Washington, Mar 4 (ANI): Scientists have found that "knocking down" a gene called transcriptional coactivator PPARg coactivator-1b (PGC-1b) can protect 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. (ANI)