PCK1 and Insulin resistance: For example, we observed suppressed postprandial lipogenic gene expression (e.g., Fasn and Aacs) and disrupted preprandial gluconeogenic gene expression (e.g., G6pc and Pck1. Interestingly, however, the disrupted feeding response in this experimental setup contradicts the general notion that diet-induced hyperinsulimia and insulin resistance leads to increased expression of lipogenenic and gluconeogenic genes by unresolved mechanisms [56].