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Study reveals trigger for insulin resistance in liver, potential drug targets

In the July issue of Cell Metabolism, researchers report the discovery of a trigger for insulin resistance in the liver. Hepatic insulin resistance is a silent condition that increases the chances of developing diabetes and heart disease. The team's findings also identify a potential target for drugs to prevent or treat the condition, the researchers said.

The livers of mice lacking an enzyme called mitochondrial acyl-CoA:glycerol-sn-3-phosphate acyltransferase 1 (mtGPAT1) remain sensitive to insulin's effects when fed a high-fat diet. The mice also exhibit lower concentrations of a lipid metabolite that might play a key role in triggering the liver to become insulin resistant, the researchers found.

Along with the existing epidemic of obesity, fatty liver, also known as hepatic steatosis, is rapidly becoming a major health care problem, said Howard Hughes Medical Institute investigator Gerald Shulman of Yale University, senior author of the study. Fatty liver can lead to altered liver function, elevated lipids such as cholesterol and triglycerides in the bloodstream, and progression to liver cirrhosis, he said. Characterized by scarring, cirrhosis of the liver is the twelfth leading cause of death by disease, according to the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK).

Furthermore, Shulman added, recent studies have demonstrated an important role of hepatic steatosis in causing insulin resistance in the liver, resulting in increased liver production of glucose, and high blood sugar in patients with type 2 diabetes.

"Through noninvasive measurements of hepatic triglyceride content in humans, we've learned that elevated liver fat is fairly ubiquitous in patients with poorly controlled type 2 diabetes," Shulman said. "It's been an underappreciated aspect of the disease."

The researchers examined whether or not mice deficient for the mtGPAT1 enzyme would be protected from fatty liver and liver insu
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Contact: Heidi Hardman
hhardman@cell.com
617-397-2879
Cell Press
19-Jul-2005


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