Endocrinology, Vol 133, 1783-1788, Copyright © 1993 by Endocrine Society

ARTICLES

Mesangial cells from diabetic NOD mice constitutively secrete increased amounts of insulin-like growth factor-I

SJ Elliot, LJ Striker, M Hattori, CW Yang, CJ He, EP Peten and GE Striker
Renal Cell Biology Section, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892.

Experimental evidence has suggested that insulin-like growth factor-I (IGF-I) may contribute to diabetic complications. Previously, we and others have shown that normal glomerular mesangial cells have receptors for, synthesize, and exhibit a mitogenic response to IGF-I. We investigated the IGF-I response in cells derived from a genetic model of diabetes, the nonobese diabetic (NOD) mouse. Mesangial cell lines were derived from diabetic (D-NOD) and nondiabetic adult mice. D-NOD cells released more IGF-I into the supernatant and had a decreased binding of IGF-I to surface receptors. Analysis according to Scatchard revealed a decreased number of receptor sites on D-NOD cells, although the structure of the IGF-I receptor visualized by cross-linking was identical for both cell types. Preincubation of D-NOD cells with an antibody to IGF-I resulted in an increase in the number of receptor sites. This suggested that autocrine IGF-I was responsible for the decrease in D-NOD receptor number and that diabetes had resulted in a stable phenotypic change.

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