These studies provided compelling evidence that the antihypertensive agent candesartan, a drug that inhibits obesity-associated intracellular Ca2+ overload and lipid accumulation, ameliorated obesity-induced insulin resistance by enhancing the postprandial membrane localization of PH domain-carrying AKT, leading to increased insulin sensitivity and signaling. Here, AKT1 is linked to obesity due to melanocortin 4 receptor deficiency.