Does Bariatric Surgery Work By Changing Gut Bugs?Friday, June 14, 2013
As readers are well aware, bariatric surgery is currently the most effective treatment for severe obesity. Yet, we are still not quite sure how exactly surgery works.
For one, we know that simplistic notions of surgery “mechanically” inhibiting food intake are simply wrong – were that the case, simply having your jaws wired shut would be as effective.
Nor does caloric malabsorption account for much of the weight loss (except perhaps with biliopancreatic diversion) – there is indeed good evidence that with contemporary bypass procedures, the remaining gut has no problem extracting all the calories it needs from the diet.
One of the reasons bariatric surgery works in the long term is because it changes gut hormones (e.g. ghrelin, GLP-1, PYY) and thus counteracts the homeostatic mechanisms that counteract weight loss.
But recent observations that bariatric surgery also prevents much of the decrease in metabolic rate normally associated with weight loss suggests that there is more going on than meets the eye.
Now, a study by Ling-Chun Kong and colleagues from Paris, France, in a paper published in the American Journal of Clinical Nutrition supports the notion that bariatric surgery may have additional effects on energy homeostasis by affecting the gut microbiome.
The researchers profiled the gut microbiota from fecal samples and adipose tissue samples in severely obese individuals, before as well as three and six months after roux-en-Y gastric bypass surgery.
In these patients, surgery resulted in a remarkable increase in richness of gut microbiota (previous studies have shown that gut microbiota phylogenetic richness is lower in obese than in lean subjects), whereby almost 40% of the increase in gut bacteria belonged to the phylum Proteobacteria. Most of these changes occurred early, with no further differences noted between the three and six month samples.
The researchers also found significant associations between gut microbiota composition and adipose tissue gene expression (including numerous genes related to metabolism and inflammation) as well as clinical phenotype – as substantial proportion of which were independent of any changes in caloric intake.
As to the cause or clinical implications of these changes, the authors can only speculate. As they point out, some of these changes may be due to alterations in diet composition, eating behaviour (e.g. increased chewing), or biological changes that include differences in pH and other aspects of intestinal milieu.
Although such “correlational” studies cannot prove cause and effect, this study does document profound changes in the gut bacteriome with gastric bypass surgery and given our understanding that gut bugs may very much influence energy metabolism, it will be certainly be of considerable interest to examine whether these changes contribute to the success of bariatric surgery.
Kong LC, Tap J, Aron-Wisnewsky J, Pelloux V, Basdevant A, Bouillot JL, Zucker JD, Doré J, & Clément K (2013). Gut microbiota after gastric bypass in human obesity: increased richness and associations of bacterial genera with adipose tissue genes. The American journal of clinical nutrition PMID: 23719559