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Obesity Surgery May Cure Diabetes in Nonobese Patients
Am Fam Physician. 2003 Feb 15;67(4):866-869.
Although optimal treatment for patients with type 2 diabetes involves tight glucose control, this is rarely achieved. Morbid obesity, defined as weighing at least 100 lb (45.5 kg) more than ideal body weight or more than 200 percent of ideal body weight, is associated with serious comorbid diseases such as hypertension, dyslipidemia, and diabetes. Obesity surgery, including gastric bypass (GBP), biliopancreatic diversion (BPD), and gastroplasties that reduce the volume of the stomach, can ease some of these comorbidities by bringing about a weight loss of 60 to 70 percent of excess body weight. Rates of operative mortality and major complications with these procedures are low. Rubino and Gagner review the literature and discuss the possibility that weight-reducing surgical procedures may have a positive effect on patients with type 2 diabetes.
Many patients who undergo GBP or BPD report long-term normalization of plasma glucose levels. The operations appear to restore insulin sensitivity, prevent progression from impaired glucose metabolism to frank diabetes, and decrease the rate of mortality from diabetes in persons who were previously morbidly obese. Potential mechanisms for this beneficial effect on glucose metabolism include weight loss or decreased food intake. However, the positive effect of surgery occurs before significant weight loss occurs, and the fact that gastroplasty has a significantly less beneficial effect on glucose metabolism makes these explanations appear unlikely.
A more likely reason for the positive effect of weight-reducing surgery on glucose control is the subsequent change in the pattern of secretion of gastrointestinal hormones, including enteroglucagon and leptin. When BPD is performed on persons who are not morbidly obese, the beneficial effects on glucose metabolism hint that a portion of the etiology of type 2 diabetes is probably the same among obese and nonobese patients. Bypassing of the duodenum and proximal jejunum, which is included in both procedures, probably decreases production of a hormone or neuronal signal secondary to the passage of food that is responsible for the impaired action or secretion of insulin that occurs in type 2 diabetes. This outcome is not related to a decrease in food intake or a drop in weight.
The authors conclude that morbid-obesity surgery may be a specific, primary treatment for type 2 diabetes. They recommend GBP over BPD in nonmorbidly obese patients with diabetes because of the lower complication rate and the lower incidence of important late metabolic sequelae, and because the procedure can be performed laparoscopically. Further studies of this surgical effect on diabetes are recommended.
Rubino F, Gagner M. Potential of surgery for curing type 2 diabetes mellitus. Ann Surg. November 2002;236:554–9.
editor's note:Surgical literature has proposed bariatric surgery as the most effective method of diabetes management and cure in morbidly obese patients. Bypassing the hormonally active foregut and causing malabsorption provide dramatic effects on diabetes. Gastric banding and gastroplasty work in a restrictive manner to improve diabetes through decreasing food intake and body weight by slowing gastric emptying. Procedures that cause malabsorption as well as restriction result in even greater weight loss and an increase in insulin sensitivity. This improvement in metabolic fitness is related to reduction in insulin resistance and occurs over a range of glucose tolerance statuses, from normal to diabetic. A strong link between leptin and body mass index is noted after surgery, but changes in insulin levels and metabolic parameters do not appear to correlate with changes in leptin levels (Geloneze B, et al. Serum leptin levels after bariatric surgery across a range of glucose tolerance from normal to diabetes. Obesity Surgery December 2001;11:693–8.) The role of other circulating enterohormones in improved insulin sensitivity after surgery needs further study.—R.S.
Copyright © 2003 by the American Academy of Family Physicians.
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