Vinexin β deficiency exacerbates diet-induced obesity, hepatosteatosis, insulin resistance and endoplasmic reticulum stress in mice.

Vinexin β is a member of an adaptor protein family. Previous research has elucidated its role in cell adhesion and growth factor signaling. Recently, several studies demonstrated its role in metabolic abnormality, such as obesity and atherosclerosis. In this study, we found that vinexin β-knockout (KO) mice were more obese and gained more obvious visceral fat accumulation than their wildtype (WT) littermates fed with high fat diet (HFD). KO mice also showed more severe hepatosteatosis when compared with the WT control, which was in line with the significant increase of key serum lipids in KO mice. Furthermore, we confirmed the inhibited Akt signaling and exacerbated insulin resistance which resulted in high fasting blood glucose in KO mice. The endoplasmic reticulum stress response was found obviously activated which may mediate the metabolic changes in KO mice. Our studies indicated that vinexin β deficiency promotes the diet-induced metabolic disorders.