Endocrinology and Metabolism

Review Article

Mineral, bone & muscle
Sarcopenia and Muscle Aging: Updated Insights into Molecular Mechanisms and Translational Therapeutics: Thanh T. Nguyen, Tam Dao, Ha Thu Nguyen, Jun-Hyeon Park, Seung-Jun Jeong, Sei Kim, Yunju Jo, Nhung T.H. Thieu, Jiangqi Zhao, Fuan Ding, Ying Yu, Vu Chi Dung, Karim Gariani, Beom-Jun Kim, Dongryeol Ryu; Endocrinol Metab. 2026;41(1):57-85. Published online February 12, 2026; DOI: https://doi.org/10.3803/EnM.2025.2656

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Sarcopenia is a progressive, age-related condition characterized by the loss of skeletal muscle mass, strength, and function, which increases the risk of falls, frailty, and loss of independence. Despite growing recognition and its incorporation into geriatric assessments, there is still no approved pharmacological treatment. This review provides an updated overview of sarcopenia, encompassing diagnostic criteria, biological mechanisms, and emerging therapeutic strategies. Key molecular features include mitochondrial dysfunction, nicotinamide adenine dinucleotide (NAD⁺) decline, fiber-type alterations, and dysregulation of myokines. Recent singlecell and multi-omics studies have revealed the heterogeneity of muscle tissue and distinct cell-type-specific aging patterns. Therapeutic efforts are evolving beyond lifestyle interventions toward targeted approaches, including myostatin inhibitors, NAD⁺ boosters, senolytics, and microbiome modulators. However, clinical translation remains constrained by heterogeneity in trial design and the absence of standardized outcome measures. Future sarcopenia care will likely involve precision medicine guided by biomarkers and supported by digital monitoring tools. Progressing from molecular discovery to clinical application will be essential for preserving muscle health and function in aging populations.

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Molecular Mechanisms and Nutritional Modulation in Sarcopenia: A Narrative Review
Hui San Chin, Ling Liu, Pei-Ju Liao, Alexandra L. R. M. Wee, Xiu-Yi Kwek, Bin Tean Teh, Frederick H. Koh
Nutrients.2026; 18(7): 1161. CrossRef
Elevated Circulating Ceramides 18:0 and 24:1 as a Risk Factor for Sarcopenia: In Vitro, Animal, and Clinical Evidence
So Jeong Park, Ji Yeon Baek, Shibo Wei, Jin Young Lee, Yuna Lee, Sang‐Hoon Lee, Il‐Young Jang, Hyuk Sakong, Hyun Ju Yoo, Hee‐Won Jung, Eunju Lee, Su Jung Kim, Yunju Jo, Kyunggon Kim, Dongryeol Ryu, Beom‐Jun Kim
Journal of Cachexia, Sarcopenia and Muscle.2026;[Epub] CrossRef
Dysregulation of the ubiquitin–proteasome system in aging skeletal muscle
Gunju Song, Boo-Yong Lee, Kwang-Hyun Baek
Biomedicine & Pharmacotherapy.2026; 199: 119504. CrossRef
Trends in Low Muscle Mass and Sarcopenia Prevalence in Korea Using Korea National Health and Nutrition Examination Survey (KNHANES) 2024 and 2008–2011: The KSBMR-KSOS KNHANES DXA Joint Task Force Report
Namki Hong, Jun-Il Yoo, Jeonghoon Ha, Seong Hee Ahn, Young-Kyun Lee, Hyun Sik Gong, Ki-Hyun Baek, Yumie Rhee, Yong-Chan Ha
Journal of Bone Metabolism.2026; 33(2): 197. CrossRef
Differential Effects of Stroke Stage and Age on Sarcopenia in Stroke Patients: A Cross-Sectional Study
Guan-Bo Chen, I-Hsiu Liou, Shu-Fen Sun, Chien-Hui Li, Sheng-Hui Tuan
Life.2026; 16(7): 1073. CrossRef
From organ age gaps to precision geromedicine: Multi-omic and imaging frameworks for heterogeneous biological aging
Qian-Man Li, Xiao-Xuan Ge, Tian-Jiao Wen, Li-Wen Zhang, Hao-Yu Liu, Xiu-Wen Shi, Lu Liu, Ting-Ting Gong, Qi-Jun Wu, Shan-Yan Gao
Ageing Research Reviews.2026; 121: 103238. CrossRef
Effect of moderate-intensity aerobic exercise on early oxidative stress and muscle atrophy in SAMP8 mice through modulation of the DAO/SRR and Nrf2/Keap1 pathways
Xiangli Tong, Jinkun Xue, Zixuan Chen, Rongsiqing Luo, Zihan Huang, Fengxuan Chen, Ying Liu, Jingran Xiao, Jia Jiang, Zhiyuan Wang, Wenfeng Liu
Cellular Signalling.2026; 147: 112760. CrossRef
A Stimulus-Resolved Framework for Investigating Putative Neurotrophic Secretome–Metabolome Coupling in Aging Skeletal Muscle: CNTF and CLCF1 as Non-Equivalent Nodes
Fei Tong, Yirui Chen, Hongxin Gui, Aowei Li, Hongyu Li, Yusen Pei, Zimu Wu, Mengyang Wang
Metabolites.2026; 16(8): 562. CrossRef

Original Article

Diabetes, obesity and metabolism
Irisin Attenuates Hepatic Stellate Cell Activation and Liver Fibrosis in Bile Duct Ligation Mice Model and Improves Mitochondrial Dysfunction: Thuy Linh Lai, So Young Park, Giang Nguyen, Phuc Thi Minh Pham, Seon Mee Kang, Jeana Hong, Jae-Ho Lee, Seung-Soon Im, Dae-Hee Choi, Eun-Hee Cho; Endocrinol Metab. 2024;39(6):908-920. Published online November 5, 2024; DOI: https://doi.org/10.3803/EnM.2024.1984

