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Insulin Resistance Following Weight Loss Surgery for Morbid Obesity
Abstract & Commentary
By Namir Katkhouda, MD, FACS, Professor of Surgery, Chief, Minimally Invasive Surgery, University of Southern California (USC)-Los Angeles, CA. Dr. Katkhouda is a consultant for Baxter, Ethicon, Storz, and Gore.
Synopsis: Both LAGB and LRYGBP significantly improved insulin resistance during the first 3 months following surgery. Both operations generated similar changes in HOMA IR, although postoperative HOMA IR levels were significantly lower after LRYGBP.
Source: Ballantyne GH, et al. Short-term changes in insulin resistance following weight loss surgery for morbid obesity: Laparoscopic adjustable gastric banding versus laparoscopic Roux-en-Y gastric bypass. Obes Surg. 2006;16:1189-1197.
Background: Laparoscopic adjustable gastric banding (LAGB) and laparoscopic Roux-en-Y gastric bypass (LRYGBP) both effectively treat insulin resistance associated with type 2 diabetes mellitus (T2DM). Restriction of caloric consumption, alterations in the enteroinsular axis, or weight loss may contribute to lowering insulin resistance after these procedures. The relative importance of these mechanisms, however, following LAGB and LRYGBP, remain unclear. The aim of this study was to compare directly the short-term changes in insulin resistance following LAGB and LRYGBP in similar populations of patients.
Methods: Patient preference determined operation type. The Homeostasis Model Assessment for Insulin Resistance (HOMA IR) was used to measure insulin resistance. Preoperative values were compared to postoperative levels obtained within 90 days of surgery. Significant differences between groups were tested by ANOVA.
Results: There were no significant preoperative differences between the groups. The 56 LAGB patients had a mean age of 42.5 years (25.7-63), BMI of 45.5 kg/m2 (35-66), and preoperative HOMA IR of 4.1 (1.4-39.2). Seventy-five percent of LAGB patients were female, and 43% had T2DM. The 61 LRYGBP patients had a median age of 39.9 years (22.1-64.3), BMI of 45.0kg/m2 (36-62), and preoperative HOMA IR of 5.0 (0.6-56.5). Seventy-nine percent of LRYGBP patients were women, and 44.3% had T2DM. Median follow-up for LAGB patients was 45 days (18-90) and 46 days for LRYGBP patients (8-88 days). LAGB patients had a median of 14.8% excess weight loss (6.9%-37.0%) and LRYGB patients had 24.2% (9.8%-51.4%). Postoperative HOMA IR was significantly less after LRYGBP, 2.2 (0.7-12.2), than LAGB, 2.6 (0.8-29.6), although change in HOMA IR was not significantly different. Change in HOMA IR for both groups did not vary with length of follow-up or weight loss, but correlated best with preoperative HOMA IR (LAGB, r = 0.8264; LRYGBP, r = 0.9711).
Conclusions: Both LAGB and LRYGBP significantly improved insulin resistance during the first 3 months following surgery. Both operations generated similar changes in HOMA IR, although postoperative HOMW IR levels were significantly lower after LRYGBP. These findings suggest that caloric restriction plays a significant role in improving insulin resistance after both LAGB and LRYTBP.
This paper by Ballantyne and colleagues shows that both the lapband and lap bypass improve type 2 diabetes through an improvement of insulin resistance. Both operations showed similar lowering of Homa IR, an indicator of insulin resistance, even if the Roux-en-Y was slightly better. He concluded that calorie restriction is a fundamental factor in the improvement of insulin resistance.
This contradicts many other authors including Rubino and Cummings who have championed the "gut" theory for improvement of type 2 diabetes. In other words, they believe that the bypassed duodenum is critical in rapid improvement of type 2 diabetes. Rubino has proposed that the duodenum produces not only the incretin hormone glucose dependent insulinotropic polypeptide (GIP) but also an unidentified anti-incretin factor which is hyperactive in the diabetic state. The 2 opposing factors are stimulated by enteral nutrients so exclusion of the upper intestine from digestive continuity silences both of them. In patients with diabetes, the result is an improvement in glycemic control because the anti-incretin dominates in this setting. These findings are supported by several rat studies.
According to Cummings, this is the real mechanism for improvement of type 2 diabetes rather than calorie and weight loss. He quotes the results published by Buchwald in a 2004 issue of JAMA that shows that the lap band which does not bypass the duodenum improved diabetes in 48% only as compared with 84% and more than 95% in lap roux en y and BPD respectively to support his theory. In the BPD, it is possible that a distal gut theory might come to play through the GLP 1 mechanism
What to think about all this? It is difficult at this point to make any final conclusions. If I had to bet, I would go with Rubino because of the current clinical evidence but it is not a sure bet. More body of evidence will emerge as this is currently the one of the most researched topic. Maybe at the end all the mechanisms will be involved in a combined fashion and there will be no winner after all!