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Obesity and the GI microbiota


Obesity is an enormous public health problem, arising as a consequence of alterations in eating behavior and how the body regulates energy intake, expenditure, and storage. Although an increased intake of energy-dense foods, especially when combined with reduced physical activity, contributes to the high prevalence of obesity, the existence of complex systems that regulate energy balance requires that this paradigm be considered in a larger context. In particular, recent evidence suggests that the gut microbiota may play a role in by increasing the host's energy-harvesting efficiency.

For further information visit:

DiBaise JK et al. Gut Microbiota and Its Possible Relationship With Obesity. Mayo Clin Proc. 2008;83(4):460-469

Armougom F et al. Monitoring Bacterial Community of Human Gut Microbiota Reveals an Increase in Lactobacillus in Obese Patients and Methanogens in Anorexic Patients. PLoS ONE 4(9): e7125 (2009)

Fleissner CK et al. Absence of intestinal microbiota does not protect mice from diet-induced obesity. Br J Nutr. 2010 Sep;104(6):919-29

Tsukumo DM et al. Translational research into gut microbiota: new horizons in obesity treatment. Arq Bras Endocrinol Metab. 2009;53(2):139-144



Mechanisms by which the intestinal microbiota may contribute to obesity:



AMPK = adenosine monophosphate activated protein kinase
ChREBP = carbohydrate response element binding protein
FIAF = fasting induced adipocyte
LPL = lipoprotein lipase



For further information download Skinner C and Lin S. Effects of calorie restriction on life span of microorganisms. Appl Microbiol Biotechnol. 2010 Oct;88(4):817-28 or read about the following study on how probiotics can reduce the risk of overweight development:

A recent hypothesis envisages the gut microbiota as instrumental in the control of bodyweight and energy metabolism, affecting the two main causes of obesity: energy acquisition and storage.

Moreover, the composition of the gut microbiota contributes to the insulin resistance and theinflammatory state characterizing obesity. High prepregnancy body mass index (BMI) and excessive weight gain during pregnancy are associated with aberrancies in the gut microbiota composition of the mother, this acting as the inoculum for the development of the infant gut microbiota, and thus carrying a potential to interfere with the healthy stepwise colonization of the infant gut.

In a similar manner, breast milk, the composition of which also depends on the mother's nutritional and immunological state and gut microbiota composition, guides the compositional development of the infant gut microbiota. Early Bifidobacterium microbiota appear to protect against gut barrier dysfunction, metabolic endotoxemia, insulin resistance and obesity. The composition of gut microbiota may thus be taken to represent a novel contributor to obesity above the traditional and well-known risk factors, excessive energy intake and sedentary behavior.

On this basis, we here hypothesized that early modification of the gut microbial and immunological environment with probiotics will reduce the risk of overweight development and, thus, beneficially influence the child's early growth pattern. We therefore followed the growth of 113 children who were given probiotics or placebo perinatally in a double-blind, allergy prevention study until 10 years of age, with special attention to reducing the risk of allergic disease and the critical age for the development of overweight and the impact, if any, of this intervention on the child's BMI. The justification for the evaluation of overweight development and the importance of a healthy host–microbiome interaction in a population at high risk of allergic diseases, in addition to the probiotic intervention accomplished, is further supported by the similar environmental influences underlying obesity and allergic diseases, that is, a low-grade systemic inflammation.
Read more about this study from Luoto et al. (2010).





Proposed mechanisms by which periodontal inflammatory mediators may contribute to the development of insulin resistance in individuals with both type 2 diabetes and periodontitis. The inflammatory mediators originating from periodontal sources can interact systemically with lipids, free fatty acids and advanced glacation end products (AGES), all of which are characteristic of diabetes. This interaction induces or perpetuates activation of the intracellular pathways, such as the I-kappa-B (IkB), I-kappa B kinase-ß (IKKß), nuclear factor-kappa B (NF-kß) and the protein c-Jun N-terminal kinase (JNK) axes, all of which are associates with insulin resistance. The activation of these infalmmatory pathways in immune cells (monocytes or macrophages), endothelium cells, adipocytes, hepatocytes and muscle cells promotes and contributes to an increase in the overall insulin resistance, which makes it difficult to achieve metabolic control in patients with both type 2 diabetes and periodontitis.





IL = interleukin, IRS-1 = insulin receptor substrate-1, LPS = lipopolysaccharide, PGE2 = prostaglandin E2, PKCs = protein kinases C, PRRs = pattern-recognition receptors, pS302 (serine-302) and p5307 (serine-307) = examples of serine sites, ROS = reactive oxygen species, TNF-alpha = tumour necrosis factor alpha.