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

Cell metabolism | Nov 3, 2009

http://www.ncbi.nlm.nih.gov/pubmed/19883618

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.

Pubmed ID: 19883618 RIS Download

Mesh terms: Animals | Dietary Fats | Insulin Resistance | Leptin | Lipid Metabolism | Liver | Mice | Mice, Knockout | Mice, Obese | Obesity | Protein-Serine-Threonine Kinases | Proto-Oncogene Proteins c-akt | Triglycerides

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Associated grants

  • Agency: NIDDK NIH HHS, Id: 1F30 DK081283
  • Agency: NIDDK NIH HHS, Id: P30 DK19525
  • Agency: NIDDK NIH HHS, Id: R01 DK040936
  • Agency: NIDDK NIH HHS, Id: R01 DK056886
  • Agency: NIDDK NIH HHS, Id: R01 DK056886-10
  • Agency: NIDDK NIH HHS, Id: R01 DK56886
  • Agency: NIGMS NIH HHS, Id: T32 GM07229
  • Agency: NIDDK NIH HHS, Id: U24 DK059635
  • Agency: Howard Hughes Medical Institute, Id:

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