Through the activation of GPCR (GLP-1R), GLP-1 exerts its effects in lipid metabolism, protecting hepatocytes against steatosis [148,149]: HFD and lipotoxicity, typical of obesity, induce the loss of GLP-1 responsiveness, but butyrate has the capability to upregulate hepatic GLP-1R expression, with a decrease in fatty acid synthesis lead by the involvement of (AMP)-activated protein kinase/AcetylCoA carboxylase (AMPK/ACC) signaling [150,151]. Here, GCG is linked to steatosis.