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International Journal of Experimental Diabetes Research
Volume 2 (2001), Issue 1, Pages 47-54
http://dx.doi.org/10.1155/EDR.2001.47

High Insulin Requirements and Poor Metabolic Control do not Modify the Expression, Regulation and PKC Mediated Activation of the p21ras Pathway in PBMC from Type II Diabetic Patients

1Diabetes and Endocrinology Unit, Assaf Harofeh Medical Center, the Sackler Facilty of Medicine, Tel-Aviv University, Zerifin 70300, Israel
2Department of Internal Medicine “C”, Assaf Harofeh Medical Center, the Sackler Facilty of Medicine, Tel-Aviv University, Zerifin 70300, Israel
3Department of Cell Biology , Baylor College of Medicine, Houston, Texas, USA
4Department of lmmunology, Assaf Harofeh Medical Center, the Sackler Facilty of Medicine, Tel-Aviv University, Zerifin 70300, Israel
5Department of Nephrology, Assaf Harofeh Medical Center, the Sackler Facilty of Medicine, Tel-Aviv University, Zerifin 70300, Israel

Received 22 August 2000; Accepted 15 December 2000

Copyright © 2001 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Aims To asses whether clinically severe insulin resistance and poor metabolic control in patients with type II diabetes are associated with aberrant expression or function of the p21ras pathway.

Methods We examined the expression and function of the p21ras pathway in resting and activated PBMC from 10 insulin treated patients with type II diabetes characterized by high insulin requirements and poor metabolic control (IR group) and 10 age and sex matched well controlled patients treated by diet alone or oral hypoglycemic medications (WC group).

Results Levels of p21ras and its regulatory elements: p21rasGAP and hSOS1, were comparable in the two groups. The induced activities of p21ras and its associated down-stream regulatory enzyme MAP-kinase following TPA stimulation were also comparable in the IR and WC patients.

Conclusions Taken together, these data indicate that clinically significant severe insulin resistance does not modify the expression, regulation and activation of p21ras pathway in PBMC of patients with type II diabetes.