Interplay Between Weight Loss and Gut Microbiota Composition in Overweight Adolescents

Abstract

The aim of this study was to determine the influence of an obesity treatment program on the gut microbiota and body weight of overweight adolescents. Thirty‐six adolescents (13–15 years), classified as overweight according to the International Obesity Task Force BMI criteria, were submitted to a calorie‐restricted diet (10–40%) and increased physical activity (15–23 kcal/kg body weight/week) program over 10 weeks. Gut bacterial groups were analyzed by quantitative real‐time PCR before and after the intervention. A group of subjects (n = 23) experienced >4.0 kg weight loss and showed significant BMI (P = 0.030) and BMI z‐score (P = 0.035) reductions after the intervention, while the other group (n = 13) showed <2.0 kg weight loss. No significant differences in dietary intake were found between both groups. In the whole adolescent population, the intervention led to increased Bacteroides fragilis group (P = 0.001) and Lactobacillus group (P = 0.030) counts, and to decreased Clostridium coccoides group (P = 0.028), Bifidobacterium longum (P = 0.031), and Bifidobacterium adolescentis (P = 0.044) counts. In the high weight–loss group, B. fragilis group and Lactobacillus group counts also increased (P = 0.001 and P = 0.007, respectively), whereas C. coccoides group and B. longum counts decreased (P = 0.001 and P = 0.044, respectively) after the intervention. Total bacteria, B. fragilis group and Clostridium leptum group, and Bifidobacterium catenulatum group counts were significantly higher (P < 0.001–0.036) while levels of C. coccoides group, Lactobacillus group, Bifidobacterium, Bifidobacterium breve, and Bifidobacterium bifidum were significantly lower (P < 0.001–0.008) in the high weight–loss group than in the low weight–loss group before and after the intervention. These findings indicate that calorie restriction and physical activity have an impact on gut microbiota composition related to body weight loss, which also seem to be influenced by the individual's microbiota.

Surgical control of obesity and diabetes: The role of intestinal vs. gastric mechanisms in the regulation of body weight and glucose homeostasis

“…Other plausible mechanisms for the improvement of glucose homeostasis after procedures that like DJB involve a bypass of the small intestine include: (1) alteration in gut microbiota (19,20); (2) bile acid perturbations (17,18); (3) changes in neuroendocrine signaling (21); and (4) alterations in putative gut factors regulated by the duodenum, that may be involved in the diabetic alterations of glucose homeostasis (''anti-incretin'' theory) (9,24). A recent study by Lam et al (7) demonstrates that duodenal-jejunal bypass surgery activates nutrient-sensing signals in the jejunum and rapidly lowers endogenous hepatic glucose production in nonobese rats with uncontrolled diabetes, suggesting a possible contribution of intestinal nutrient sensing to the glucose-lowering effects of bypass procedures.…”

“…In addition, the physiology of the digestive system and its role in glucose and energy homeostasis are complex and yet incompletely understood. Over the last decades the study of GI physiology has advanced at cellular and molecular levels revealing roles for several GI factors in the regulation of energy and glucose homeostasis including gut hormones (14)(15)(16) bile acids (17,18), miocrobiota (19,20), neural signals (21), and intestinal nutrient sensing (7). Paradoxically, however, the understanding of how anatomical segments of the GI tract contribute to metabolic regulation remains rudimentary.…”

“…Glucagon was measured using antibody against the C-terminal fragment (19,28) of glucagon which has high specificity to pancreatic glucagon and shows no cross reactivity with intestinal glucagon, GLP-1 and GLP-2.…”

Changes in gut microbiota due to supplemented fatty acids in diet-induced obese mice

“…The significance of the protective role of the GM has been highlighted by the profound impact seen when the GM is absent or disrupted. Germ-free mice have poorly developed mucosal architecture and rudimentary development of the mucosa-associated lymphoid tissue, being generally small and underweight, and also highly susceptible to intestinal infection (10) .In obese patients, there is a significant change in the composition of the GM compared with lean controls (11,12) , and, in rats, these modifications can be induced by the ingestion of a HFD (13) . Furthermore, host nutritional status may be markedly influenced by the composition and activities of the GM since the Bacteroidetes:Firmicutes ratio seems to be decreased in obese individuals and genetically obese mice harbour an 'obese microbiome', with a transferable elevated capacity for energy sequestration (14) .…”

The Epidemiologic Evidence and Potential Biological Mechanisms for a Protective Effect of Dietary Fiber on the Risk of Colorectal Cancer

“…It is possible that obesity could be linked to colorectal cancer via lower levels of bifidobacteria, which has been noted in obese women (who have higher levels of Bacteroides, Clostridium, and Staphylococcus) who gain excessive weight during pregnancy and also in people with type 2 diabetes-itself a putative risk factor for colorectal cancer [5•, 38, 39]. Weight loss also has been associated with reduced level of Bifidobacterium bifidum and Bifidobacterium breve counts and increased Bifidobacterium catenulatum [40]. The level of Bifidobacterium genus also is decreased upon weight loss after bariatric surgery [41].…”