Insulin Resistance and a Diabetes Mellitus-Like Syndrome in Mice Lacking the Protein Kinase Akt2 (PKBβ)

Author:

Cho Han1,Mu James23,Kim Jason K.34,Thorvaldsen Joanne L.53,Chu Qingwei23,Crenshaw E. Bryan6,Kaestner Klaus H.7,Bartolomei Marisa S.53,Shulman Gerald I.34,Birnbaum Morris J.23

Affiliation:

1. Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA.

2. Department of Medicine,

3. Howard Hughes Medical Institute and the

4. Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.

5. Department of Cell and Developmental Biology,

6. Department of Neuroscience, and

7. Department of Genetics, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.

Abstract

Glucose homeostasis depends on insulin responsiveness in target tissues, most importantly, muscle and liver. The critical initial steps in insulin action include phosphorylation of scaffolding proteins and activation of phosphatidylinositol 3-kinase. These early events lead to activation of the serine-threonine protein kinase Akt, also known as protein kinase B. We show that mice deficient in Akt2 are impaired in the ability of insulin to lower blood glucose because of defects in the action of the hormone on liver and skeletal muscle. These data establish Akt2 as an essential gene in the maintenance of normal glucose homeostasis.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference36 articles.

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