Although the protection of AMPKα1 deletion in SF1 neurons against HFD-induced obesity was mainly associated with increased energy expenditure, slight alterations in glucose balance (decreased glycemia and improved glucose tolerance without changes in insulin sensitivity and insulin levels) found in mutant mice fed with an HFD, could be involved [56]. The gene discussed is PRKAA1; the disease is obesity due to melanocortin 4 receptor deficiency.