Potential of surgery for curing type 2 diabetes mellitus

Abstract

Objective: To review the effect of morbid obesity surgery on type 2 diabetes mellitus, and to analyze data that might explain the mechanisms of action of these surgeries and that could answer the question of whether surgery for morbid obesity can represent a cure for type 2 diabetes in nonobese patients as well.

Summary background data: Diabetes mellitus type 2 affects more than 150 million people worldwide. Although the incidence of complications of type 2 diabetes can be reduced with tight control of hyperglycemia, current therapies do not achieve a cure. Some operations for morbid obesity not only induce significant and lasting weight loss but also lead to improvements in or resolution of comorbid disease states, especially type 2 diabetes.

Methods: The authors reviewed data from the literature to address what is known about the effect of surgery for obesity on glucose metabolism and the endocrine changes that follow this surgery.

Results: Series with long-term follow-up show that gastric bypass and biliopancreatic diversion achieve durable normal levels of plasma glucose, plasma insulin, and glycosylated hemoglobin in 80% to 100% of severely obese diabetic patients, usually within days after surgery. Available data show a significant change in the pattern of secretion of gastrointestinal hormones. Case reports have also documented remission of type 2 diabetes in nonmorbidly obese individuals undergoing biliopancreatic diversion for other indications.

Conclusions: Gastric bypass and biliopancreatic diversion seem to achieve control of diabetes as a primary and independent effect, not secondary to the treatment of overweight. Although controlled trials are needed to verify the effectiveness on nonobese individuals, gastric bypass surgery has the potential to change the current concepts of the pathophysiology of type 2 diabetes and, possibly, the management of this disease.

Figure 1. We hypothesize that the complex reaction of the endocrine bowel to meal ingestion in normal subjects includes production of both incretins (which stimulate insulin secretion and action) and other unknown factors that inhibit the effects of incretins as a sort of negative feedback mechanism.

Figure 2. We speculate that type 2 diabetes might be the result of an imbalance in the equilibrium between anti-incretin factors and incretins, which eventually leads to delayed insulin response and impaired insulin action (A). The anti-incretin factors are most likely overproduced in the proximal foregut of diabetics.

Figure 3. Hypothesis as to the mechanism responsible for the control of diabetes after gastric bypass.