Obesity is a multifactorial condition that results from the interaction of individual genetics with the environment. From the 1970s to the 1980s, the prevalence of obesity in the world continued to rise steadily, so much so that in 2014 the World Health Organization estimated that around 2 billion adults worldwide were overweight. Undoubtedly the increasingly convenient, easily available, high energy density and poor quality food, as well as excess nutrition are among the most important causes of the increase in obesity. The same factors also have a considerable importance in the alteration of the microbiota. It is the focus of ‘Ferments, the secret of life‘, the fortnightly column edited by the immunologist Mauro Minelli under the aegis of the Foundation for Personalized Medicine and in collaboration with AdnKronos Salute,
“One of the first studies that confirmed the relationship between microbiota, weight gain and obesity dates back to 2006. That study highlighted the ability of the microbiota to make a greater amount of absorbable energy available to the host. In particular, it demonstrated that the transplantation of microbiota from obese ob/ob mice into germ-free mice, i.e. completely devoid of any microorganism inside them, determined an increase in weight in the transplanted mice – observes Minelli – The weight increase was not observed when, with the same intake of food, was transplanted into germ-free mice microbiota of non-obese mice.Among other things, metformin, a well-known hypoglycaemic drug, administered to mice, is associated with the increase of Akkermansia muciniphila, a relatively recently identified bacterium that has a positive impact on obesity and diabetes by inducing weight loss, an improvement in glycemic control and, last but not least, a reduction in systemic inflammation not.
That 2006 study was followed by others which demonstrated how the bacteria constituting the “obesogenic” microbiota possess enzymes capable of inducing hydrolysis and fermentation of polysaccharides which, without those bacteria, would be indigestible, and those polysaccharides increase the energy available for ‘guest. Studies on homozygous twins discordant for weight have allowed us to determine the link between microbiota, weight and diet”
“In detail, the microbiota influences the digestion by hydrolysis of indigestible carbohydrates transforming them into short-chain fatty acids (butyric acid, acetic acid, propionic acid). Butyric acid and propionic acid have an anti-obesogenic effect, while acetic acid has the opposite effect.The first two are mainly produced by the Bacteroidetes family, while acetic acid by the Firmicutes.And butyric acid, mainly released by the Bacteroidetes, stimulates the release, by the so-called ‘L-cells’ of the ileum -colon, of ‘incretins’ or hormones produced after meals at the gastrointestinal level, capable of exercising an important function of blood sugar control by increasing the secretion of insulin by the beta cells of the pancreas, slowing down gastric emptying and therefore making it softer the postprandial glycemic curve, and decreasing appetite,” emphasizes the immunoloo.
“From this we can understand how the microbiota that inhabits the intestinal tract can positively or negatively influence the metabolism, the use of sugars but also of fats and, therefore, favor or not obesity. As mentioned, it is now established that obesity is linked to a microbiota with a prevalence of Firmicutes compared to Bacteroidetes and that this dysbiosis also generates greater intestinal permeability with high translocation of bacterial-derived pathogenic factors into the bloodstream. chronic inflammation, are the basis of the metabolic syndrome since they are able to negatively interfere, among other things, with insulin function.Hence – he concludes – the link with type 2 diabetes, the not easy control of type 1 diabetes, the allergic states, celiac disease.This mechanism would appear to be the basis of as many pathologies on a neurodegenerative basis, mainly Alzheimer’s disease and but Parkinson’s disease, who see a clear clinical-pathological reversal in a resolution of dysbiosis and in an enrichment of the microbiota”.
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