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Insulin resistance in uremia: Insulin receptor kinase activity in liver and muscle from chronic uremic rats

Journal Article · · American Journal of Physiology; (USA)
OSTI ID:6727492
; ; ;  [1]
  1. East Carolina Univ. School of Medicine, Greenville, NC (USA)
The authors have studied the structure and function of the partially purified insulin receptors from liver and skeletal muscle in a rat model of severe chronic uremia. {sup 125}I-insulin binding was higher in the liver from uremic rats when compared with ad libitum- and pair-fed controls. Furthermore, the ability of insulin to stimulate the autophosphorylation of the {beta}-subunit and insulin receptor kinase activity using Glu{sup 80}, Tyr{sup 20} as exogenous phosphoacceptor was increased in the liver of the uremic animals. The structural characteristics of the receptors, as determined by electrophoretic mobilities of affinity labeled {alpha}-subunit and the phosphorylated {beta}-subunit, were normal in uremia. {sup 125}I-insulin binding and insulin receptor kinase activity were similar in the skeletal muscle from uremic and pair- and ad libitum-fed animals. Thus the data are supportive of the hypothesis that in liver and muscle of chronic uremic rats, insulin resistance is due to a defect(s) distal to the insulin receptor kinase.
OSTI ID:
6727492
Journal Information:
American Journal of Physiology; (USA), Journal Name: American Journal of Physiology; (USA) Vol. 254:4; ISSN 0002-9513; ISSN AJPHA
Country of Publication:
United States
Language:
English