee Cho, Ji-Young Lee; Diabetes Metab J. 2020;44(2):234-244. Published online March 24, 2020; DOI: https://doi.org/10.4093/dmj.2019.0243

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Abstract PDF PubReader

As a member of the class IIa histone deacetylases (HDACs), HDAC9 catalyzes the deacetylation of histones and transcription factors, commonly leading to the suppression of gene transcription. The activity of HDAC9 is regulated transcriptionally and post-translationally. HDAC9 is known to play an essential role in regulating myocyte and adipocyte differentiation and cardiac muscle development. Also, recent studies have suggested that HDAC9 is involved in the pathogenesis of chronic diseases, including cardiovascular diseases, osteoporosis, autoimmune disease, cancer, obesity, insulin resistance, and liver fibrosis. HDAC9 modulates the expression of genes related to the pathogenesis of chronic diseases by altering chromatin structure in their promotor region or reducing the transcriptional activity of their respective transcription factors. This review summarizes the current knowledge of the regulation of HDAC9 expression and activity. Also, the roles of HDAC9 in the pathogenesis of chronic diseases are discussed, along with potential underlying mechanisms.

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Original Articles

Clinical Diabetes & Therapeutics
Association between Serum Selenium Level and the Presence of Diabetes Mellitus: A Meta-Analysis of Observational Studies: Juno Kim, Hye Soo Chung, Min-Kyu Choi, Yong Kyun Roh, Hyung Joon Yoo, Jung Hwan Park, Dong Sun Kim, Jae Myung Yu, Shinje Moon; Diabetes Metab J. 2019;43(4):447-460. Published online January 2, 2019; DOI: https://doi.org/10.4093/dmj.2018.0123

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Background

Epidemiological studies have suggested an association between selenium (Se) and diabetes mellitus (DM). However, different studies have reported conflicting results. Therefore, we performed a comprehensive meta-analysis to clarify the impact of Se on DM.

Methods

We searched the PubMed database for studies on the association between Se and DM from inception to June 2018.

Results

Twenty articles evaluating 47,930 participants were included in the analysis. The meta-analysis found that high levels of Se were significantly associated with the presence of DM (pooled odds ratios [ORs], 1.88; 95% confidence interval [CI], 1.44 to 2.45). However, significant heterogeneity was found (I²=82%). Subgroup analyses were performed based on the Se measurement methods used in each study. A significant association was found between high Se levels and the presence of DM in the studies that used blood (OR, 2.17; 95% CI, 1.60 to 2.93; I²=77%), diet (OR, 1.61; 95% CI, 1.10 to 2.36; I²=0%), and urine (OR, 1.49; 95% CI, 1.02 to 2.17; I²=0%) as samples to estimate Se levels, but not in studies on nails (OR, 1.24; 95% CI, 0.52 to 2.98; I²=91%). Because of significant heterogeneity in the studies with blood, we conducted a sensitivity analysis and tested the publication bias. The results were consistent after adjustment based on the sensitivity analysis as well as the trim and fill analysis for publication bias.

Conclusion

This meta-analysis demonstrates that high levels of Se are associated with the presence of DM. Further prospective and randomized controlled trials are warranted to elucidate the link better.

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Others
Evaluation of a Novel Glucose Area Under the Curve (AUC) Monitoring System: Comparison with the AUC by Continuous Glucose Monitoring: Satoshi Ugi, Hiroshi Maegawa, Katsutaro Morino, Yoshihiko Nishio, Toshiyuki Sato, Seiki Okada, Yasuo Kikkawa, Toshihiro Watanabe, Hiromu Nakajima, Atsunori Kashiwagi; Diabetes Metab J. 2016;40(4):326-333. Published online July 26, 2016; DOI: https://doi.org/10.4093/dmj.2016.40.4.326

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Abstract PDF PubReader

Background

Management of postprandial hyperglycemia is a key aspect in diabetes treatment. We developed a novel system to measure glucose area under the curve (AUC) using minimally invasive interstitial fluid extraction technology (MIET) for simple monitoring of postprandial glucose excursions. In this study, we evaluated the relationship between our system and continuous glucose monitoring (CGM) by comparing glucose AUC obtained using MIET with that obtained using CGM for a long duration.

Methods

Twenty diabetic inpatients wearing a CGM system were enrolled. For MIET measurement, a plastic microneedle array was applied to the skin as pretreatment, and hydrogels were placed on the pretreated area to collect interstitial fluid. Hydrogels were replaced every 2 or 4 hours and AUC was predicted on the basis of glucose and sodium ion levels.

Results

AUC predicted by MIET correlated well with that measured by CGM (r=0.93). Good performances of both consecutive 2- and 4-hour measurements were observed (measurement error: 11.7%±10.2% for 2 hours and 11.1%±7.9% for 4 hours), indicating the possibility of repetitive measurements up to 8 hours. The influence of neither glucose fluctuation nor average glucose level over the measurement accuracy was observed through 8 hours.

Conclusion

Our system showed good relationship with AUC values from CGM up to 8 hours, indicating that single pretreatment can cover a large portion of glucose excursion in a day. These results indicated possibility of our system to contribute to convenient monitoring of glucose excursions for a long duration.

Citations

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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
Diabetes & Metabolism Journal.2017; 41(4): 265. CrossRef

Review

Others
Novel Molecular Mechanisms in the Development of Non-Alcoholic Steatohepatitis: Davide Povero, Ariel E. Feldstein; Diabetes Metab J. 2016;40(1):1-11. Published online February 19, 2016; DOI: https://doi.org/10.4093/dmj.2016.40.1.1

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Abstract PDF PubReader

Non-alcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease in adults and children worldwide. NAFLD has become a severe health issue and it can progress towards a more severe form of the disease, the non-alcoholic steatohepatitis (NASH). A combination of environmental factors, host genetics, and gut microbiota leads to excessive accumulation of lipids in the liver (steatosis), which may result in lipotoxicity and trigger hepatocyte cell death, liver inflammation, fibrosis, and pathological angiogenesis. NASH can further progress towards liver cirrhosis and cancer. Over the last few years, cell-derived extracellular vesicles (EVs) have been identified as effective cell-to-cell messengers that transfer several bioactive molecules in target cells, modulating the pathogenesis and progression of NASH. In this review, we focused on recently highlighted aspects of molecular pathogenesis of NASH, mediated by EVs via their bioactive components. The studies included in this review summarize the state of art regarding the role of EVs during the progression of NASH and bring novel insight about the potential use of EVs for diagnosis and therapeutic strategies for patients with this disease.

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