WEDNESDAY, July 20, 2005 (HealthDay News) -- U.S. researchers say they've identified a trigger for insulin resistance in the liver, as well as a potential target to prevent or treat the silent condition.
Cellular resistance to the effects of insulin is a key factor in the development of type 2 diabetes, and hepatic (liver) insulin resistance greatly increases the odds of developing full-blown diabetes, experts say.
Yale University researchers led by Gerald Shulman noted that the livers of mice lacking an enzyme called mitochondrial acyl-CoA:glycerol-sn-3-phosphate acyltransferase 1 (mtGPAT1) remained sensitive to insulin's effects when the mice were fed a high-fat diet. These mice also exhibited lower concentrations of a lipid metabolite that may play a critical role in triggering insulin resistance in the liver, the study found.
After being fed a high-fat diet for three weeks, mice lacking mtGPAT1 had much lower than normal concentrations of liver lipid metabolites called hepatic triacylglycerol and diacylglycerol.
Compared to normal mice, mice lacking mtGPAT1 were also protected from insulin resistance in the liver.
"Taken together, these data implicate diacylglycerol in the liver as an important trigger in causing fat-induced hepatic insulin resistance. These data also suggest that mtGPAT1 might be a potent therapeutic target to treat hepatic insulin resistance," Shulman said in a prepared statement.
The findings appear in the July issue of Cell Metabolism.
More information
The American Liver Foundation has more about diseases that affect the liver.
