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Diabetes and Obesity: Protein Tyrosine Phosphatases
 
 
Their Role in Diabetes and Obesity
Insulin binding to the a-subunit of the insulin receptor stimulates the tyrosine kinase activity of the b-subunit, which results in phosphorylation of insulin-receptor substrates to propagate insulin signaling. Protein tyrosine phosphatases (PTP), particularly the protein tyrosine phosphatase-1B (PTP-1B), reduce the degree of phosphorylation of the insulin receptor, which diminishes insulin signaling and insulin sensitivity. A negative regulatory role for protein tyrosine phosphatases in insulin signaling and in the development of insulin resistance associated with Type 2 diabetes has been well established.PTP-1B is considered as a negative regulator of insulin signaling and several genetic studies have supported the association between PTP-1B and insulin resistance. Mice lacking PTP-1B exhibit enhanced insulin sensitivity and even when fed a high fat diet maintain their insulin sensitivity. They are resistant to diabetes and diet-induced obesity. Hence, PTP-1B is considered as an effective target for the treatment of both Type 2 diabetes and obesity. A variety of vanadium compounds have been known to mimic the effects of insulin by inhibition of tyrosine phosphatases.
 
 
 
 
 
 
 
 
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