Tweaking With A Particular Gene Prevents Fructose-Induced Insulin Resistance

by Tanya Thomas on  March 6, 2009 at 10:34 AM Research News
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 Tweaking With A Particular Gene Prevents Fructose-Induced Insulin Resistance
Transcriptional coactivator PPARg coactivator-1b (PGC-1b) - Wonder what that is? Well, that's the name of the gene, scientists say, when "knocked down" has protected mice on a diet loaded with high-fructose from insulin resistance.

Usually, insulin resistance is induced by diets full of high-fructose corn syrup, a sweetener found in most sodas and many other processed foods.

PGC-1b coactivates a number of transcription factors that control the activity of other genes, including one responsible for building fat in the liver.

And thus killing the gene in the animals' liver and fat tissue can even prevent the ill effects of insulin resistance.

"There has been a remarkable increase in consumption of high-fructose corn syrup. 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," said Gerald Shulman of Yale University School of Medicine.

NAFLD, in turn, leads to hepatic insulin resistance and type II diabetes.

The researchers claimed that the wide and increasing use of high-fructose corn syrup sweeteners had made metabolic syndrome and type 2 diabetes to reach epidemic proportions worldwide.

It was earlier shown that fructose is more readily converted to fatty acids than glucose, and that there's a link between high-fructose diets and high blood levels of triglycerides (a condition known as hypertriglyceridemia), NAFLD and insulin resistance. lthough the scientists implicated a gene known as SREBP-1, a master regulator of lipids' manufacture in the liver, not much was known about the underlying molecular connections between fructose and those metabolic disorders.

In the new study, the researchers focussed on PGC-1b, a gene known for boosting SREBP-1 levels.

For testing its role in the effects of fructose, they blocked its activity in mice fed a diet high in that sugar for four weeks.

The treatments improved the animals' metabolic profiles by lowering levels of SREBP-1, and other fat-building genes in their livers.

The mice also showed a reversal of their fructose-induced insulin resistance and a threefold increase in glucose uptake in their fat tissue.

"These data support an important role for PGC-1b in the pathogenesis of fructose-induced insulin resistance and suggest that PGC-1b inhibition may be a therapeutic target for treatment of NAFLD, hypertriglyceridemia, and insulin resistance associated with increased de novo lipogenesis," concluded the researchers.

The study has been published in the journal Cell Metabolism.

Source: ANI

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High fructose corn syrup, sugar, and several fruit juices are all nutritionally the same.

High fructose corn syrup has the same number of calories as sugar and is handled similarly by the body.

As noted by the American Medical Association in June 2008, “Because the composition of HFCS and sucrose are so similar, particularly on absorption by the body, it appears unlikely that HFCS contributes more to obesity or other conditions than sucrose.”

There is no scientific evidence to suggest that high fructose corn syrup is responsible for diabetes. All caloric sweeteners trigger an insulin response in the body. In fact, table sugar, honey and high fructose corn syrup trigger about the same insulin release, because they contain nearly equal amounts of fructose and glucose.

Many confuse pure “fructose” with “high fructose corn syrup,” a sweetener that never contains fructose alone, but always in combination with a roughly equivalent amount of a second sugar (glucose). Recent studies that have examined pure fructose - often at abnormally high levels - have been inappropriately applied to high fructose corn syrup and have caused significant consumer confusion.

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