Effects of Genistein on Differentiation and Viability of Human Visceral Adipocytes

Nutrients

Giacomo Deiro¹  Sergio Gentilli¹  Serena Farruggio²  David Mary²  Elena Grossini²  Giulia Raina² 

[1] General Surgery Unit, Department of Health Sciences, University of Eastern Piedmont, Via Solaroli 17, 28100 Novara, Italy;Laboratory of Physiology, Department of Translational Medicine, University of Eastern Piedmont, Via Solaroli 17, 28100 Novara, Italy;

关键词: adiponectin;    browning;    cell survival;    differentiation;    genistein;    mitochondria;    peroxidation;   

DOI  :  10.3390/nu10080978

来源: DOAJ

【 摘 要 】

Obesity can lead to pathological growth of adipocytes by inducing inflammation and oxidative stress. Genistein could be a potential candidate for the treatment of obesity due to its antioxidant properties. Specific kits were used to examine the effects of genistein vs adiponectin on human visceral pre-adipocytes differentiation, cell viability, mitochondrial membrane potential, and oxidative stress in pre-adipocytes and in white/brown adipocytes. Western Blot was performed to examine changes in protein activation/expression. Genistein increased human visceral pre-adipocytes differentiation and browning, and caused a dose-related improvement of cell viability and mitochondrial membrane potential. Similar effects were observed in brown adipocytes and in white adipocytes, although in white cells the increase of cell viability was inversely related to the dose. Moreover, genistein potentiated AMP-activated protein kinase (AMPK)/mitofusin2 activation/expression in pre-adipocytes and white/brown adipocytes and protected them from the effects of hydrogen peroxide. The effects caused by genistein were similar to those of adiponectin. The results obtained showed that genistein increases human visceral pre-adipocytes differentiation and browning, protected against oxidative stress in pre-adipocytes and white/brown adipocytes through mechanisms related to AMPK-signalling and the keeping of mitochondrial function.

【 授权许可】

Unknown