In addition to its preventive actions in diet-induced disease models, butyrate is also effective in treating obesity through the promotion of energy expenditure and the induction of mitochondrial function: the mechanism of butyrate action for obesity is related to the activation of AMPK, increasing ATP consumption, and the induction of PGC-1α activity, the molecular mechanism by which butyrate stimulates mitochondrial function in association with up-regulated expression of genes involved in lipolysis and fatty acid β-oxidation [125,126,127]. This evidence concerns the gene PPARGC1A and obesity due to melanocortin 4 receptor deficiency.