1. Muscle-Specific Pten Deletion Protects against Insulin Resistance and Diabetes.
- Author
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Wijesekara, Nadeeja, Konrad, Daniel, Eweida, Mohamed, Jefferies, Craig, Liadis, Nicole, Giacca, Adria, Crackower, Mike, Suzuki, Akira, Mak, Tak W., Kahn, C. Ronald, Klip, Amira, and Woo, Minna
- Subjects
HORMONES ,HYPOGLYCEMIC agents ,INSULIN ,PANCREATIC secretions ,PHYSIOLOGY ,GLUCOSE ,SUCROSE - Abstract
Pten (phosphatase with tensin homology), a dual-specificity phosphatase, is a negative regulator of the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. Pten regulates a vast array of biological functions including growth, metabolism, and longevity. Although the PI3K/Akt pathway is a key determinant of the insulin-dependent increase in glucose uptake into muscle and adipose cells, the contribution of this pathway in muscle to whole-body glucose homeostasis is unclear. Here we show that muscle-specific deletion of Pten protected mice from insulin resistance and diabetes caused by high-fat feeding. Deletion of muscle Pten resulted in enhanced insulin-stimulated 2-deoxyglucose uptake and Akt phosphorylation in soleus but, sur- prisingly, not in extensor digitorum longus muscle compared to littermate controls upon high-fat feeding, and these mice were spared from developing hyperinsulinemia and islet hyperplasia. Muscle Pten may be a potential target for treatment or prevention of insulin resistance and diabetes. [ABSTRACT FROM AUTHOR]
- Published
- 2005
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