FABP4- deficient mice are protected from obesity-induced insulin resistance and hyperglycemia because of the increase in AT (88, 89), which results from reduced lipolysis and increased de novo lipogenesis, especially that of palmitoleate (90, 91), Moreover, FABP4 deficiency in macrophages also increases de novo lipogenesis, with increased palmitoleate production, which reduces lipid-induced endoplasmic reticulum (ER) stress (92). This evidence concerns the gene FABP4 and obesity due to melanocortin 4 receptor deficiency.