Hepatocyte KCTD17 deletion in HFD-fed mice improved glucose intolerance and fatty liver by increasing carbohydrate response element-binding protein (ChREBP) protein stability via the degradation of O-GlcNAcase (OGA), suggesting that KCTD17 is a key regulatory node in multiple liver metabolic processes and a novel therapeutic option for the treatment of obesity-induced insulin resistance and NAFLD98. This evidence concerns the gene MLXIPL and Insulin resistance.