Diabetes & Metabolism Journal

Original Articles

Basic Research
Peroxisomal Fitness: A Potential Protective Mechanism of Fenofibrate against High Fat Diet-Induced Non-Alcoholic Fatty Liver Disease in Mice: Songling Jiang, Md Jamal Uddin, Xiaoying Yu, Lingjuan Piao, Debra Dorotea, Goo Taeg Oh, Hunjoo Ha; Diabetes Metab J. 2022;46(6):829-842. Published online June 24, 2022; DOI: https://doi.org/10.4093/dmj.2021.0274

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Background
Non-alcoholic fatty liver disease (NAFLD) has been increasing in association with the epidemic of obesity and diabetes. Peroxisomes are single membrane-enclosed organelles that play a role in the metabolism of lipid and reactive oxygen species. The present study examined the role of peroxisomes in high-fat diet (HFD)-induced NAFLD using fenofibrate, a peroxisome proliferator-activated receptor α (PPARα) agonist.
Methods
Eight-week-old male C57BL/6J mice were fed either a normal diet or HFD for 12 weeks, and fenofibrate (50 mg/kg/day) was orally administered along with the initiation of HFD.
Results
HFD-induced liver injury as measured by increased alanine aminotransferase, inflammation, oxidative stress, and lipid accumulation was effectively prevented by fenofibrate. Fenofibrate significantly increased the expression of peroxisomal genes and proteins involved in peroxisomal biogenesis and function. HFD-induced attenuation of peroxisomal fatty acid oxidation was also significantly restored by fenofibrate, demonstrating the functional significance of peroxisomal fatty acid oxidation. In Ppara deficient mice, fenofibrate failed to maintain peroxisomal biogenesis and function in HFD-induced liver injury.
Conclusion
The present data highlight the importance of PPARα-mediated peroxisomal fitness in the protective effect of fenofibrate against NAFLD.

Citations

Citations to this article as recorded by

Pharmacological potential of ginseng and ginsenosides in nonalcoholic fatty liver disease and nonalcoholic steatohepatitis
Young-Su Yi
Journal of Ginseng Research.2024; 48(2): 122. CrossRef
Fenofibrate alleviates NAFLD by enhancing the PPARα/PGC-1α signaling pathway coupling mitochondrial function
Xuemei Wang, Jieying Wang, Cao Ying, Yuan Xing, Xuan Su, Ke Men
BMC Pharmacology and Toxicology.2024;[Epub] CrossRef
Role of Fenofibrate Use in Dyslipidemia and Related Comorbidities in the Asian Population: A Narrative Review
Chaicharn Deerochanawong, Sin Gon Kim, Yu-Cheng Chang
Diabetes & Metabolism Journal.2024; 48(2): 184. CrossRef
Current Therapeutical Approaches Targeting Lipid Metabolism in NAFLD
Manuela Vitulo, Elisa Gnodi, Giulia Rosini, Raffaella Meneveri, Roberto Giovannoni, Donatella Barisani
International Journal of Molecular Sciences.2023; 24(16): 12748. CrossRef
PPARα agonist fenofibrate prevents postoperative cognitive dysfunction by enhancing fatty acid oxidation in mice
Tiantian Liu, Xinlu Chen, Ziqi Wei, Xue Han, Yujia Liu, Zhengliang Ma, Tianjiao Xia, Xiaoping Gu
Translational Neuroscience.2023;[Epub] CrossRef
Fenofibrate enhances lipid deposition via modulating PPARγ, SREBP-1c, and gut microbiota in ob/ob mice fed a high-fat diet
Ying Zhang, Xiu-Bin Jia, Yun-Chao Liu, Wen-Qian Yu, Yan-Hong Si, Shou-Dong Guo
Frontiers in Nutrition.2022;[Epub] CrossRef

Basic Research
Vimentin Deficiency Prevents High-Fat Diet-Induced Obesity and Insulin Resistance in Mice: SeoYeon Kim, Inyeong Kim, Wonkyoung Cho, Goo Taeg Oh, Young Mi Park; Diabetes Metab J. 2021;45(1):97-108. Published online June 15, 2020; DOI: https://doi.org/10.4093/dmj.2019.0198

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233 Download
16 Web of Science
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Background

Obesity and type 2 diabetes mellitus are world-wide health problems, and lack of understanding of their linking mechanism is one reason for limited treatment options. We determined if genetic deletion of vimentin, a type 3 intermediate filament, affects obesity and type 2 diabetes mellitus.

Methods

We fed vimentin-null (Vim^−/−) mice and wild-type mice a high-fat diet (HFD) for 10 weeks and measured weight change, adiposity, blood lipids, and glucose. We performed intraperitoneal glucose tolerance tests and measured CD36, a major fatty acid translocase, and glucose transporter type 4 (GLUT4) in adipocytes from both groups of mice.

Results

Vim^−/− mice fed an HFD showed less weight gain, less adiposity, improved glucose tolerance, and lower serum level of fasting glucose. However, serum triglyceride and non-esterified fatty acid levels were higher in Vim^−/− mice than in wild-type mice. Vimentin-null adipocytes showed 41.1% less CD36 on plasma membranes, 27% less uptake of fatty acids, and 50.3% less GLUT4, suggesting defects in intracellular trafficking of these molecules.

Conclusion

We concluded that vimentin deficiency prevents obesity and insulin resistance in mice fed an HFD and suggest vimentin as a central mediator linking obesity and type 2 diabetes mellitus.

Citations

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Irina Tikhonova, Alsu Dyukina, Elvira Shaykhutdinova, Valentina Safronova
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Blueberry and Blackberry Anthocyanins Ameliorate Metabolic Syndrome by Modulating Gut Microbiota and Short-Chain Fatty Acids Metabolism in High-Fat Diet-Fed C57BL/6J Mice
Lanlan Du, Han Lü, Yan Chen, Xiaohua Yu, Tunyu Jian, Huifang Zhao, Wenlong Wu, Xiaoqin Ding, Jian Chen, Weilin Li
Journal of Agricultural and Food Chemistry.2023; 71(40): 14649. CrossRef
An analogue of the Prolactin Releasing Peptide reduces obesity and promotes adult neurogenesis
Sara KM Jörgensen, Alena Karnošová, Simone Mazzaferro, Oliver Rowley, Hsiao-Jou Cortina Chen, Sarah J Robbins, Sarah Christofides, Florian T Merkle, Lenka Maletínská, David Petrik
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Cytoskeleton alterations in non-alcoholic fatty liver disease
João Pessoa, José Teixeira
Metabolism.2022; 128: 155115. CrossRef
Recent Advances in the Treatment of Insulin Resistance Targeting Molecular and Metabolic Pathways: Fighting a Losing Battle?
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Roles of vimentin in health and disease
Karen M. Ridge, John E. Eriksson, Milos Pekny, Robert D. Goldman
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Plasma Membrane Localization of CD36 Requires Vimentin Phosphorylation; A Mechanism by Which Macrophage Vimentin Promotes Atherosclerosis
Seo Yeon Kim, Se-Jin Jeong, Ji-Hae Park, Wonkyoung Cho, Young-Ho Ahn, Youn-Hee Choi, Goo Taeg Oh, Roy L. Silverstein, Young Mi Park
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