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Background
Liver fibrosis is a common outcome of chronic liver disease and is primarily driven by hepatic stellate cell (HSC) activation. Irisin, a myokine released during physical exercise, is beneficial for metabolic disorders and mitochondrial dysfunction. This study aimed to explore the effects of irisin on liver fibrosis in HSCs, a bile duct ligation (BDL) mouse model, and the associated mitochondrial dysfunction.
Methods
In vitro experiments utilized LX-2 cells, a human HSC line, stimulated with transforming growth factor-β1 (TGF-β1), a major regulator of HSC fibrosis, with or without irisin. Mitochondrial function was assessed using mitochondrial fission markers, transmission electron microscopy, mitochondrial membrane potential, and adenosine triphosphate (ATP) production. In vivo, liver fibrosis was induced in mice via BDL, followed by daily intraperitoneal injections of irisin (100 μg/kg/day) for 10 days.
Results
In vitro, irisin mitigated HSC activation and reduced reactive oxygen species associated with the TGF-β1/Smad signaling pathway. Irisin restored TGF-β1-induced increases in fission markers (Fis1, p-DRP1) and reversed the decreased expression of TFAM and SIRT3. Additionally, irisin restored mitochondrial membrane potential and ATP production lowered by TGF-β1 treatment. In vivo, irisin ameliorated the elevated liver-to-body weight ratio induced by BDL and alleviated liver fibrosis, as evidenced by Masson’s trichrome staining. Irisin also improved mitochondrial dysfunction induced by BDL surgery.
Conclusion
Irisin effectively attenuated HSC activation, ameliorated liver fibrosis in BDL mice, and improved associated mitochondrial dysfunction. These findings highlight the therapeutic potential of irisin for the treatment of liver fibrosis.

Citations

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Lulu Pei, Xing Du, Zehao Mao, Kai Ding, Jiangyu Li, Tianqing Liu, Yongmei Zhao
Molecular Pharmaceutics.2026; 23(2): 662. CrossRef
From bench to bedside: Molecular mechanisms, diagnostic tools, and therapeutic strategies in liver fibrosis
Zhen Yang, Weizhao Tong, Kanglong Zhang, Guoxin Hu
Liver Research.2026; 10(2): 133. CrossRef
SREBP2 links ACSS2-dependent acetyl-CoA biosynthesis to metaboloepigenetic activation of hepatic stellate cells and liver fibrosis
Yu Wang, Aoqi Kang, Shunjie Wang, Zhen Yang, Hong Liu, Linbo Yue, Hao Li, Caiyi Wu, Wenjing Ren, Xiulian Miao, Zilong Li, Yong Xu, Zhiwen Fan
Metabolism.2026; 179: 156597. CrossRef
Synthesis and application of encapsulated Bifidobacterium Longum for mitigation of liver fibrosis via modulation of oxidative stress and inflammation in BDL rat model
Siavash Amiri, Mitra Motallebi, Mohsen Hemmati-Dinarvand, Merat Karimi, Maryam Akhavan Taheri, Sahar Ahmadi Asouri, Mohammad Esmaeil Shahaboddin
World Journal of Microbiology and Biotechnology.2026;[Epub] CrossRef
Irisin Attenuates Pulmonary Vascular Remodeling in Pulmonary Arterial Hypertension via Ubiquitin‐Mediated Regulation of ENO1
Na Sun, Yong‐Bing Wang, Jing Huang, Run‐Wei Deng, Hui‐Yu He, Lei Gao, Xuan Gao, You‐Li Fan, Yan Cong, Yao‐Lei Guo, Yi‐Qiang Chen, Gui‐Jia Wang, Shao‐Hong Fang, Xia Gu, Bo Yu, Bing‐Xiang Wu
Advanced Science.2025;[Epub] CrossRef
The Influence of Irisin on Selected Organs—The Liver, Kidneys, and Lungs: The Role of Physical Exercise
Maria Ciałowicz, Marek Woźniewski, Eugenia Murawska-Ciałowicz, Piotr Dzięgiel
Cells.2025; 14(16): 1228. CrossRef
Metabolic and immune links between sarcopenia and liver disease
Stanislav Nikolaevich Kotlyarov
World Journal of Hepatology.2025;[Epub] CrossRef
Irisin, the Myokine: Guardian and Mediator in Cardiovascular System
Tian Lan, Xueru Yan, Jie Li, Haoran Gu, Qi Hou, Enpeng He, Qingyuan Yang
Endocrinology, Diabetes & Metabolism.2025;[Epub] CrossRef
Inflammation—Insulin Resistance Crosstalk and the Central Role of Myokines
Maria-Zinaida Dobre, Bogdana Virgolici, Daciana Costina Andrada Dunca-Stefan, Ioana-Cristina Doicin, Iulia-Ioana Stanescu-Spinu
International Journal of Molecular Sciences.2025; 27(1): 60. CrossRef

Review Article

Diabetes, obesity and metabolism
The Emerging Importance of Mitochondria in White Adipocytes: Neither Last nor Least: Juan Cai, Fenfen Wang, Mengle Shao; Endocrinol Metab. 2023;38(5):493-503. Published online October 10, 2023; DOI: https://doi.org/10.3803/EnM.2023.1813

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The growing recognition of mitochondria’s crucial role in the regulation of white adipose tissue remodeling and energy balance underscores its significance. The marked metabolic diversity of mitochondria provides the molecular and cellular foundation for enabling adipose tissue plasticity in response to various metabolic cues. Effective control of mitochondrial function at the cellular level, not only in thermogenic brown and beige adipocytes but also in energy-storing white adipocytes, exerts a profound influence on adipose homeostasis. Furthermore, mitochondria play a pivotal role in intercellular communication within adipose tissue via production of metabolites with signaling properties. A more comprehensive understanding of mitochondrial regulation within white adipocytes will empower the development of targeted and efficacious strategies to enhance adipose function, leading to advancements in overall metabolic health.

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Aerobic glycolysis drives differentiation of unilocular adipocytes
Alice Maestri, Min Cai, Ruby Schipper, Julia Backman, Alana Vannay, Anneli Olsson, Ewa Ehrenborg, Roland Nilsson, Carolina E. Hagberg
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The Multiple Roles and Targeting Strategies of LonP1 in the Occurrence and Development of Cancer
Qun Zeng, Shitian Huang, Tingting Jiang
BioFactors.2026;[Epub] CrossRef
AAV-mediated FGF21 gene therapy promotes health span extension by whole-body tissue-specific adaptations
Veronica Jimenez, Victor Sacristan, Miquel Garcia, Claudia Jambrina, Estefania Casana, Sergio Muñoz, Laia Vilà, Ignasi Grass, Maria Luisa Jaén, Carles Roca, Xavier León, Sara Marcó, Maria Molas, Albert Ribera, Ivet Elias, Jordi Rodó, Tura Ferré, Fatima Bo
Molecular Therapy.2026; 34(8): 4546. CrossRef
Combining small extracellular vesicles with decellularized adipose tissue hydrogel for the construction of tissue-engineered adipose
Pengyu Hong, Shengmeng Yuan, Jian Yang, Zhiwei Cao, Xiangyun Sun, Ling Du, Dianri Wang, Jian Pan
Materials & Design.2025; 256: 114331. CrossRef
Unraveling the complexities of diet induced obesity and glucolipid dysfunction in metabolic syndrome
Babi Dutta, Aparna Tripathy, P. R. Archana, Shobha U. Kamath
Diabetology & Metabolic Syndrome.2025;[Epub] CrossRef
Protocol for differentiating murine 3T3-L1 and SVF-derived preadipocytes and isolating crude mitochondrial fractions
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International Journal of Obesity.2024;[Epub] CrossRef
Dissecting human adipose tissue heterogeneity using single‐cell omics technologies
Giuliana Di Rocco, Angelo Trivisonno, Giovanni Trivisonno, Gabriele Toietta
Stem Cell Research & Therapy.2024;[Epub] CrossRef
Decreased mitochondrial‐related gene expression in adipose tissue after acute sprint exercise in humans: A pilot study
Mona Esbjörnsson, Håkan C. Rundqvist, Barbara Norman, Ted Österlund, Eric Rullman, Jens Bülow, Eva Jansson
Physiological Reports.2024;[Epub] CrossRef
Brown Fat and Metabolic Health: The Diverse Functions of Dietary Components
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Original Articles

