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Publication : Akt2 is required for hepatic lipid accumulation in models of insulin resistance.

First Author  Leavens KF Year  2009
Journal  Cell Metab Volume  10
Issue  5 Pages  405-18
PubMed ID  19883618 Mgi Jnum  J:155432
Mgi Id  MGI:4413648 Doi  10.1016/j.cmet.2009.10.004
Citation  Leavens KF, et al. (2009) Akt2 is required for hepatic lipid accumulation in models of insulin resistance. Cell Metab 10(5):405-18
abstractText  Insulin drives the global anabolic response to nutrient ingestion, regulating both carbohydrate and lipid metabolism. Previous studies have demonstrated that Akt2/protein kinase B is critical to insulin's control of glucose metabolism, but its role in lipid metabolism has remained controversial. Here, we show that Akt2 is required for hepatic lipid accumulation in obese, insulin-resistant states induced by either leptin deficiency or high-fat diet feeding. Lep(ob/ob) mice lacking hepatic Akt2 failed to amass triglycerides in their livers, associated with and most likely due to a decrease in lipogenic gene expression and de novo lipogenesis. However, Akt2 is also required for steatotic pathways unrelated to fatty acid synthesis, as mice fed high-fat diet had reduced liver triglycerides in the absence of hepatic Akt2 but did not exhibit changes in lipogenesis. These data demonstrate that Akt2 is a requisite component of the insulin-dependent regulation of lipid metabolism during insulin resistance.
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