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Chem Biol Interact. 2018 Jun 25;290:77-87. doi: 10.1016/j.cbi.2018.05.014. Epub 2018 May 29.

Ganoderic Acid A improves high fat diet-induced obesity, lipid accumulation and insulin sensitivity through regulating SREBP pathway.

Author information

1
Department of Infectious Diseases, Hangzhou First People's Hospital, Nanjing Medical University, 310006, Hangzhou, Zhejiang, China.
2
Central Laboratory, Hangzhou First People's Hospital, Nanjing Medical University, 310006, Hangzhou, Zhejiang, China.
3
Department of Laboratory, Tongde Hospital of Zhejiang Province, 310012, Hangzhou, Zhejiang, China.
4
Department of Pulmonary Medicine Hangzhou First People's Hospital, Nanjing Medical University, 310006, Hangzhou, Zhejiang, China. Electronic address: xjb47@126.com.

Abstract

Obesity and its major co-morbidity, type 2 diabetes, have been an alarming epidemic prevalence without an effective treatment available. Sterol regulatory element-binding proteins (SREBPs) are major transcription factors regulating the expression of genes involved in biosynthesis of cholesterol, fatty acid and triglyceride. Therefore, inhibition of SREBP pathway may be a useful strategy to treat obesity with type 2 diabetes. Here, we identify a small molecule, Ganoderic Acid A (GAA), inhibits the SREBP expression and decreases the cellular levels of cholesterol and fatty acid in vitro. GAA also ameliorates body weight gain and fat accumulation in liver or adipose tissues, and improves serum lipid levels and insulin sensitivity in high fat diet (HFD)-induced obese mice. Consistently, GAA regulates SREBPs target genes and metabolism associated genes in liver or adipose tissues, which may directly contribute to the lower lipid level and improvement of insulin resistance. Taken together, GAA could be a potential leading compound for development of drugs for the prevention of obesity and insulin resistance.

KEYWORDS:

Ganoderic Acid A; Insulin resistance; Lipid accumulation; Obesity; SREBPs

PMID:
29852127
DOI:
10.1016/j.cbi.2018.05.014
[Indexed for MEDLINE]

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