Diabetes, Obesity and Metabolism
Gemigliptin Alleviates Succinate-Induced Hepatic Stellate Cell Activation by Ameliorating Mitochondrial Dysfunction: Giang Nguyen, So Young Park, Dinh Vinh Do, Dae-Hee Choi, Eun-Hee Cho; Endocrinol Metab. 2022;37(6):918-928. Published online November 15, 2022; DOI: https://doi.org/10.3803/EnM.2022.1530

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Background
Dipeptidyl peptidase-4 inhibitors (DPP-4Is) are used clinically as oral antidiabetic agents. Although DPP-4Is are known to ameliorate liver fibrosis, the protective mechanism of DPP-4Is in liver fibrosis remains obscure. In this study, gemigliptin was used to investigate the potential of DPP-4Is to alleviate the progression of liver fibrosis.
Methods
To clarify the effects and mechanisms of gemigliptin, we conducted various experiments in LX-2 cells (immortalized human hepatic stellate cells [HSCs], the principal effectors of hepatic fibrogenesis), which were activated by succinate and exhibited elevated expression of α-smooth muscle actin, collagen type 1, and pro-inflammatory cytokines and increased cell proliferation. In vivo, we examined the effects and mechanisms of gemigliptin on a high-fat, high-cholesterol–induced mouse model of nonalcoholic steatohepatitis (NASH).
Results
Gemigliptin decreased the expression of fibrogenesis markers and reduced the abnormal proliferation of HSCs. In addition, gemigliptin reduced the succinate-induced production of mitochondrial reactive oxygen species (ROS), intracellular ROS, and mitochondrial fission in HSCs. Furthermore, in the mouse model of NASH-induced liver fibrosis, gemigliptin alleviated both liver fibrosis and mitochondrial dysfunction.
Conclusion
Gemigliptin protected against HSC activation and liver fibrosis by alleviating mitochondrial dysfunction and ROS production, indicating its potential as a strategy for preventing the development of liver disease.

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Mitochondrial dysfunction in MASH: Focusing on chronic inflammation and intercellular communication
Wanyi Luo, Muxin Yu, Chuwei Zheng, Xiaowen Li, Xiaotian Ma, Guocheng Zeng, Jinming Zhang, Xia Ji, Liyan Sun
Biochemical and Biophysical Research Communications.2026; 804: 153356. CrossRef
Sensing succinate: SUCNR1 as a context-dependent metabolic and cellular signal integrator
Aenne-Dorothea Liebing, Claudia Stäubert
Frontiers in Molecular Biosciences.2026;[Epub] CrossRef
Tearing Down the Wall: emu-miR-745-3p in Echinococcus multilocularis Exosomes Attenuates Host Liver Fibrosis to Permit Invasive Lesion Development
Ning Yang, Hongbin Zhang, Bowen Shi, Junlong Xue, Jin Chu, Xue Zhang, Liang Li, Hui Liu, Guodong Lü, Xiaojuan Bi, Renyong Lin
The Journal of Infectious Diseases.2026;[Epub] CrossRef
Omarigliptin attenuates thioacetamide-induced hepatic fibrosis in rats by activating SIRT1/Nrf2 and inhibiting NF-κB/TGF-β1 pathways
Abdulaziz Alarifi, Marwa Qadri, Daniyah A. Almarghalani, Ali Alquraini, Faisal K. Alkholifi, Fadhel A. Alomar, Moudi M. Alasmari, Aya A. Shokry, Passant E. Moustafa, Hany M. Fayed, Marwa E. Shabana
Immunopharmacology and Immunotoxicology.2026; 48(4): 630. CrossRef
SUCNR1 Deficiency Alleviates Liver Ischemia–Reperfusion Injury by Regulating Kupffer Cell Activation and Polarization Through the ERK/NF-κB Pathway in Mice
Huan Yang, An Wei, Xinting Zhou, Zhiwei Chen, Yiheng Wang
Inflammation.2025; 48(5): 3649. CrossRef
Metabolic Sparks in the Liver: Metabolic and Epigenetic Reprogramming in Hepatic Stellate Cells Activation and Its Implications for Human Metabolic Diseases
Yeon Jin Roh, Hyeonki Kim, Dong Wook Choi
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Andi Endang Kusuma Intan, Kanokwan Jarukamjorn, Tarapong Srisongkram
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Emerging roles of the metabolite succinate in bone-related diseases
Zuping Wu, Qiaoli Dai, Ying Wang, Na Wu, Chenyu Wang, Jiejun Shi
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Insulin Resistance, Non-Alcoholic Fatty Liver Disease and Type 2 Diabetes Mellitus: Clinical and Experimental Perspective
Inha Jung, Dae-Jeong Koo, Won-Young Lee
Diabetes & Metabolism Journal.2024; 48(3): 327. CrossRef
Improvement effect of gemigliptin on salivary gland dysfunction in exogenous methylglyoxal-injected rats
Woo Kwon Jung, Su-Bin Park, Hwa Young Yu, Junghyun Kim
Heliyon.2024; 10(8): e29362. CrossRef
Gemigliptin mitigates TGF-β-induced renal fibrosis through FGF21-mediated inhibition of the TGF-β/Smad3 signaling pathway
Jun-Kyu Byun, Gwon-Soo Jung
Biochemical and Biophysical Research Communications.2024; : 150425. CrossRef
Interference with mitochondrial function as part of the antifibrogenic effect of Rilpivirine: A step towards novel targets in hepatic stellate cell activation
Ana M. Benedicto, Federico Lucantoni, Isabel Fuster-Martínez, Pedro Diaz-Pozo, Dimitri Dorcaratto, Elena Muñoz-Forner, Victor M. Victor, Juan V. Esplugues, Ana Blas-García, Nadezda Apostolova
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DPP-IV as a potential candidate in anti-obesity and obesity-related diseases treatment
Xin Guo, Huolun Feng, Liyang Cai, Jiabin Zheng, Yong Li
Biomedicine & Pharmacotherapy.2024; 180: 117464. CrossRef
Irisin Attenuates Hepatic Stellate Cell Activation and Liver Fibrosis in Bile Duct Ligation Mice Model and Improves Mitochondrial Dysfunction
Thuy Linh Lai, So Young Park, Giang Nguyen, Phuc Thi Minh Pham, Seon Mee Kang, Jeana Hong, Jae-Ho Lee, Seung-Soon Im, Dae-Hee Choi, Eun-Hee Cho
Endocrinology and Metabolism.2024; 39(6): 908. CrossRef
Gemigliptin, a DPP4 inhibitor, ameliorates nonalcoholic steatohepatitis through AMP-activated protein kinase-independent and ULK1-mediated autophagy
Youngmi Song, Hyekyung Yang, Juhee Kim, Yoonjin Lee, Sung-Ho Kim, In-Gu Do, Cheol-Young Park
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Miscellaneous
Clinical Value of Serum Mitochondria-Inhibiting Substances in Assessing Renal Hazards: A Community-Based Prospective Study in Korea: Hoon Sung Choi, Jin Taek Kim, Hong Kyu Lee, Wook Ha Park, Youngmi Kim Pak, Sung Woo Lee; Endocrinol Metab. 2021;36(6):1298-1306. Published online November 26, 2021; DOI: https://doi.org/10.3803/EnM.2021.1226

