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Am J Physiol Renal Physiol 271: F114-F119, 1996;
0363-6127/96 $5.00
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AJP - Renal Physiology, Vol 271, Issue 1 114-F119, Copyright © 1996 by American Physiological Society


ARTICLES

Insulin resistance but IGF-I sensitivity in chronic renal failure

R. H. Mak
Department of Pediatrics, Stanford University School of Medicine, California 94305-5119, USA.

The effects of insulin-like growth factor I (IGF-I) and insulin on glucose metabolism were compared in awake, chronically catheterized rats with chronic renal failure (CRF) and sham-operated, pair-fed controls. In control rats, IGF-I (5 micrograms.kg-1.min-1) and insulin (2 mU.kg-1.min-1) infusions produced similar twofold increases in total body glucose uptake from fasting values under euglycemic conditions (euglycemic clamps). Total body glucose uptake during euglycemic IGF-I clamps at 5 and 10 micrograms.kg-1.min-1 was not different between CRF and control rats. Total body glucose uptake during euglycemic insulin clamps at 2 and 4 mU.kg-1.min-1 was significantly lower in CRF rats compared with corresponding values in control rats. Hepatic glucose production was suppressed by insulin equally but not by IGF-I in both groups. Correction of metabolic acidosis by NaHCO3 partially improved insulin resistance in rats with CRF, whereas an equimolar amount of NaCl had no effect. Thus the capacity of IGF-I infusion to stimulate total body glucose uptake is maintained in CRF rats that are insulin resistant.


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Z. Guan, S. Y. Buckman, L. D. Baier, and A. R. Morrison
IGF-I and insulin amplify IL-1beta -induced nitric oxide and prostaglandin biosynthesis
Am J Physiol Renal Physiol, April 1, 1998; 274(4): F673 - F679.
[Abstract] [Full Text] [PDF]




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