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In support of a critical mediatory role of aPKCs, in both models, inhibition of hepatic aPKC by adenovirally mediated expression of kinase-inactive aPKC markedly diminished diet/insulin-dependent activation of hepatic SREBP1c and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-B), and concomitantly improved hepatosteatosis, hypertriglyceridemia, hyperinsulinemia, and hyperglycemia