• Register
X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

X

Leaving Community

Are you sure you want to leave this community? Leaving the community will revoke any permissions you have been granted in this community.

No
Yes

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

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

Authors

  • Leavens KF
  • Easton RM
  • Shulman GI
  • Previs SF
  • Birnbaum MJ

Journal

Cell metabolism

Publication Data

November 3, 2009

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:

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