Gastric bypass surgery often improves the symptoms of type 2 diabetes, even before patients start to lose weight. Why?
“What we found is that the secret for the cure of diabetes after gastric bypass lies in the intestine,” said Dr. Nicholas Stylopoulos, principal investigator at the Division of Endocrinology at Children's Hospital Boston and Boston Medical School, in an interview with Healthline. “The key message is that after gastric bypass the intestine becomes the most important tissue for glucose use and this decreases blood sugar levels.”
His research was published last week in the journal Science.
Doctors are hopeful they can find a way to mimic the processes that lead to improvements for type 2 diabetics after gastric bypass without actually doing the surgery.
Small Intestine to the Rescue
how it works: After gastric bypass, which is a common weight loss
solution for the severely obese, the small intestine spontaneously
begins to produce a molecule called GLUT-1 that helps the body use
“The quite amazing thing is that this is not present normally in the small intestine of adults, but only in the fetus,” said Dr. Erini Nestoridi, a research fellow in Stylopoulos' lab, in an interview with Healthline. “This happens most likely because the intestine has to work harder to do its job, for example to absorb the nutrients or move the food further down. Also, it may be that the mechanical stress of 'dumping' the food directly to the intestine, since the stomach is bypassed, contributes to these changes.”
Although weight loss and improved diabetes symptoms go hand in hand, previous research has shown that gastric bypass surgery helps resolve the disease even before weight loss occurs.
According to the U.S. Centers for Disease Control and Prevention,
diabetes affects almost 26 million people—more than eight percent of
the population. The condition can lead to eye, kidney, and nerve damage,
and puts patients at greater risk of heart attacks and stroke.
“The problem becomes even bigger if one considers that type 2 diabetes rates will only increase because of the increased obesity rates, and since obesity and type 2 diabetes are linked," Stylopoulos said. "And to add another scary thing, the childhood obesity rates have tripled since 1980s, so all these complications will start appearing in younger people.”
Bypassing the Bypass
Stylopoulos' initial research has focused on rats. He has yet to determine whether GLUT-1 also appears in humans who have gastric bypass surgery. Next, the research team will test whether non-surgical techniques can re-create the effects of gastric bypass in animals.
Their goal is to find a way to turn the small intestine into a "depot" to "dump" glucose from the bloodstream, Stylopoulos said. That would be a novel way to get rid of some circulating glucose in the body. This would be a boon for patients with diabetes, since lowering blood glucose levels can prevent diabetic complications.
“With more research, we hope that we can find ways to, as we say, bypass the bypass,” Stylopoulos said. “This mechanism we found is very promising because unlike other organs, such as the brain for example, intestines are easily accessible, and the life of those cells is only about two days, so we can easily study and manipulate these cells without having long-term problems.”
Charles Mobbs, a professor of neuroscience, endocrinology, and geriatrics at the Icahn School of Medicine at Mount Sinai Medical Center in New York, told Healthline the new study may make the medical community more willing to approve gastric bypass surgery to treat diabetes, independent of a patient's body weight. He said more research is needed, however, to figure out why gastric bypass surgery causes the small intestine to make GLUT-1.
“It may be possible to pharmacologically mimic the effect of the undigested food to induce glucose metabolism in the intestine (which of course is highly accessible to oral drugs) independent of surgery,” Mobbs said. “This could lead to a revolution in the treatment of diabetes, possibly including type 1 as well as type 2.”