title: [Physiological patterns of intestinal microbiota. The role of dysbacteriosis in obesity, insulin resistance, diabetes and metabolic syndrome].
abstract: The intestinal microbiota is well-known for a long time, but due to newly recognized functions, clinician's attention has turned to it again in the last decade. About 100 000 billion bacteria are present in the human intestines. The composition of bacteriota living in diverse parts of the intestinal tract is variable according to age, body weight, geological site, and diet as well. Normal bacteriota defend the organism against the penetration of harmful microorganisms, and has many other functions in the gut wall integrity, innate immunity, insulin sensitivity, metabolism, and it is in cross-talk with the brain functions as well. It's a recent recognition, that intestinal microbiota has a direct effect on the brain, and the brain also influences the microbiota. This two-way gut-brain axis consists of microbiota, immune and neuroendocrine system, as well as of the autonomic and central nervous system. Emerging from fermentation of carbohydrates, short-chain fatty acids develop into the intestines, which produce butyrates, acetates and propionates, having favorable effects on different metabolic processes. Composition of the intestinal microbiota is affected by the circadian rhythm, such as in shift workers. Dysruption of circadian rhythm may influence intestinal microbiota. The imbalance between the microbiota and host organism leads to dysbacteriosis. From the membrane of Gram-negative bacteria lipopolysacharides penetrate into the blood stream, via impaired permeability of the intestinal mucosa. These processes induce metabolic endotoxaemia, inflammation, impaired glucose metabolism, insulin resistance, obesity, and contribute to the development of metabolic syndrome, type 2 diabetes, inflammarory bowel diseases, autoimmunity and carcinogenesis. Encouraging therapeutic possibility is to restore the normal microbiota either using pro- or prebiotics, fecal transplantation or bariatric surgery. Human investigations seem to prove that fecal transplant from lean healthy individuals into obese diabetic patients improved all the pathological parameters. Wide spread use of bariatric surgery altered gut microbiota and improved metabolic parameters apart from surgery itself. Pathomechanism is not yet completely clarified. Clinicians hope, that deeper understanding of complex functions of intestinal microbiota will contribute to develop more effective therapeutic proceedings against diabetes, metabolic syndrome, and obesity.
authors.affiliation: Metabolikus Ambulancia, Mazsihisz Szeretet Kórház Budapest.
authors.forename: Tamás
authors.initials: T
authors.lastname: Halmos
authors.affiliation: Tüdőgondozó, Bajcsy-Zsilinszky Kórház-Rendelőintézet Budapest.
authors.forename: Ilona
authors.initials: I
authors.lastname: Suba
mesh_terms: D001921:Brain / Q000378:metabolism; D002940:Circadian Rhythm; D003920:Diabetes Mellitus / Q000378:metabolism / Q000382:microbiology*; D064806:Dysbiosis / Q000378:metabolism / Q000382:microbiology / Q000503:physiopathology; D019446:Endotoxemia / Q000209:etiology / Q000378:metabolism; D000069467:Fecal Microbiota Transplantation; D005247:Feeding Behavior; D000069196:Gastrointestinal Microbiome; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000382:microbiology; D015212:Inflammatory Bowel Diseases / Q000378:metabolism / Q000382:microbiology; D007333:Insulin Resistance; D007422:Intestines / Q000382:microbiology*; D024821:Metabolic Syndrome / Q000378:metabolism / Q000382:microbiology*; D064307:Microbiota; D009765:Obesity / Q000378:metabolism / Q000382:microbiology*; D056692:Prebiotics / Q000008:administration & dosage; D019936:Probiotics / Q000008:administration & dosage
chemical_list: D056692:Prebiotics
keywords: agy–bél tengely; bariatric surgery; bariátrikus sebészet; dysbiosis; fecal transplantation; fekális transzplantáció; gut–brain axis; metabolic endotoxemia; metabolikus endotoxaemia; microbiota; mikrobióta; rövid láncú zsírsavak (SCFA-k); short-chain fatty acids