Sulforaphane Improves Lipid Metabolism by Enhancing Mitochondrial Function and Biogenesis In Vivo and In Vitro
Lei P, Tian S, Teng C, Huang L, Liu X, Wang J, Zhang Y, Li B, Shan Y
Molecular nutrition & food research · 69 citations
Review labels
Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.
How it was studied
- Design
- Animal study (classified by our AI screen)
- Studied in
- People, plus animal or lab work
- Main outcome
- Mechanisms only
Who paid for it
- Funding
- Independent funding
- Government
- National Science Foundation
- Nonprofit
- Foundation for the National Institutes of Health
- University or hospital
- University of East Anglia
- University or hospital
- University of Glasgow
- Government
- National Natural Science Foundation of China
- University or hospital
- Heilongjiang University of Chinese Medicine
- Government
- National Institutes of Natural Sciences
- Grants
- Heilongjiang University of Chinese Medicine (2018RCD14); National Natural Science Foundation of China (81573135)
Based on 7 listed funder(s).
Publication
- Published
- 2018-12-22 · Mol Nutr Food Res · vol. 63 · issue 4 · p. e1800795
- Publisher
- Wiley
- Cited
- 90 citations · more than 93% of similar papers · 2.9× the field average
- Impact
- Top 10% most cited in its field
- References
- 52 works
- Access
- Paywalled
- Research areas
- Genomics, phytochemicals, and oxidative stress · Lipid metabolism and biosynthesis · Sirtuins and Resveratrol in Medicine
- Keywords
- TFAM, Sulforaphane, Mitochondrial biogenesis, Adipose triglyceride lipase, Lipid metabolism, Mitochondrion, NRF1, Cell biology, Lipolysis, Chemistry, Lipid droplet, Biochemistry, Biology, Adipose tissue
- MeSH
- cell line, mitochondria, liver, hepatocytes, animals, humans, rats, wistar, isothiocyanates, sulfoxides, antioxidants, gene expression regulation, male, lipid metabolism, nf-e2-related factor 2, membrane potential, mitochondrial, diet, high-fat, non-alcoholic fatty liver disease, peroxisome proliferator-activated receptor gamma coactivator 1-alpha
9 authors
From CN
- Peng LeiHarbin Institute of Technology; Heilongjiang Institute of Technology
- Si-Cong TianHarbin Institute of Technology; Heilongjiang Institute of Technology
- Chunying TengHarbin Institute of Technology; Heilongjiang Institute of Technology
- Lei HuangHarbin Institute of Technology; Heilongjiang Institute of Technology
- Xiaodong LiuHarbin Institute of Technology; Heilongjiang Institute of Technology
- Jiaojiao WangHeilongjiang University of Chinese Medicine
Abstract
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.
Abstract via Europe PMC. Copyright remains with the authors or publisher.
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