Bariatric Times - January 2009 - (Page 22)

22 Metabolic Perspective Bariatric Times • January 2009 Failure to show an adequate rise in GLP-1 with consequent high serum insulin level needs to be treated followed other similar reports.11,12 Bantle et al13 demonstrated successful treatment of three such patients with a low carbohydrate diet. This dietary management should be tried before resorting to pancreatectomy. intestinal bypass.5 Nãslund’s paper led to my suggestion of moving a portion of ileum to a juxtaduodenal position to cure T2D without bypassing the upper digestive tract.17 This paper discouraged use of transposition of the ileum in humans without further animal study. Strader performed ileal transposition in rats and showed that it increased GLP-1 secretion, decreased food intake, and decreased body weight compared improvement in T2D in four patients unrelated to any change in weight was similar to that observed after RYGB. Measurements of plasma GLP1 were not obtained but would provide additional evidence regarding the hindgut hypothesis: that any procedure that exposes ileum to glucose will stimulate GLP-1 secretion. GASTRIC CONTRACTILITY MODULATION If the defect causing T2D is a failure of sufficiently strong initial gushing to cause overflow of hypertonic gastric contents into the jejunum, then stimulation of the antrum to augment gastric emptying should be an effective way to treat T2D. The Tantalus Gastric Contractility Modulator (GCM) has been reported to provoke an early response of the gut typical of a full meal.20 It has also been reported to improve diabetes. Measurements of plasma GLP-1 levels are needed. DUODENAL-JEJUNAL BYPASS SLEEVE The duodenal-jejunal bypass sleeve has been shown to eliminate need for medications to treat T2D in four patients.19 This is a 60cm plastic liner that is anchored in the proximal duodenum. It causes stomach contents to bypass the glucose-regulating cells and osmoreceptors in the duodenum so that stomach contents enter the duodenum without dilution to TREATMENT WITH BYPASS OPERATION Bypass operations (whether intestinal or gastric) cause ingested glucose to reach the ileum and GLP1 secretion results. GLP-1 has numerous effects.14,15 It is a brake hormone that causes contraction of the pyloric muscle to stop gastric emptying and slows intestinal peristalsis. It is also an incretin. It stimulates insulin secretion provided the concentration of blood glucose is above normal. GLP-1 also stimulates growth of beta cells. GLP-1 blocks glucagon stimulated production of glucose in the liver. It promotes glycogenesis in liver and muscle and lipogenesis in fat. GLP1 causes satiety through the arcuate nucleus in the hypothalamus. The cure of T2D after gastric bypass led some surgeons to postulate that there was a foregut hormone that was responsible.16 There has not been any hormone forthcoming to support this hypothesis. Nãslund’s paper provided evidence of failure of glucose to reach the hindgut and stimulate GLP-1 secretion in patients who were candidates for and surgeons know that all patients with severe obesity are candidates for treatment with the sham operation controls.18 Strader also showed greater reduction of plasma glucose concentration after the same dose of intraperitoneal insulin in ilealtransposed rats compared with sham animals. This indicated that ileal transposition increased GLP-1 secretion and improved insulin receptor function. isotonicity or an optimum glucose concentration. The stomach contents pass through the duodenum within the sleeve while bile and pancreatic juice pass through the duodenum between the sleeve and the duodenal wall. Weight loss in 10 patients over 12 weeks was 23.6 percent. The sleeve is a temporary duodenal bypass procedure. The rapidity of ROUX-EN-Y GASTRIC BYPASS RYGB is the standard of care today for the treatment of severe obesity. It cures T2D unless the beta cells have been exhausted, in which case type-1 diabetes also exists. Ideally, obesity should be eliminated before the beta cells are exhausted. Many patients with newly diagnosed T2D and with BMIs greater than 35 could probably be successfully treated with exendin-4, although this needs further documentation. There are other GLP-1 mimetics that might be substituted. If treatment with GLP1 mimetics failed, a surgical operation might then be indicated. My preference beginning in 1971 was to use a restriction operation when possible because of the complications of bypass operations.21 this increases the number of candidates with T2D in the United States from 23 MILLION TO 100 MILLION. CONCLUSION Even though T2D is usually cured by bypass operations, the normal control of GLP-1 secretion is lost. Medication can be stopped or given as needed. If hyperinsulinemic

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Bariatric Times - January 2009

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