A Yale-led research team has identified the molecular mechanism by which insulin normally inhibits production of glucose by the liver and why this process stops working in patients with type 2 diabetes, leading to hyperglycemia.
The findings are published Feb. 5 in the journal Cell.
"In the study, we set out to examine how insulin normally works to turn off production of glucose by the liver and why this process goes awry in patients with type 2 diabetes," said Gerald I. Shulman, the George R. Cowgill professor of physiological chemistry, professor of medicine and cellular & molecular physiology at Yale School of Medicine, and an investigator with the Howard Hughes Medical Institute.
Experts have long debated how insulin suppresses glucose production by the liver. Many have asserted that insulin's suppression of glucose production was due to the direct action of insulin on the liver. But the Yale-led team uncovered a different process that challenges current theories and may lead to new targets for treatment.
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