Low-Dose Alcohol Improves Lipid Metabolism through Store-Operated Ca2+ Channel-Induced PPARγ Expression in Obese Mice

Abstract

The relationship between low-dose alcohol consumption and lipid metabolism has been extensively studied during the last few decades. It has been reported that low-dose alcohol consumption upregulates the expression of peroxisome proliferator-activated receptor γ (PPARγ), a vital nuclear transcription factor involved in glucose and lipid metabolism. However, the possible molecular mechanism remains unclear. In the present study, the obese mouse model was established by HFD feeding for 12 weeks, and then alcohol was administered for 4 weeks. The results showed that low-dose alcohol consumption ameliorated HFD-induced glucose tolerance and insulin resistance in mice and decreased markedly the serum lipoprotein profiles levels and the size of lipid droplets that accumulated in the liver. Furthermore, low-dose alcohol consumption upregulated PPARγ and its target genes in obese mice and augmented the expression of relative proteins in store-operated Ca2+ channels (SOCs). Both ethylene glycol tetraacetic acid (EGTA), a Ca2+ chelator, and 2-aminoethoxydiphenyl borate (2-APB), a blocker of SOCs, abolished the alcohol-induced PPARγ upregulation. In conclusion, these results suggested that low-dose alcohol consumption could improve lipid metabolism through SOC-induced PPARγ expression in obese mice.