Molecular nutrition & food research, 2019-02, Vol.63 (4), p.e1800795-n/a
2019
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- Autor(en) / Beteiligte
- Titel
- Sulforaphane Improves Lipid Metabolism by Enhancing Mitochondrial Function and Biogenesis In Vivo and In Vitro
- Ist Teil von
- Molecular nutrition & food research, 2019-02, Vol.63 (4), p.e1800795-n/a
- Ort / Verlag
- Germany: Wiley Subscription Services, Inc
- Erscheinungsjahr
- 2019
- Quelle
- Wiley Online Library - AutoHoldings Journals
- Beschreibungen/Notizen
- Scope Sulforaphane (SFN) is reported to reduce the accumulation of lipids. However, the underling mechanism remains unclear. In this study, the potential of SFN to improve lipid metabolism is investigated through altering mitochondrial function and biogenesis‐related mechanisms. Methods and Results The abnormal lipid metabolism model was established both in HHL‐5 cells and in rats by feeding a high‐fat diet (HFD) for 10 weeks. The current findings suggest that SFN alleviates the swelling of mitochondria and stimulates mitochondrial biogenesis. The reduced expression of NRF1 and TFAM, were reversed by SFN. SFN increases the levels of antioxidant compounds via nuclear factor erythroid‐2‐related factor (Nrf2) activation. Furthermore, SFN improves multiple mitochondrial bioactivities, such as mitochondrial membrane potential, ATP, and the electron transfer chain based on PGC‐1α pathway. SFN also activates lipolysis by transcriptionally upregulating adipose triglyceride lipase (ATGL) and hormone‐sensitive lipase (HSL). Conclusions SFN enhances utilization of lipids via both the PGC‐ 1α‐dependent promotion of mitochondrial biogenesis and Nrf2 dependent improvement of mitochondrial function. Dysfunction of mitochondria and decreased mitochondrial contents have been observed in free fatty acids (FFAs) treated HHL‐5 cells and high‐fat‐diet‐treated rats. It is shown that sulforaphane not only enhances the utilization of FFAs via both PGC‐1α dependent mitochondrial biogenesis and Nrf‐2‐dependent mitochondrial function, but also activates lipolysis by upregulating the mRNA expression of adipose triglyceride lipase and hormone‐sensitive lipase.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1613-4125eISSN: 1613-4133DOI: 10.1002/mnfr.201800795Titel-ID: cdi_proquest_journals_2331792457
- Format
- –
- Schlagworte
- Animals, Antioxidants, Antioxidants - metabolism, Biosynthesis, Cell Line, Diet, High-Fat - adverse effects, Electron transfer, Gene Expression Regulation - drug effects, Hepatocytes - drug effects, Hepatocytes - metabolism, High fat diet, Humans, Isothiocyanates - pharmacology, Lipase, Lipid metabolism, Lipid Metabolism - drug effects, Lipids, Lipolysis, Male, Membrane potential, Membrane Potential, Mitochondrial - drug effects, Metabolism, Mitochondria, Mitochondria, Liver - drug effects, Mitochondria, Liver - metabolism, NF-E2-Related Factor 2 - genetics, Non-alcoholic Fatty Liver Disease - drug therapy, Non-alcoholic Fatty Liver Disease - etiology, nonalcholic fatty liver disease, Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics, Rats, Wistar, Sulforaphane, Transcription, Triglycerides