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Background
Mitochondrial dysfunction is strongly associated with several kidney diseases. However, no studies have evaluated the potential renal hazards of serum mitochondria-inhibiting substance (MIS) and aryl hydrocarbon receptor ligand (AhRL) levels.
Methods
We used serum level of MIS and AhRL and clinical renal outcomes from 1,511 participants of a prospective community-based cohort in Ansung. MIS was evaluated based on intracellular adenosine triphosphate (MIS-ATP) or reactive oxygen species (MIS-ROS) generation measured using cell-based assays.
Results
During a mean 6.9-year follow-up, 84 participants (5.6%) developed a rapid decline in kidney function. In the lowest quartile group of MIS-ATP, patients were older and had metabolically deleterious parameters. In multivariate logistic regression analysis, higher MIS-ATP was associated with decreased odds for rapid decline: the odds ratio (OR) of 1% increase was 0.977 (95% confidence interval [CI], 0.957 to 0.998; P=0.031), while higher MIS-ROS was marginally associated with increased odds for rapid decline (OR, 1.014; 95% CI, 0.999 to 1.028; P=0.055). However, serum AhRL was not associated with the rapid decline in kidney function. In subgroup analysis, the renal hazard of MIS was particularly evident in people with hypertension and low baseline kidney function.
Conclusion
Serum MIS was independently associated with a rapid decline in kidney function, while serum AhRL was not. The clinical implication of renal hazard on serum MIS requires further evaluation in future studies.

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An Interactive Online App for Predicting Diabetes via Machine Learning from Environment-Polluting Chemical Exposure Data
Rosy Oh, Hong Kyu Lee, Youngmi Kim Pak, Man-Suk Oh
International Journal of Environmental Research and Public Health.2022; 19(10): 5800. CrossRef

Namgok Lecture 2020

Diabetes, Obesity and Metabolism
Cellular and Intercellular Homeostasis in Adipose Tissue with Mitochondria-Specific Stress: Min Jeong Choi, Saet-Byel Jung, Joon Young Chang, Minho Shong; Endocrinol Metab. 2021;36(1):1-11. Published online February 24, 2021; DOI: https://doi.org/10.3803/EnM.2021.956

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Paracrine interactions are imperative for the maintenance of adipose tissue intercellular homeostasis, and intracellular organelle dysfunction results in local and systemic alterations in metabolic homeostasis. It is currently accepted that mitochondrial proteotoxic stress activates the mitochondrial unfolded protein response (UPR^mt) in vitro and in vivo. The induction of mitochondrial chaperones and proteases during the UPR^mt is a key cell-autonomous mechanism of mitochondrial quality control. The UPR^mt also affects systemic metabolism through the secretion of cell non-autonomous peptides and cytokines (hereafter, metabokines). Mitochondrial function in adipose tissue plays a pivotal role in whole-body metabolism and human diseases. Despite continuing interest in the role of the UPR^mt and quality control pathways of mitochondria in energy metabolism, studies on the roles of the UPR^mt and metabokines in white adipose tissue are relatively sparse. Here, we describe the role of the UPR^mt in adipose tissue, including adipocytes and resident macrophages, and the interactive roles of cell non-autonomous metabokines, particularly growth differentiation factor 15, in local adipose cellular homeostasis and systemic energy metabolism.

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The role and mechanism of UPRmt in adipocytes
Hao Liu, Jie Chen, Dan-Qi Qiu, Miao-Wei Jiang, Hao-Qi Chen, Li Li, Shu-Qin Chen
Adipocyte.2026;[Epub] CrossRef
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Masaru Tanaka, László Vécsei
Biomedicines.2025; 13(8): 2020. CrossRef
Imeglimin modulates mitochondria biology and facilitates mitokine secretion in 3T3-L1 adipocytes
Nobuhiko Takahashi, Atsushi P. Kimura, Takayuki Yoshizaki, Kazumasa Ohmura
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Mitochondrial stress-induced GFRAL signaling controls diurnal food intake and anxiety-like behavior
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Review Articles

Miscellaneous
Sarcopenia and Muscle Aging: A Brief Overview: Tam Dao, Alexander E. Green, Yun A Kim, Sung-Jin Bae, Ki-Tae Ha, Karim Gariani, Mi-ra Lee, Keir J. Menzies, Dongryeol Ryu; Endocrinol Metab. 2020;35(4):716-732. Published online December 23, 2020; DOI: https://doi.org/10.3803/EnM.2020.405; [Original]

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The world is facing the new challenges of an aging population, and understanding the process of aging has therefore become one of the most important global concerns. Sarcopenia is a condition which is defined by the gradual loss of skeletal muscle mass and function with age. In research and clinical practice, sarcopenia is recognized as a component of geriatric disease and is a current target for drug development. In this review we define this condition and provide an overview of current therapeutic approaches. We further highlight recent findings that describe key pathophysiological phenotypes of this condition, including alterations in muscle fiber types, mitochondrial function, nicotinamide adenine dinucleotide (NAD⁺) metabolism, myokines, and gut microbiota, in aged muscle compared to young muscle or healthy aged muscle. The last part of this review examines new therapeutic avenues for promising treatment targets. There is still no accepted therapy for sarcopenia in humans. Here we provide a brief review of the current state of research derived from various mouse models or human samples that provide novel routes for the development of effective therapeutics to maintain muscle health during aging.

