In the first phase of insulin resistance, as seen in mouse models of diet-dependent obesity that are produced either by a moderate increase in dietary fat or carbohydrate intake, or by hyperphagia secondary to genetic (ob/ob) leptin deficiency, hepatic aPKC activity is inordinately increased, and, presumably because of co-localization of aPKC, Akt and FoxO1on the same ProF platform [13,38,39], and because of the ability of aPKC to bind, phosphorylate and inhibit Akt [40,41,42], the effects of Akt on FoxO1 phosphorylation are selectively diminished [13]. This evidence concerns the gene AKT1 and Insulin resistance.