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.