Corn syrup more easily metabolizes to fat in liver, which may trigger disease, study says
FRIDAY, March 6 (HealthDay News) -- A gene called PGC-1b appears to play a role in insulin resistance that can be caused by consuming large amounts of high-fructose corn syrup, a sweetener found in most sodas and many processed foods.
Researchers found that mice fed a high-fructose diet were protected from insulin resistance when PGC-1b activity was blocked in the rodents' liver and fat tissue. The findings were published in the March issue of Cell Metabolism.
"There has been a remarkable increase in consumption of high-fructose corn syrup," Gerald Shulman, of the Yale School of Medicine, said in a journal news release. "Fructose is much more readily metabolized to fat in the liver than glucose is, and, in the process, can lead to nonalcoholic fatty liver disease (NAFLD)," which, in turn, leads to hepatic insulin resistance and type 2 diabetes.
High-fructose corn syrup -- a mixture of the simple sugars fructose and glucose -- came into use in the 1970s. By 2005, the average American consumed about 60 pounds of high-fructose corn syrup a year.
The study authors said their findings indicate that PGC-1b plays an important role in the development of fructose-induced insulin resistance. The gene may offer a target for new drugs to treat insulin resistance, NAFLD and hypertriglyceridemia, they concluded.
In an accompanying commentary, two experts said the study shows that PGC-1b is "a missing link between fructose intake and metabolic disorders."
"The findings ... support the emerging role of gene/environment interaction in modulating the metabolic phenotype and disease pathogenesis. Thus, perturbations of the same regulatory motif may produce vastly different metabolic responses, depending on the specific combinations of dietary nutrients," wrote Carlos Hernandez and Jiandie Lin of the University of Michigan Medical Center, in Ann Arbor.
The U.S. National Institute of Diabetes and Digestive and Kidney Diseases has more about insulin resistance.
-- Robert Preidt
SOURCE: Cell Press, news release, March 3, 2009
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