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Diabetes, Obesity and Metabolism
Implications of Mitochondrial Unfolded Protein Response and Mitokines: A Perspective on Fatty Liver Diseases: Hyon-Seung Yi; Endocrinol Metab. 2019;34(1):39-46. Published online March 21, 2019; DOI: https://doi.org/10.3803/EnM.2019.34.1.39

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The signaling network of the mitochondrial unfolded protein response (UPR^mt) and mitohormesis is a retrograde signaling pathway through which mitochondria-to-nucleus communication occurs in organisms. Recently, it has been shown that the UPR^mt is closely associated with metabolic disorders and conditions involving insulin resistance, such as alcoholic and non-alcoholic fatty liver and fibrotic liver disease. Scientific efforts to understand the UPR^mt and mitohormesis, as well as to establish the mitochondrial proteome, have established the importance of mitochondrial quality control in the development and progression of metabolic liver diseases, including non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). In this review, we integrate and discuss the recent data from the literature on the UPR^mt and mitohormesis in metabolic liver diseases, including NAFLD/NASH and fibrosis.

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Original Article

Endocrine Research
Deficiency of Sphingosine-1-Phosphate Reduces the Expression of Prohibitin and Causes β-Cell Impairment via Mitochondrial Dysregulation: Seok-Woo Hong, Jinmi Lee, Hyemi Kwon, Se Eun Park, Eun-Jung Rhee, Cheol-Young Park, Ki-Won Oh, Sung-Woo Park, Won-Young Lee; Endocrinol Metab. 2018;33(3):403-412. Published online September 18, 2018; DOI: https://doi.org/10.3803/EnM.2018.33.3.403

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Background

Emerging evidence suggests that sphingolipids may be involved in type 2 diabetes. However, the exact signaling defect through which disordered sphingolipid metabolism induces β-cell dysfunction remains unknown. The current study demonstrated that sphingosine-1-phosphate (S1P), the product of sphingosine kinase (SphK), is an essential factor for maintaining β-cell function and survival via regulation of mitochondrial action, as mediated by prohibitin (PHB).

Methods

We examined β-cell function and viability, as measured by mitochondrial function, in mouse insulinoma 6 (MIN6) cells in response to manipulation of cellular S1P and PHB levels.

Results

Lack of S1P induced by sphingosine kinase inhibitor (SphKi) treatment caused β-cell dysfunction and apoptosis, with repression of mitochondrial function shown by decreases in cellular adenosine triphosphate content, the oxygen consumption rate, the expression of oxidative phosphorylation complexes, the mitochondrial membrane potential, and the expression of key regulators of mitochondrial dynamics (mitochondrial dynamin-like GTPase [OPA1] and mitofusin 1 [MFN1]). Supplementation of S1P led to the recovery of mitochondrial function and greatly improved β-cell function and viability. Knockdown of SphK2 using small interfering RNA induced mitochondrial dysfunction, decreased glucose-stimulated insulin secretion (GSIS), and reduced the expression of PHB, an essential regulator of mitochondrial metabolism. PHB deficiency significantly reduced GSIS and induced mitochondrial dysfunction, and co-treatment with S1P did not reverse these trends.

Conclusion

Altogether, these data suggest that S1P is an essential factor in the maintenance of β-cell function and survival through its regulation of mitochondrial action and PHB expression.

Citations

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Review Article

Diabetes-Related Cardiac Dysfunction: Lamario J. Williams, Brenna G. Nye, Adam R. Wende; Endocrinol Metab. 2017;32(2):171-179. Published online June 23, 2017; DOI: https://doi.org/10.3803/EnM.2017.32.2.171

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The proposal that diabetes plays a role in the development of heart failure is supported by the increased risk associated with this disease, even after correcting for all other known risk factors. However, the precise mechanisms contributing to the condition referred to as diabetic cardiomyopathy have remained elusive, as does defining the disease itself. Decades of study have defined numerous potential factors that each contribute to disease susceptibility, progression, and severity. Many recent detailed reviews have been published on mechanisms involving insulin resistance, dysregulation of microRNAs, and increased reactive oxygen species, as well as causes including both modifiable and non-modifiable risk factors. As such, the focus of the current review is to highlight aspects of each of these topics and to provide specific examples of recent advances in each area.

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Original Article

Endocrine Research
The Effects of High Fat Diet and Resveratrol on Mitochondrial Activity of Brown Adipocytes: Cheol Ryong Ku, Yoon Hee Cho, Zhen-Yu Hong, Ha Lee, Sue Ji Lee, Seung-soo Hong, Eun Jig Lee; Endocrinol Metab. 2016;31(2):328-335. Published online April 8, 2016; DOI: https://doi.org/10.3803/EnM.2016.31.2.328

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Background

Resveratrol (RSV) is a polyphenolic phytoalexin that has many effects on metabolic diseases such as diabetes and obesity. Given the importance of brown adipose tissue (BAT) for energy expenditure, we investigated the effects of RSV on brown adipocytes.

Methods

For the in vitro study, interscapular BAT was isolated from 7-week-old male Sprague Dawley rats. For the in vivo study, 7-week-old male Otsuka Long Evans Tokushima Fatty (OLETF) rats were divided into four groups and treated for 27 weeks with: standard diet (SD); SD+RSV (10 mg/kg body weight, daily); high fat diet (HFD); HFD+RSV. RSV was provided via oral gavage once daily during the in vivo experiments.

Results

RSV treatment of primary cultured brown preadipocytes promoted mitochondrial activity, along with over-expression of estrogen receptor α (ER-α). In OLETF rats, both HFD and RSV treatment increased the weight of BAT and the differentiation of BAT. However, only RSV increased the mitochondrial activity and ER-α expression of BAT in the HFD-fed group. Finally, RSV improved the insulin sensitivity of OLETF rats by increasing the mitochondrial activity of BAT, despite having no effects on white adipocytes and muscles in either diet group.

