A new study in mice sheds light on at least part of the reason for the insulin resistance that can come from diets high in high-fructose corn syrup, a sweetener found in most sodas and many other processed foods.
Fructose is much more readily metabolized to fat in the liver than glucose, and in the process can lead to nonalcoholic fatty liver disease. NAFLD in turn leads to hepatic insulin resistance and type II diabetes.
Researchers showed that mice fed a high-fructose diet could be protected from insulin resistance if a gene known as transcriptional coactivator PPARg coactivator-1b (PGC-1b) was "knocked down" in the animals' liver and fat tissue. PGC-1b controls the activity of several other genes, including one responsible for building fat in the liver. This suggests an important role for PGC-1b in the pathogenesis of fructose-induced insulin resistance.