Increased dose-response relationship of liver plasma membrane adenylate cyclase to glucagon stimulation in diabetic rats. A possible role of the guanyl nucleotide-binding regulatory protein.
In view of controversial findings regarding the mechanism for the increased intracellular hepatic cyclic 3':5' adenosine monophosphate levels in diabetic rats, we studied the dose-response relationship of the adenylate cyclase to glucagon stimulation in severely diabetic and in diabetic, insulin-treated rats. An enhanced response to glucagon and an additional augmenting effect of guanosine triphosphate on hormonal stimulation of the adenylate cyclase activity were found in diabetes which were reversible with insulin treatment. The results suggest a role of the regulatory guanyl nucleotide-binding protein in diabetes leading to an increased dose response relationship of the hepatic adenylate cyclase system to glucagon.
D000262:Adenylyl Cyclases / Q000378:metabolism*; D000818:Animals; D002462:Cell Membrane / Q000201:enzymology; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy / Q000201:enzymology*; D004305:Dose-Response Relationship, Drug; D019204:GTP-Binding Proteins; D005934:Glucagon / Q000494:pharmacology*; D006160:Guanosine Triphosphate / Q000494:pharmacology; D007328:Insulin / Q000627:therapeutic use; D008099:Liver / Q000201:enzymology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D011956:Receptors, Cell Surface / Q000502:physiology*; D012969:Sodium Fluoride / Q000494:pharmacology; D013311:Streptozocin
D007328:Insulin; D011956:Receptors, Cell Surface; D013311:Streptozocin; D006160:Guanosine Triphosphate; D012969:Sodium Fluoride; D005934:Glucagon; D019204:GTP-Binding Proteins; D000262:Adenylyl Cyclases