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• W3008266194 abstract "Using animal models of diabetes, hepatic guanine nucleotide regulatory protein (G protein) function has been investigated. Diabetes mellitus can be classified into two major catagories; type I (I. D. D. M.) an insulin-dependent form of the disease and type II (N. I. D. D. M.) a non-insulin dependent form of the disease often associated with obesity. Guanine nucleotide regulatory proteins (G proteins) are membrane associated components which are involved in the transduction of chemical signals across cell plasma membranes. The G protein Gi, inhibits adenylate cyclase activity and the G protein Gs, stimulates adenylate cyclase activity. Adenylate cyclase is an integral membrane protein which catalyzes the formation of cAMP from ATP. cAMP is an important cellular signal for the control of metabolism. In both type I and type II diabetic rats, activity of the inhibitory G protein, Gi, is absent in hepatocytes . It is proposed that in type I diabetic animals, hepatic Gi expression is abolished. In type II diabetic rats, hepatic Gi is modified, but present in a non-functional state. Insulin has the ability to inhibit glucagon-stimulated adenylate cyclase activity. This action of insulin is reduced in liver plasma membranes prepared from type II diabetic rats and is absent in liver plasma membranes prepared from type I diabetic rats. Insulin administration to type I diabetic animals resulted in the return Gi function and insulin's ability to inhibit adenylate cyclase activity. It is therefore proposed that the loss of Gi function and insulin mediated inhibition of adenylate cyclase activity is a result of insulin deficiency in this type I diabetic condition. The mechanism by which insulin mediates inhibition of adenylate cyclase activity was investigated. It is proposed that insulin activates a G protein which is distinct from Gi, and inhibits glucagon-stimulated adenylate cyclase activity by the release of subunits from a distinct G protein subunit (a B g) complex. These B7 subunits inhibit the stimulatory G protein , Gs, from interacting with and thereby stimulating the activity of the adenylate cyclase catalytic unit. In addition, the effect of the hvpoglycaemic drug metformin, was assessed. This drug has been used in human diabetic therapy and is reported to have post-receptor effects. This drug was found to restore insulin's ability to inhibit hepatic adenylate cyclase activity in type I diabetic animals and enhance this insulin action in type II diabetic animals. Finally, insulin has the ability to stimulate a high affinity GTPase activity associated with a G protein which is distinct from the G proteins Gi, Gs and a putative G protein Gp. This insulin activated G protein may be the G protein through which insulin is able to regulate the activity of adenylate cyclase . The activity of this G protein may be altered in diabetic states. It is proposed that alterations in G protein function may reflect post-receptor defects in the diabetic state. Transraembrane signal transduction may resultantly be suppressed and therefore the ability of hormones to control metabolism would be reduced." @default.
• W3008266194 created "2020-03-06" @default.
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• W3008266194 date "1987-01-01" @default.
• W3008266194 modified "2023-09-27" @default.
• W3008266194 title "Diabetes-induced changes in hormonal and G protein regulation of adenylate cyclase activity" @default.
• W3008266194 hasPublicationYear "1987" @default.
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