Abstract
The Spontaneously Diabetic Torii (SDT) rat is a nonobese type 2 diabetic model, showing the overt hyperglycemia after about 16 weeks of age. In this study, we investigated the protein tyrosine phosphatase (PTPase) activities in insulin-sensitive tissues in SDT rats. PTPase activities in the liver, muscle, and fat were examined at 8 weeks (pre-diabetes), 16 weeks (onset-diabetes), and 24 weeks (diabetes). SDT rats showed glucose intolerance at 8 weeks and hyperglycemia after 16 weeks. The PTPase activities in fat increased at 8 weeks and the increase was sustained to 24 weeks. In the liver, PTPase activities increased only at 24 weeks. On the other hand, the PTPase activities in muscle did not change. The increase of PTPase activity in fat might be related to progression of glucose intolerance and diabetes in SDT rats.
Highlights
The hyperglycemia is attributed to two major defects, namely insulin resistance in insulin-sensitive tissues and depletion of glucose-stimulated insulin secretion (GSIS) from the pancreas
It has been speculated that a specific phosphotyrosine phosphatases (PTPase) is involved in the dephosphorylation and inactivation of insulin receptor (IR), attenuating insulin signaling, and disequilibrium between IR and the PTPase could be a contributing factor to the insulin resistance observed in type 2 diabetes mellitus [6,7,8]
In this study we investigated the PTPase activities in liver, muscle, and fat in Spontaneously Diabetic Torii (SDT) rats at 8, 16, and 24 weeks of age
Summary
The hyperglycemia is attributed to two major defects, namely insulin resistance in insulin-sensitive tissues and depletion of glucose-stimulated insulin secretion (GSIS) from the pancreas. The intracellular phosphotyrosyl phosphorylation levels proteins in signal chains will reflect the balance of activities of phosphotyrosine kinases and phosphotyrosine phosphatases (PTPase). It has been speculated that a specific PTPase is involved in the dephosphorylation and inactivation of IR, attenuating insulin signaling, and disequilibrium between IR and the PTPase could be a contributing factor to the insulin resistance observed in type 2 diabetes mellitus [6,7,8]. SDT rats show glucose intolerance before the onset of diabetes. SDT rats show remarkable hyperglycemia after the onset of diabetes mellitus. In this study we investigated the PTPase activities in liver, muscle, and fat in SDT rats at 8 (pre-diabetes), 16 (onset-diabetes), and 24 (diabetes) weeks of age
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