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. |