Bariatric surgery is a procedure that alters the digestive tract to treat obesity.  Unlike gastric lap-band procedures that implant an inflatable cuff to increase a patient’s sense of fullness, bariatric surgery involves the substantial removal of stomach tissue (sleeve gastrectomy) or the formation of a small gastric pouch and by-pass of the stomach proper (Roux-en-Y gastric by-pass).  There is another important distinction between these two surgeries:  Bariatric surgery favourably alters the patient’s metabolism while lap-band devices do not.

Several changes contribute to improved insulin sensitivity following bariatric surgery, with the primary effect being an increase in levels of GLP-1.  This hormone is produced by cells in the intestines and helps the body’s pancreas make better use of insulin.  A recent study elucidated a novel mechanism that helps to explain this effect.  Remarkably, bariatric surgeries in neither humans nor mice had a significant effect on the identity or activity of hormone-producing cells in the intestines.

In other words, increased GLP-1 in those who had undergone surgery was not due to changes in the number of hormone-producing cells and the surgery itself had no effect on the activity of those cells. Rather, increases in GLP-1 were correlated with an intestinal transit score.  This means that more sugar was transported to distant parts of the intestines and this led to improved metabolism.

Two important details are missing from this analysis:  First, the vast majority of glucose uptake in the digestive tract occurs in the small intestine, which means that glucose making it to the large intestine in bariatric surgery patients will not be absorbed.  This is similar to Acarbose, a type 2 diabetes drug that inhibits our body’s enzymes from converting starch into absorbable sugar.  In both bariatric surgery and acarbose therapy, less sugar is absorbed by the body for a given meal than would be in a healthy person.

My second point relates to prebiotics.  These fibers naturally escape digestion and travel to the large intestine where they are fermented by the microbiome, eventually stimulating the release of insulin-sensitizing hormones like GLP-1.  The same has been documented for individuals taking Acarbose, which inhibits digestion to increase the abundance of fermentable, prebiotic resistant starch in the large intestine.  It is therefore likely that increased transit time in bariatric surgery patients produces a prebiotic effect from normal sugars and the fermentation products stimulate endocrines cells to release more GLP-1.

The finding that there are similar blood glucose-lowering effects for bariatric surgery, acarbose, and prebiotics is most surprising because all three interventions appear to converge on the gut microbiome.  As the appreciation for this important acquired organ grows, it will be interesting to see how many other health interventions are unexpectedly mediated via the microbiome.



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Prebiotics vs Probiotics: What’s The Difference?

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