Glucagon binding and lipolytic response in isolated adipocytes from streptozotocin-diabetic rats.
Evidence for pre-receptor, receptor and post-receptor glucagon defects was investigated in adipocytes from streptozotocin-diabetic rats. For this purpose male Wistar rats were injected by cardiac puncture with streptozotocin (65 mg/Kg body-weight) or saline solution and sacrificed after 7 and 15 days of drug administration. Increased glucagon levels and increased glucagon degradation in serum together with a decrease in glucagon binding were found in both groups of diabetic rats. The decrease in glucagon binding was related to a decrease in the number of glucagon receptors/cell rather than to a change in receptor affinity. The lipolytic response of glucagon was increased. However, the ability of glucagon to increase basal or theophylline-stimulated cAMP accumulation in the incubation medium of adipocytes from diabetic rats was decreased. Such alterations could represent a counter-regulatory mechanism of the hyperglucagonemia detected in streptozotocin-diabetic rats.
Mayor
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Department of Biochemistry, School of Medicine, Complutense University, Madrid, Spain.
Calle
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D000273:Adipose Tissue / Q000166:cytology*; D000818:Animals; D002469:Cell Separation; D000242:Cyclic AMP / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D005934:Glucagon / Q000378:metabolism* / Q000494:pharmacology; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
D005934:Glucagon; D000242:Cyclic AMP