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.

Keywords

AKT2Insulin resistanceProtein kinase BInternal medicineGlucose homeostasisEndocrinologyAKT1HomeostasisInsulinProtein kinase ASkeletal muscleDiabetes mellitusInsulin receptorKinaseBiologyPhosphorylationMedicineBiochemistry

MeSH Terms

AnimalsBlood GlucoseDeoxyglucoseDiabetes MellitusType 2FemaleGene TargetingGlucoseGlucose Clamp TechniqueGlucose Tolerance TestHomeostasisInsulinInsulin ResistanceIslets of LangerhansLiverMaleMiceMiceInbred C57BLMiceTransgenicMuscleSkeletalProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktSignal Transduction

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Publication Info

Year
2001
Type
article
Volume
292
Issue
5522
Pages
1728-1731
Citations
1815
Access
Closed

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Cite This

Han Cho, James Mu, Jason K. Kim et al. (2001). Insulin Resistance and a Diabetes Mellitus-Like Syndrome in Mice Lacking the Protein Kinase Akt2 (PKBβ). Science , 292 (5522) , 1728-1731. https://doi.org/10.1126/science.292.5522.1728

Identifiers

DOI
10.1126/science.292.5522.1728
PMID
11387480

Data Quality

Data completeness: 81%