Gene Explains Fructose-Insulin Resistance Link
Reported March 04, 2009
(Ivanhoe Newswire) A common sweetener found in sodas and other food products has been linked to insulin resistance. Now researchers are explaining why.
Investigators from Yale University School of Medicine studied high-fructose corn syrup in mice in which a gene called transcriptional co activator PPARg coactivator-1b (PGC-1b) was blocked. PGC-1b is responsible for controlling other genes, one of which builds fat in the liver.
According to the researchers, problems arise because the sweetener is more easily metabolized into fat in the liver than the traditional form of sugar, glucose. That build up in the liver then causes nonalcoholic fatty liver disease, which itself is linked to insulin resistance, the precursor to diabetes.
In the study, blocking the activity of PGC-1b in mice led to lower levels of genes known to build fat in the liver. All of the mice were fed diets high in fructose, but blocking the gene resulted in a reversal of their fructose-induced insulin resistance and a threefold increase in glucose uptake in their fat tissue.
The authors believe this line of study may one day lead to new therapies for the treatment of nonalcoholic fatty liver disease, insulin resistance, and other problems related to the build up of fat in the liver.
The consumption of high-fructose corn syrup has skyrocketed since its introduction in the 1970s, with estimates suggesting the average person consumes 60 pounds a year.
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SOURCE: Cell Metabolism, published online March 3, 2009
