The findings could also advance the search for better diabetes treatments that target the small intestine and not the pancreas, researchers say.
"It is increasingly clear that the intestine is not just a conduit for food transit," gastric bypass surgeon Francesco Rubino, MD, tells WebMD. "We now know that it is also a very important organ for the regulation of glucose."
Because weight loss alone cannot explain the rapid remission of disease in many gastric bypass patients, researchers have looked for other causes.
One theory has been that surgery alters the expression of hormones that help control appetite, blood sugar, and weight.
But studies designed to test this hypothesis have proven contradictory, diabetes researcher Gilles Mithieux tells WebMD.
In their newly published study, reported in the September issue of the journal Cell Metabolism, Mithieux and colleagues looked elsewhere for answers.
"We know from earlier work that the small intestine can produce glucose," he says. "We showed that with gastric bypass surgery you essentially double the capacity of the intestine to do this."
By studying mice treated with either gastric bypass or banding, researchers confirmed that the bypass operation was associated with increased production of glucose, or blood sugar, in the small intestine, while gastric banding was not.
Gastric bypass surgery essentially produces a "double intestine," Mithieux says. The portion of the small intestine that is closest to the stomach is bypassed so that it no longer received nutrients. The lower small intestine is then attached to the stomach where it becomes the main nutrient receiver.
By surgically repositioning the lower small intestine, which usually does not produce much glucose, it ramps up intestinal glucose production and improves insulin sensitivity, he says.