Conclusion

RSV could improve insulin resistance, which might be associated with mitochondrial activity of brown adipocyte. Further studies evaluating the activity of RSV for both the differentiation and mitochondrial activity of BAT could be helpful in investigating the effects of RSV on metabolic parameters.

Citations

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Response: The Effects of High Fat Diet and Resveratrol on Mitochondrial Activity of Brown Adipocytes (Endocrinol Metab2016;31:328-35, Cheol Ryong Ku et al.)
Cheol Ryong Ku, Eun Jig Lee
Endocrinology and Metabolism.2016; 31(3): 482. CrossRef
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Endocrinology and Metabolism.2016; 31(3): 480. CrossRef

Review Article

Mechanisms of Vascular Calcification: The Pivotal Role of Pyruvate Dehydrogenase Kinase 4: Jaechan Leem, In-Kyu Lee; Endocrinol Metab. 2016;31(1):52-61. Published online March 16, 2016; DOI: https://doi.org/10.3803/EnM.2016.31.1.52

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Vascular calcification, abnormal mineralization of the vessel wall, is frequently associated with aging, atherosclerosis, diabetes mellitus, and chronic kidney disease. Vascular calcification is a key risk factor for many adverse clinical outcomes, including ischemic cardiac events and subsequent cardiovascular mortality. Vascular calcification was long considered to be a passive degenerative process, but it is now recognized as an active and highly regulated process similar to bone formation. However, despite numerous studies on the pathogenesis of vascular calcification, the mechanisms driving this process remain poorly understood. Pyruvate dehydrogenase kinases (PDKs) play an important role in the regulation of cellular metabolism and mitochondrial function. Recent studies show that PDK4 is an attractive therapeutic target for the treatment of various metabolic diseases. In this review, we summarize our current knowledge regarding the mechanisms of vascular calcification and describe the role of PDK4 in the osteogenic differentiation of vascular smooth muscle cells and development of vascular calcification. Further studies aimed at understanding the molecular mechanisms of vascular calcification will be critical for the development of novel therapeutic strategies.

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Original Articles

Endocrine Research
Selective Mitochondrial Uptake of MKT-077 Can Suppress Medullary Thyroid Carcinoma Cell Survival In Vitro and In Vivo: Dmytro Starenki, Jong-In Park; Endocrinol Metab. 2015;30(4):593-603. Published online December 31, 2015; DOI: https://doi.org/10.3803/EnM.2015.30.4.593

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Background

Medullary thyroid carcinoma (MTC) is a neuroendocrine tumor mainly caused by mutations in the rearranged during transfection (RET) proto-oncogene. Not all patients with progressive MTC respond to current therapy inhibiting RET, demanding additional therapeutic strategies. We recently demonstrated that disrupting mitochondrial metabolism using a mitochondria-targeted agent or by depleting a mitochondrial chaperone effectively suppressed human MTC cells in culture and in mouse xenografts by inducing apoptosis and RET downregulation. These observations led us to hypothesize that mitochondria are potential therapeutic targets for MTC. This study further tests this hypothesis using1-ethyl-2-[[3-ethyl-5-(3-methylbenzothiazolin-2-yliden)]-4-oxothiazolidin-2-ylidenemethyl] pyridinium chloride (MKT-077), a water-soluble rhodocyanine dye analogue, which can selectively accumulate in mitochondria.

Methods

The effects of MKT-077 on cell proliferation, survival, expression of RET and tumor protein 53 (TP53), and mitochondrial activity were determined in the human MTC lines in culture and in mouse xenografts.

Results

MKT-077 induced cell cycle arrest in TT and MZ-CRC-1. Intriguingly, MKT-077 also induced RET downregulation and strong cell death responses in TT cells, but not in MZ-CRC-1 cells. This discrepancy was mainly due to the difference between the capacities of these cell lines to retain MKT-077 in mitochondria. The cytotoxicity of MKT-077 in TT cells was mainly attributed to oxidative stress while being independent of TP53. MKT-077 also effectively suppressed tumor growth of TT xenografts.

Conclusion

MKT-077 can suppress cell survival of certain MTC subtypes by accumulating in mitochondria and interfering with mitochondrial activity although it can also suppress cell proliferation via other mechanisms. These results consistently support the hypothesis that mitochondrial targeting has therapeutic potential for MTC.

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Endocrine Research
Diastolic Dysfunction Induced by a High-Fat Diet Is Associated with Mitochondrial Abnormality and Adenosine Triphosphate Levels in Rats: Ki-Woon Kang, Ok-Soon Kim, Jung Yeon Chin, Won Ho Kim, Sang Hyun Park, Yu Jeong Choi, Jong Ho Shin, Kyung Tae Jung, Do-Seon Lim, Seong-Kyu Lee; Endocrinol Metab. 2015;30(4):557-568. Published online December 31, 2015; DOI: https://doi.org/10.3803/EnM.2015.30.4.557

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Background

Obesity is well-known as a risk factor for heart failure, including diastolic dysfunction. However, this mechanism in high-fat diet (HFD)-induced obese rats remain controversial. The purpose of this study was to investigate whether cardiac dysfunction develops when rats are fed with a HFD for 10 weeks; additionally, we sought to investigate the association between mitochondrial abnormalities, adenosine triphosphate (ATP) levels and cardiac dysfunction.

Methods

We examined myocardia in Wistar rats after 10 weeks of HFD (45 kcal% fat, n=6) or standard diet (SD, n=6). Echocardiography, histomorphologic analysis, and electron microscopy were performed. The expression levels of mitochondrial oxidative phosphorylation (OXPHOS) subunit genes, peroxisome-proliferator-activated receptor γ co-activator-1α (PGC1α) and anti-oxidant enzymes were assessed. Markers of oxidative stress damage, mitochondrial DNA copy number and myocardial ATP level were also examined.

Results

After 10 weeks, the body weight of the HFD group (349.6±22.7 g) was significantly higher than that of the SD group (286.8±14.9 g), and the perigonadal and epicardial fat weights of the HFD group were significantly higher than that of the SD group. Histomorphologic and electron microscopic images were similar between the two groups. However, in the myocardium of the HFD group, the expression levels of OXPHOS subunit NDUFB5 in complex I and PGC1α, and the mitochondrial DNA copy number were decreased and the oxidative stress damage marker 8-hydroxydeoxyguanosine was increased, accompanied by reduced ATP levels.

