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Protein defect in diabetes?

Protein defect in diabetes?

An absence of protein activity thataffects the transfer of chemicals across cell membranes--including the interaction of the hormone insulin with liver cells--may be responsible for many of the medical problems associated with diabetes, researchers reported this week.

Using diabetic rats, scientists at theUniversity of Glasgow in Scotland, Rockefeller University in New York City and the National Institute of Diabetes in Bethesda, Md., found that a protein called G(i) appears to be inactive in the animals' livers. The protein is one of several grouped under the name "G proteins,' which play a role in the movement of chemical signals between a cell's interior and the outside.

Previous research had shown that G(i)is one of two G proteins that serve as a link between a cellular enzyme called adenylate cyclase and hormone receptors found on the cell surface: In a complex regulatory process, G(s) stimulates and G(i) inhibits adenylate cyclase's response to hormones. However, in diabetic rats with very low blood levels of insulin, there apparently is no G(i) activity; thus, part of the normal feedback process is missing, the scientists say in the May 21 NATURE.

Using specially prepared antibodies,the scientists found that the amount of one G(i) subunit is abnormally low in liver cell membranes from diabetic rats. Although the activity of G(i) is restored when the diabetic animals are injected with insulin, it is unclear how the low levels of insulin seen in type I diabetes are related to the deficiency in G(i), say the authors. Nonetheless, given adenylate cyclase's broad influence on cellular metabolism, the authors suggest that the loss of inhibitory activity by G(i) could account for many diabetic complications, including those of the nervous, immune and cardiovascular systems.
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Author:Edwards, Diane D.
Publication:Science News
Date:May 23, 1987
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