A new study by the Free University of Brussels in Belgium shows a relationship between the number of bacteria in the intestines and the susceptibility to medical complications associated with obesity. Belgian researchers have shown that people with low numbers of bacteria in their intestines are most likely to develop obesity-related complications, such as cardiovascular disease and diabetes, as "intestinal bacterial germination" reduces the number of bacteria.
The human intestine is colonized by millions of bacteria which form the intestinal flora, known as gut flora. Studies reveal that lean and overweight human may present a difference in the composition of their intestinal flora. Several mechanisms explain the correlation between intestinal flora and obesity. The intestinal flora would increase the energetic extraction of non-digestible polysaccharides. In addition, the lipopolysaccharide from intestinal flora bacteria could trigger a chronic sub-clinical inflammatory process, leading to obesity and diabetes. Another mechanism through which the intestinal flora could lead to obesity would be through the regulation of genes of the host involved in energy storage and expenditure. In the past five years data coming from different sources established causal effects between intestinal microbiota and obesity/insulin resistance, and it is clear that this area will open new avenues of therapeutic to obesity, insulin resistance and DM2.
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Gut microbiota also may contribute for metabolic disturbances observed in obesity by triggering systemic inflammation . Lipopolysaccharides (LPS) from gut microbiota, present in cell membrane of those gram-negative bacteria ...
Gut microbiota also may contribute for metabolic disturbances observed in obesity by triggering systemic inflammation . Lipopolysaccharides (LPS) from gut microbiota, present in cell membrane of those gram-negative bacteria ...
Yes. Possible role exists. Gut microbiota can influence energy extraction from food, lipid metabolism, immune response and endocrine functions and its profile has shown to differs between obese and lean subjects.
The resident bacteria within the GI tract are responsible for a significant portion of our energy intake, allowing us access to energy sources that may have otherwise been indigestible.
Peter J. Turnbaugh et al (2006) reported that the comparisons of the distal gut microbiota of genetically obese mice and their lean littermates, as well as those of obese and lean human volunteers have revealed that obesity is associated with changes in the relative abundance of the two dominant bacterial divisions, the Bacteroidetes and the Firmicutes.
Their results indicated that the obese microbiome has an increased capacity to harvest energy from the diet. Furthermore, this trait is transmissible: colonization of germ-free mice with an ‘obese microbiota’ results in a significantly greater increase in total body fat than colonization with a ‘lean microbiota’.
They identify the gut microbiota as an additional contributing factor to the pathophysiology of obesity
Composition of gut microbiota is affected by many factors such as diet, disease state, medications as well as host genetics to name a few. As a result, the composition of the gut microbiota is constantly changing affecting the health and well-being of the host such as disease state as well as the use of various medicines such as antibiotics