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OBJECTIVE-Obesity alters gut microbiota ecology and associates with low-grade inflammation in humans. Roux-en-Y gastric bypass (RYGB) surgery is one of the most efficient procedures for the treatment of morbid obesity resulting in drastic weight loss and improvement of metabolic and inflammatory status. We analyzed the impact of RYGB on the modifications of gut microbiota and examined links with adaptations associated with this procedure.
RESEARCH DESIGN AND METHODS-Gut microbiota was profiled from fecal samples by real-time quantitative PCR in 13 lean control subjects and in 30 obese individuals (with seven type 2 diabetics) explored before (MO), 3 months (MS), and 6 months (M6) after RYGB.
RESULTS-Four major findings are highlighted: 1) Bacteroides/ Prevotella group was lower in obese subjects than in control subjects at M0 and increased at M3. It was negatively correlated with corpulence, but the correlation depended highly on caloric intake; 2) Escherichia, coli species increased at M3 and inversely correlated with fat mass and leptin levels independently of changes in food intake; 3) lactic acid bacteria including Lactobacillus/Leuconostoc/Pediococcus group and Bifidobacterium genus decreased at M3; and 4) Faecalibacterium prausnitzii species was lower in subjects with diabetes and associated negatively with inflammatory markers at M0 and throughout the follow-up after surgery independently of changes in food intake.
CONCLUSIONS-These results suggest that components of the dominant gut microbiota rapidly adapt in a starvation-like situation induced by RYGB while the F. prausnitzii species is directly linked to the reduction in low-grade inflarnmation state in obesity and diabetes independently of calorie intake. Diabetes 59: 3049-3057, 2010
Obesity is characterized by increased fat mass accumulation and the development of comorbidities mcliiding other metabolic and cardiovascular diseases. Even though some but not all environmental factors have been elucidated, the increasing epidemic of obesity appears virtually impossible to control, and the mechanisms associated with fat mass expansion need to be identified. Obesity is considered a low-grade inflammatory disease with adipose tissue contributing to this state via the secretion of molecules capable of altering metabolic homeostasis (1,2). A novel factor identified to play a role in human obesity and associated metabolic risks is the commensal microbiota of the mtestine (3).
A role for the intestinal microbiota in harvesting energy from food (4) and regulating body fat storage (5) was proposed...