In both obesity models, we found that hepatic Akt activity is in fact increased, presumably by hyperinsulinemia owing to increased hepatic gluconeogenesis and resultant glucose intolerance, and hepatic aPKC activity is increased, apparently owing to both hyperinsulinemia and dietary lipid-induced increases in hepatic ceramides that directly activate aPKC [13,18]. This evidence concerns the gene AKT1 and hyperinsulinism.