Conclusion

Diastolic dysfunction was accompanied by the mitochondrial abnormality and reduced ATP levels in the myocardium of 10 weeks-HFD-induced rats.

Citations

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Brief Report

Diabetes, Obesity and Metabolism
Glucagon-Like Peptide-1 Increases Mitochondrial Biogenesis and Function in INS-1 Rat Insulinoma Cells: Mi Yeon Kang, Tae Jung Oh, Young Min Cho; Endocrinol Metab. 2015;30(2):216-220. Published online June 30, 2015; DOI: https://doi.org/10.3803/EnM.2015.30.2.216

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Glucagon-like peptide-1 (GLP-1) is a gut-derived incretin hormone that increases glucose-stimulated insulin secretion in pancreatic β-cells. Since mitochondrial function is crucial to insulin secretion, we hypothesized that GLP-1 may increase mitochondrial biogenesis in pancreatic β-cells. We treated INS-1 rat insulinoma cells with GLP-1 or exendin-4 for 48 hours and measured mitochondrial mass and function. Both GLP-1 and exendin-4 increased mitochondrial mass by approximately 20%. The mitochondria/cytosol ratio was increased from 7.60±3.12% to 10.53±2.70% by exendin-4. In addition, GLP-1 increased the mitochondrial membrane potential and oxygen consumption. Proliferator-activated receptor-gamma coactivator 1α expression was increased approximately 2-fold by GLP-1 treatment. In conclusion, the present study presents evidence for a new mechanism of action by which GLP-1 improves pancreatic β-cell function via enhanced mitochondrial mass and performance.

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Review Article

Thyroid
Mitochondrial Energy Metabolism and Thyroid Cancers: Junguee Lee, Joon Young Chang, Yea Eun Kang, Shinae Yi, Min Hee Lee, Kyong Hye Joung, Kun Soon Kim, Minho Shong; Endocrinol Metab. 2015;30(2):117-123. Published online June 30, 2015; DOI: https://doi.org/10.3803/EnM.2015.30.2.117

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Primary thyroid cancers including papillary, follicular, poorly differentiated, and anaplastic carcinomas show substantial differences in biological and clinical behaviors. Even in the same pathological type, there is wide variability in the clinical course of disease progression. The molecular carcinogenesis of thyroid cancer has advanced tremendously in the last decade. However, specific inhibition of oncogenic pathways did not provide a significant survival benefit in advanced progressive thyroid cancer that is resistant to radioactive iodine therapy. Accumulating evidence clearly shows that cellular energy metabolism, which is controlled by oncogenes and other tumor-related factors, is a critical factor determining the clinical phenotypes of cancer. However, the role and nature of energy metabolism in thyroid cancer remain unclear. In this article, we discuss the role of cellular energy metabolism, particularly mitochondrial energy metabolism, in thyroid cancer. Determining the molecular nature of metabolic remodeling in thyroid cancer may provide new biomarkers and therapeutic targets that may be useful in the management of refractory thyroid cancers.

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Original Articles

Diabetes, Obesity and Metabolism
Mitochondrial Complexes I and II Are More Susceptible to Autophagy Deficiency in Mouse β-Cells: Min Joo Kim, Ok Kyong Choi, Kyung Sil Chae, Min Kyeong Kim, Jung Hee Kim, Masaaki Komatsu, Keiji Tanaka, Hakmo Lee, Sung Soo Chung, Soo Heon Kwak, Young Min Cho, Kyong Soo Park, Hye Seung Jung; Endocrinol Metab. 2015;30(1):65-70. Published online March 27, 2015; DOI: https://doi.org/10.3803/EnM.2015.30.1.65

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Background

Damaged mitochondria are removed by autophagy. Therefore, impairment of autophagy induces the accumulation of damaged mitochondria and mitochondrial dysfunction in most mammalian cells. Here, we investigated mitochondrial function and the expression of mitochondrial complexes in autophagy-related 7 (Atg7)-deficient β-cells.

Methods

To evaluate the effect of autophagy deficiency on mitochondrial function in pancreatic β-cells, we isolated islets from Atg7^F/F:RIP-Cre+ mice and wild-type littermates. Oxygen consumption rate and intracellular adenosine 5'-triphosphate (ATP) content were measured. The expression of mitochondrial complex genes in Atg7-deficient islets and in β-TC6 cells transfected with siAtg7 was measured by quantitative real-time polymerase chain reaction.

Results

Baseline oxygen consumption rate of Atg7-deficient islets was significantly lower than that of control islets (P<0.05). Intracellular ATP content of Atg7-deficient islets during glucose stimulation was also significantly lower than that of control islets (P<0.05). By Oxygraph-2k analysis, mitochondrial respiration in Atg7-deficient islets was significantly decreased overall, although state 3 respiration and responses to antimycin A were unaffected. The mRNA levels of mitochondrial complexes I, II, III, and V in Atg7-deficient islets were significantly lower than in control islets (P<0.05). Down-regulation of Atg7 in β-TC6 cells also reduced the expression of complexes I and II, with marginal significance (P<0.1).

Conclusion

Impairment of autophagy in pancreatic β-cells suppressed the expression of some mitochondrial respiratory complexes, and may contribute to mitochondrial dysfunction. Among the complexes, I and II seem to be most vulnerable to autophagy deficiency.

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Autophagy deficiency in β cells blunts incretin-induced suppression of glucagon release from α cells
Min Joo Kim, Ok Kyong Choi, Kyung Sil Chae, Hakmo Lee, Sung Soo Chung, Dong-Sik Ham, Ji-Won Kim, Kun-Ho Yoon, Kyong Soo Park, Hye Seung Jung
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A Novel Cytosolic Isoform of Mitochondrial Trans-2-Enoyl-CoA Reductase Enhances Peroxisome Proliferator-Activated Receptor α Activity: Dong-Gyu Kim, Jae Cheal Yoo, Eunju Kim, Young-Sun Lee, Oleg V. Yarishkin, Da Yong Lee, Kun Ho Lee, Seong-Geun Hong, Eun Mi Hwang, Jae-Yong Park; Endocrinol Metab. 2014;29(2):185-194. Published online June 26, 2014; DOI: https://doi.org/10.3803/EnM.2014.29.2.185

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Abstract PDF PubReader

Background

Mitochondrial trans-2-enoyl-CoA reductase (MECR) is involved in mitochondrial synthesis of fatty acids and is highly expressed in mitochondria. MECR is also known as nuclear receptor binding factor-1, which was originally reported with yeast two-hybrid screening as a binding protein of the nuclear hormone receptor peroxisome proliferator-activated receptor α (PPARα). However, MECR and PPARα are localized at different compartment, mitochondria, and the nucleus, respectively. Therefore, the presence of a cytosolic or nuclear isoform of MECR is necessary for functional interaction between MECR and PPARα.

