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For diabetics, a way to bypass the bypass

PET/CT scans of a rat before (left) and after (right) gastric bypass surgery showing increased glucose use by the intestine after the surgery.
[Image courtesy of Stylopoulos Laboratory]

A new study in the journal Science might help explain why obese individuals who undergo a special type of surgery to help reduce their weight are cured of diabetes in the process.

Very overweight individuals commonly have diabetes, a condition in which their blood sugar is too high; this causes organ damage. When these patients undergo a particular kind of gastric bypass surgery (meant to help them lose weight), doctors have observed that they also experience a reduction in blood sugar.

Recent studies have shown that a particular type of gastric bypass surgery called Roux-en-Y gastric bypass (RYGB), quickly reduces the high blood sugar associated with Type 2 diabetes. Indeed, obese diabetics who undergo RYGB can often stop taking their diabetes medication even before weight loss is observed.

The way diabetes is squashed in these patients has been unclear. Some have proposed that RYGB causes changes in gut hormones, those that tell the brain it's full after food consumption; perhaps it makes the hormones cue the brain earlier. In this report, however, researchers present an entirely new view of how RGBY induces a beneficial effect on diabetic patients.

During an RYGB procedure, the stomach is divided into a small upper pouch that collects food and a much larger lower pouch that no longer can. The smaller pouch alone is connected to the gut below, and specifically, to the small intestine. First though, the small intestine is surgically re-arranged into a Y-configuration called a "Roux limb." Several recent studies in rodents and humans have shown that the Roux limb changes following RYGB surgery, expanding in size, though the significance of this growth is not understood.

Nima Saeidi, from the Center for Basic and Translational Obesity Research at Boston Children's Hospital, and colleagues, hypothesized that the construction of the Roux limb, as well as the changes it undergoes, are what make blood glucose levels go down in RYGB patients with diabetes. They suggested that undigested food passes into the Roux limb, triggering it to expand, and that the Roux limb gathers the energy to fuel this expansion by taking up glucose, leaving less of it behind in the blood.

This process represents a special glucose metabolism, unique to the Roux limb structure.

To test their hypothesis about this special metabolism, the researchers performed RYGB surgery in obese rats and compared the metabolic activity in the Roux limb of these RYGB-treated rodents with the metabolic activity in the same part of the intestine of control rats (those who underwent general surgery in which the intestine was not reconfigured into the Roux limb).

They found that intestinal glucose in RYGP-treated rats is metabolized as it would be in non-diabetics; it enters the breakdown pathways that create the molecules and energy needed for tissue expansion. This was not the case in the non-reconfigured intestines of control rats, for which glucose lingered in the blood.

These findings confirmed the researchers' hypothesis that the beneficial effect of RYGB on diabetics comes from changes in glucose metabolism within the Roux limb.

Whether or not this process is applicable in humans remains to be seen. If it is, however, these findings may pave the way for new diabetes treatments that could replace invasive gastric bypass techniques by taking advantage of the changes in intestinal metabolism that occur after RYGB.