title: Microbiota and Obesity.
abstract: Obesity is globally the most prevalent nutritional disorder. Multifaceted therapeutic approaches are called for to halt the cascade from neonatal adiposity/high birth weight to childhood excessive weight gain/adult obesity with comorbidities. Recent experimental and clinical data provide one new target for interventions aiming to close this vicious circle: the microbiota. An aberrant gut microbiota, dysbiosis, induces immune and metabolic disturbances both locally and, consequent upon impaired gut barrier function, also systemic low-grade inflammation, which is causally linked to insulin resistance. The gut microecology could thus fill the gap between energy intake and expenditure by processing nutrients and regulating their access to and storage in the body, producing chemicals of hormonal nature and controlling the secretion of proinflammatory mediators locally and systemically. Conversely, being highly sensitive to environmental impacts, particularly to early feeding, the compositional development of the gut microbiota may prove the target of choice in efforts to reduce the risk of obesity. It has been demonstrated that a lower number of bifidobacteria precedes the development of obesity, and a dearth of butyrate-producing bacteria and an overall richness of bacteria increase the risk of metabolic disease; moreover, recognition that practices known to disrupt the early gut microbiota, e.g., cesarean section delivery and antibiotic exposure, contribute to obesity, encourages to pursue this line of research.
authors.affiliation: Department of Pediatrics and Adolescent Medicine, Turku University Hospital, and Department of Clinical Sciences, Faculty of Medicine, University of Turku, Turku, Finland.
authors.forename: Erika
authors.initials: E
authors.lastname: Isolauri
mesh_terms: D000818:Animals; D002585:Cesarean Section / Q000009:adverse effects; D004032:Diet; D064806:Dysbiosis / Q000150:complications / Q000276:immunology / Q000378:metabolism; D002149:Energy Intake; D004734:