Microbiota intestinal, sistema inmune y obesidad Intestinal microbiota, immune system and obesity

TLDR: Interactions among the intestinal microbiota, the immune system, inflammation, obesity and comorbidities suggest that the immune response could be noxious in metabolic overload conditions and that the energy accumulation as fat mainly the intra-abdominal one could be the organism response to unfavorable modifications of intestinal microbiota.

Abstract: In the development and functioning of immune system influenced essential factors like an appropriate nutritional balance and the exposition, from birth, to different microorganisms. The intestinal microbiota, although beneficial, must to be maintained within some margins. We propose that modifications in the intestinal microbiota leading to a chronic state of endotoxemia could be a key factor associated with increase in the adiposity. In obese patients Firmicutes/Bacteroidetes level is increased, which could be modified with specific changes in the lifestyle. The immune system and the metabolism have evolved in a close interrelationship with broad morphological and functional links. It is emphasize the fact that the great portion of immune system cells are located in or around the bowel and that be justly the energy accumulation as visceral fat the more associated one with the diabetes mellitus, atherosclerosis, strokes, cardiovascular disease and even some types of cancer (obesity comorbidities). The intrauterine malnutrition could a priori, to creates the immune system dysfunction, subsequently potentiated by a poor breastfeeding, an obesogenic diet and physical inactivity. All these factors will favor a more aggressive intestinal microbiota provoking a chronic inflammation characteristic of obesity. Interactions among the intestinal microbiota, the immune system, inflammation, obesity and comorbidities suggest that the immune response could be noxious in metabolic overload conditions and that the energy accumulation as fat mainly the intra-abdominal one could be the organism response to unfavorable modifications of intestinal microbiota.