Methods

To identify the expression pattern of MECR and the cytosolic form of MECR (cMECR), we performed reverse transcription polymerase chain reaction (RT-PCR) with various tissue samples from Sprague-Dawley rats. To confirm the interaction between cMECR and PPARα, we performed several binding assays such as yeast two-hybrid, coimmunoprecipitation, and bimolecular fluorescence complementation. To observe subcellular localization of these proteins, immunocytochemistry was performed. A luciferase assay was used to measure PPARα activity.

Results

We provide evidence of an alternatively spliced variant of the rat MECR gene that yields cMECR. The cMECR lacks the N-terminal 76 amino acids of MECR and shows uniform distribution in the cytoplasm and nucleus of HeLa cells. cMECR directly bound PPARα in the nucleus and increased PPARα-dependent luciferase activity in HeLa cells.

Conclusion

We found the cytosolic form of MECR (cMECR) was expressed in the cytosolic and/or nuclear region, directly binds with PPARα, and enhances PPARα activity.

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Case Reports

A Case of MELAS Syndrome Manifested by Insulin-deficient Diabetes Mellitus.: Hee Seog Jeong, Ji Young Kang, Hyun Kim, Kyu Ho Lee, Dal Sic Lee, Guan Yong Choi, Tae Geun Oh, Hyen Jeong Jeon; J Korean Endocr Soc. 2008;23(6):444-449. Published online December 1, 2008; DOI: https://doi.org/10.3803/jkes.2008.23.6.444

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Abstract PDF

MELAS (mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes) syndrome is characterized by stroke-like episodes before the age of 40, encephalopathy, seizures, dementia and lactic acidosis, and is caused by mutations in mitochondrial DNA. Diabetes mellitus and cardiac involvement are also frequently seen in MELAS syndrome. It is a classic mitochondrial disorder that shows a slow, chronic, progressive course, and presents with multiple organ involvement including the central nervous system, skeletal muscle, eye, cardiac muscle and gastrointestinal system.

Citations

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Characteristic Neuroimaging Findings in a Patient with Acute Metabolic Encephalopathy, Lactic Acidosis and Stroke-Like Episodes Syndrome Distinguishable from that of Acute Ischemic Stroke
Hyodong Kim, Jung-ju Lee, Byung-kun Kim, Ohyun Kwon, Jong-moo Park, Kyusik Kang, Woong-woo Lee
Journal of the Korean Neurological Association.2020; 38(1): 37. CrossRef

A Case of Adrenocortical Oncocytoma.: Seong Jin Lee, Ho Gwon Lee, Cheol young Park, In Kyung Jeong, Eun Gyung Hong, Gi Weon Oh, Hyeon Kyu Kim, Doo Man Kim, Jae Myung Yoo, Sung Hee Ihm, Moon Gi Choi, Hyung Joon Yoo, Sung Woo Park; J Korean Endocr Soc. 2004;19(1):82-89. Published online February 1, 2004

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Abstract PDF: Oncocytomas are neoplasms, histologically are composed of epithelial cells, with abundant, acidophilic and granular cytoplasm. Electron microscopic studies of oncocytomas have shown that the cytoplasm of oncocytes is packed with mitochondria. The adrenal gland is a very rare anatomical site for oncocytomas, and to the best of our knowledge, only thirty-six cases of adrenal oncocytomas have been described. Herein, a case of a large adrenal mass in a forty-year-old man, which was incidentally detected by abdominal ultrasonography, is presented. This patient demonstrated no clinical manifestation associated with adrenal hyperfunction. Hormonal studies showed no abnormal findings, except for a mild elevation of the 24-hour urinary VMA level. Abdominal computed tomography with enhancement revealed a large, well-defined left adrenal mass, measuring 5.0x.2 x.0cm. The patient underwent a left adrenalectomy, and a light microscopic examination confirmed an adrenocortical oncocytoma, with characteristic oncocytes and polygonal, abundant, eosinophilic and granular cytoplasm. The tumor cells were positive for cytokeratin and vimentin as well as S-100, but negative for chromogranin on immunohistochemical staining. An electron microscopic examination demonstrated closely packed mitochondria, containing intramitochondrial inclusions. After surgery, there was no evidence of a recurrent or distant metastatic disease at the 5 month follow-up. In summary, an extremely rare case of a man with an adrenocortical oncocytoma is reported, which was confirmed by histological examinations, including electron microscopy.

Original Article

The Correlation of Plasma Homocysteine and Mitochondrial DNA Content in Peripheral Blood in Healthy Women.: Soo Lim, Won Shik Shin, Kyong Soo Park, Seong Yeon Kim, Jong Ho Lee, Mi Ja Yim, Ji Hyun Song, Hong Kyu Lee; J Korean Endocr Soc. 2000;15(2):248-261. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Hyperhomocysteinemia is an independent risk factor for cardiovascular diseases. Previous reports showed that homocysteine damages mitochondrial gene expression, function and structure. In recent years, homocysteine and mitochondrial DNA (mtDNA) content are reported to relate with insulin resistance. The aim of this study is to investigate the correlation of plasma homocysteine level and mitochondrial DNA content in peripheral blood. METHODS: The mtDNA content, homocysteine and insulin resistance parameters were measured in healthy women (n=60). Plasma homocysteine level was measured by ion-exchange chromatography method and the mtDNA content in peripheral blood was measured by real time PCR method using ABI Prism 7700 machine. RESULTS: Significant correlation was found between homocysteine and mtDNA content (r=-0.507, p<0.05). Homocysteine was correlated with age (r=0.397), cholesterol (r=0.327), LDL-cholesterol (r=0.318), apolipoprotein B (r=0.387), HbA1c (r=0.274) positively and folate (r=-0.262), apolipoprotein A1 (r=-0.293), VO2max (r=-0.332) negatively. Mitochondrial DNA content was correlated with age (r=-0.535), BMI (r=-0.397), cholesterol (r=-0.340), LDL-cholesterol (r=-0.319), apolipoprotein B (r=-0.367) negatively and apolipoprotein A1 (r=0.346), lactate (r=0.307), VO2max (r=0.308) positively. All correlations were statistically significant(p<0.05). CONCLUSION: In this study, plasma homocysteine level was related with mitochondrial DNA content negatively and these two factors are estimated to be concerned with insulin resistance.

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