Calebin‐A inhibits adipogenesis and hepatic steatosis in high‐fat diet‐induced obesity via activation of AMPK signaling. Issue 10 (20th July 2015)

• Record Type: Journal Article
• Authors: Lai, Ching‐Shu; Liao, Sih‐Ning; Tsai, Mei‐Ling; Kalyanam, Nagabhushanam; Majeed, Muhammed; Majeed, Anju; Ho, Chi‐Tang; Pan, Min‐Hsiung
• Is Part Of: Molecular nutrition & food research. Volume 59:Issue 10(2015:Oct.)
• Page Start: 1883
• Page End: 1895
• Publication Date: 2015-07-20
• Subjects: Food -- Biotechnology -- Periodicals; Food -- Microbiology -- Periodicals; Nutrition -- Periodicals; Food -- Toxicology -- Periodicals; Nutrition -- Periodicals; Food Microbiology -- Periodicals; Food Technology -- Periodicals; Molecular Biology -- Periodicals; 664.0705
• DOI: 10.1002/mnfr.201400809
• Languages: English
• ISSNs: 1613-4125

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="mnfr2434-sec-0010" sec-type="section"> <title>Scope</title> <p>Diet‐induced obesity and associated nonalcoholic fatty liver disease have increased and become a major health problem worldwide. This study was conducted to investigate the chemopreventive effects of dietary Calebin‐A, a curcuminoid, on differentiation of 3T3‐L1 adipocytes and high‐fat diet (HFD) induced obesity and hepatic steatosis. Potential mechanisms contributing to these effects were also elucidated.</p> </sec> <sec id="mnfr2434-sec-0020" sec-type="section"> <title>Methods and results</title> <p>Calebin‐A effectively and dose dependently suppressed accumulation of lipid droplets in adipocytes through the suppression of adipogenic specific factor peroxisome proliferator‐activated receptor (PPAR) γ and fatty acid synthase and activated acetyl‐CoA carboxylase. Dietary Calebin‐A effectively decreased weight gain and relative perigonadal, retroperitoneal, and mesenteric fat weight in HFD‐fed mice. Furthermore, Calebin‐A markedly reduced hepatic steatosis and the serum levels of glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, total cholesterol, and triacylglycerol. These effects were associated with the downregulation of PPARγ, sterol regulatory element‐binding protein‐1, and particularly the activation of AMP‐activated protein kinase α signaling found in both adipocytes and liver tissues.</p> </sec> <sec id="mnfr2434-sec-0030" sec-type="section"> <title>Conclusion</title> <p>Taken together, these results demonstrated for the first time that Calebin‐A suppressed adipocyte differentiation, prevented HFD‐induced obesity, and improved hepatic steatosis, suggesting a novel application for the prevention and treatment of obesity and associated nonalcoholic fatty liver disease.</p> </sec> </abstract>