I read with great interest the recently published review article “Mechanisms in bariatric surgery: Gut hormones, diabetes resolution, and weight loss” by Holst et al. The study is published in Surgery for Obesity and Related Diseases journal, May 2018 issue. The authors presented a thorough and clear review on weight loss mechanisms following bariatric surgery like gastric bypass and gastric sleeve procedures. Holst and colleagues present evidence supporting accelerated nutrient passage from gastric pouch into intestines as well as nutrient absorption across gut mucosa into the blood stream. This accelerated nutrient delivery including glucose and amino acids stimulates postprandial neuroendocrine hormone secretion like GLP-1 and PYY. Within few days after weight loss surgery, GLP-1 an insulinotropic hormone and glucose plasma levels dramatically rise, creating a powerful stimulus for pancreatic beta cells. Beta cells sensitivity to glucose is enhanced and postprandial insulin secretion increases leading to improvement in postprandial blood sugar control. Administration of exendin 9-39, a GLP-1 antagonist, impairs the rise in insulin secretion and improvement of glucose homeostasis. Such evidence confirms the central role of neuroendocrine cells and GLP-1 in particular in bariatric surgery mechanism of action. The concepts of restriction and malabsorption that have been traditionally assigned to Roux-en-Y gastric bypass are no longer applicable. Indeed, studies quoted in this article have clearly demonstrated increased gastric pouch emptying and increased nutrient absorption.
The implications of such findings are significant when it comes to optimizing surgical technique. The most effective weight loss procedure is the procedure that accelerates gastro-intestinal motility the most. We no longer use the smallest size bougie to perform a sleeve gastrectomy. A smaller bougie is associated with higher leak rate without concomitant improvement in weight loss outcomes. The most optimal sleeve shape is the one that preserves certain stomach components that accelerate gastric emptying. These components include preserving the antrum (gastric pump), avoid narrowing the incisura angularis, and resecting the redundant posterior gastric fundus. The same applies to gastric pouch size in Roux-en-Y gastric bypass surgery and the futile practice of endoscopic narrowing of gastro-jejunostomy in hope of increasing gastric pouch food stasis. Food stasis is, indeed, not associated with increased satiety and weight loss.
Several years ago, I developed gastric fundus invagination as a weight loss procedure. It preserves stomach structure but at the same time eliminates gastric fundus meal accommodation. As a result, gastric fundus invagination increases gastric emptying and may possibly increase GLP-1 secretion. We don’t know if, and, how gastric fundus invagination changes pacemaker function and stomach electric activity. Does gastric fundus invagination restore emptying along the Magenstrasse pathway? Magenstrasse emptying depends on both electric waves generated in the fundus and antrum. By invaginating gastric fundus in close proximity to stomach antrum, what happens to those waves?
Metabolic and weight loss surgery research is much needed today to elucidate the role of gastro-intestinal motility in disease like obesity, type Diabetes, GERD and gastroparesis. Understanding gastro-intestinal motility may help develop more effective and less invasive solutions for diseases that have reached epidemic level in our society.