What question did this study set out to answer?

To determine the physiological role of the serine-threonine protein kinase Akt2 (PKBβ) in mediating insulin signaling and systemic glucose homeostasis.

June 1, 2001Science

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

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To determine the physiological role of the serine-threonine protein kinase Akt2 (PKBβ) in mediating insulin signaling and systemic glucose homeostasis.
Generated and examined knockout mice deficient in the Akt2 gene.
Assessed in vivo insulin responsiveness, blood glucose lowering capacity, and tissue-specific metabolic action in the liver and skeletal muscle.
Mice deficient in Akt2 exhibit marked impairment in insulin-mediated blood glucose reduction.
Defects in insulin action localize primarily to skeletal muscle and liver target tissues, resulting in a diabetes mellitus-like phenotype.

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Implication

Animal study demonstrates impaired insulin responsiveness and diabetes-like hyperglycemia in Akt2-deficient mice, indicating Akt2 is indispensable for muscle and liver glucose regulation.

Cite This Study

Cho et al. (2001) studied this question.

synapsesocial.com/papers/6a0cd468ff9c20aeb34a45aa https://doi.org/10.1126/science.292.5522.1728

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Implication

Animal study demonstrates impaired insulin responsiveness and diabetes-like hyperglycemia in Akt2-deficient mice, indicating Akt2 is indispensable for muscle and liver glucose regulation.

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

Key Points

Discussion

Implication

Cite This Study

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

Key Points

Discussion

Implication

Cite This Study

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