Neohesperidin enhances PGC-1α-mediated mitochondrial biogenesis and alleviates hepatic steatosis in high fat diet fed mice
| Autor: | Xue-Yu Fan, Li-jun Lou, Yuan-Yuan Weng, Hao Sheng, Si-wei Wang, Yong-Feng Bai, Feng Zhang |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Blood Glucose Male medicine.medical_specialty Endocrinology Diabetes and Metabolism Mitochondrion AMP-Activated Protein Kinases Diet High-Fat Article 03 medical and health sciences Mice 0302 clinical medicine Insulin resistance Non-alcoholic Fatty Liver Disease Internal medicine Nonalcoholic fatty liver disease Internal Medicine medicine Animals Humans Obesity Beta oxidation lcsh:RC620-627 Organelle Biogenesis business.industry Hesperidin AMPK Type 2 diabetes Hep G2 Cells Translational research medicine.disease Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha humanities Mitochondria Fatty Liver Mice Inbred C57BL lcsh:Nutritional diseases. Deficiency diseases 030104 developmental biology Endocrinology Mitochondrial biogenesis 030220 oncology & carcinogenesis Organelle biogenesis Steatosis Insulin Resistance business |
| Zdroj: | Nutrition & Diabetes, Vol 10, Iss 1, Pp 1-11 (2020) Nutrition & Diabetes |
| ISSN: | 2044-4052 |
| DOI: | 10.1038/s41387-020-00130-3 |
| Popis: | Backgrounds Mitochondria plays a critical role in the development and pathogenesis of nonalcoholic fatty liver disease (NAFLD). Neohesperidin (NHP) could lower blood glucose and prevent obesity in mice. However, the direct effect of NHP on hepatic steatosis has not been reported. Methods Mice were fed with either a chow diet or HFD with or without oral gavage of NHP for 12 weeks. A variety of biochemical and histological indicators were examined. In vitro cell culture model was utilized to demonstrate underlying molecular mechanism of the effect induced by NHP treatment. Results NHP increases mitochondrial biogenesis, improves hepatic steatosis and systematic insulin resistance in high fat diet (HFD) fed mice. NHP elevates hepatic mitochondrial biogenesis and fatty acid oxidation by increasing PGC-1α expression. Mechanistically, the activation of AMP-activated protein kinase (AMPK) is involved in NHP induced PGC-1α expression. Conclusions PGC-1α-mediated mitochondrial biogenesis plays a vital role in the mitigation of hepatic steatosis treated by NHP. Our result suggests that NHP is a good candidate to be dietary supplement for the auxiliary treatment of NAFLD. |
| Databáze: | OpenAIRE |
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