Insulin Resistance and a Diabetes Mellitus-Like Syndrome in Mice Lacking the Protein Kinase Akt2 (PKBβ)
2001; American Association for the Advancement of Science; Volume: 292; Issue: 5522 Linguagem: Inglês
10.1126/science.292.5522.1728
ISSN1095-9203
AutoresHan Cho, James Mu, Jason K. Kim, Joanne L. Thorvaldsen, Qingwei Chu, E. Bryan Crenshaw, Klaus H. Kaestner, Marisa S. Bartolomei, Gerald I. Shulman, Morris J. Birnbaum,
Tópico(s)Pancreatic function and diabetes
ResumoGlucose 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.
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