Experimental models of diabetes mellitus of the 1st and 2nd types in rats: regulation of activity of glycogen synthase by peptides of the insulin superfamily and by epidermal growth factor in skeletal muscles

• Published in: Žurnal ėvolûtsionnoj biohimii i fiziologii Vol. 48; no. 1; p. 22
• Main Authors: Kuznetsova, L A, Chistiakova, O V
• Format: Journal Article
• Language: Russian
• Published: Russia (Federation) 01.01.2012
• Subjects: Animals; Diabetes Mellitus, Experimental - enzymology; Diabetes Mellitus, Experimental - pathology; Diabetes Mellitus, Type 1 - enzymology; Diabetes Mellitus, Type 1 - pathology; Diabetes Mellitus, Type 2 - enzymology; Diabetes Mellitus, Type 2 - pathology; Enzyme Activation - drug effects; Epidermal Growth Factor - pharmacology; Glycogen Synthase - metabolism; Insulin - pharmacology; Male; Muscle Proteins - metabolism; Muscle, Skeletal - enzymology; Muscle, Skeletal - pathology; Peptides - pharmacology; Rats; Rats, Wistar
• ISSN: 0044-4529

The regulatory effect of peptides of the insulin hyperfamily--insulin, insulin-like growth factor (IGF-1), and relaxin, as well as of epidermal growth factor (EGF) on activity of glycogen synthase (GS) in rat skeletal muscles was studied in norm and in experimental diabetes mellitus of the 1st and 2nd types (DM1, DM2). In norm, peptides in vitro stimulated maximally the GS activity at a concentration of 10-8 M. The row of efficiency of the peptide action was as follows: insulin > IGF-1 > relaxin. In DM1 the basal GS activity did not change, while effect of insulin in vitro was decreased more sharply as compared with action of IGF-1 and relaxin at the 30th day of development of diabetes, i. e., the efficiency row was as follows: IGF-1 = relaxin > insulin. Administration of insulin in vivo did not restore sensitivity of the enzyme to the action of hormone in DM1. In DM2, the GS activity (both the total and active form) decreased. while the stimulatory effect ofpeptides and EGF on the enzyme was absent. Insulin introduced in vitro did not lead to restoration of the enzyme reaction. The conclusion has been made that the insulin resistance affects the basal GS activity in rat skeletal muscles as well as the regulation of the enzyme by peptides of the insulin nature and by EGF, which is more obvious in DM2, than in DM1.