DIMINISHED LEVELS OF INSULIN-LIKE GROWTH FACTOR-I IN LUNGS IN STREPTOZOTOCIN-INDUCED DIABETES - RELATION TO NUTRITIONAL-STATUS AND GROWTH

Citation
Af. Ofulue et al., DIMINISHED LEVELS OF INSULIN-LIKE GROWTH FACTOR-I IN LUNGS IN STREPTOZOTOCIN-INDUCED DIABETES - RELATION TO NUTRITIONAL-STATUS AND GROWTH, Experimental lung research, 20(1), 1994, pp. 27-40
Citations number
34
Categorie Soggetti
Respiratory System
Journal title
ISSN journal
01902148
Volume
20
Issue
1
Year of publication
1994
Pages
27 - 40
Database
ISI
SICI code
0190-2148(1994)20:1<27:DLOIGF>2.0.ZU;2-M
Abstract
It is yet unknown whether the impaired nutritional status of streptozo tocin-induced diabetic rats influences changes in levels of insulin-li ke growth factor-I (IGF-I) in this experimental model of diabetes. To explore this possibility, simultaneous studies were undertaken of rats made diabetic by streptozotocin (75 mg/kg body wt, intraperitoneally) and undernourished control rats with similar somatic growth rate (det ermined by body weight gain), in comparison with normal controls. Seru m ICF-I levels were diminished in the untreated diabetic and undernour ished control animals, but more so in the diabetic group. Lung IGF-I l evels (per lung and per lung DNA) and DNA contents were diminished to similar degrees in the untreated diabetic animals and the undernourish ed control group. Lung dry weights of the diabetic rats were greater t han chose of the undernourished control group, such that lung IGF-I/10 0 mg tissue dry wt in the former was significantly lower than in the l atter group. Insulin treatment of the diabetic vats restored their bod y weights, serum and lung IGF-I levels, and DNA contents to normal con trol values. Lung IGF-I levels in the diabetic rats correlated strongl y with serum glucose (r = .75) and body weight (r = .79), and moderate ly with lung weight (r = .43) and lung DNA (r = .58). These findings s uggest that the diminished lung IGF-I levels in streptozotocin-induced diabetes may be related to the impaired nutritional status and/or som atic growth of the experimental animals, and that this relationship ma y be responsible, at least in part, for the diminished lung cellular p roliferation observed in experimental diabetic animals.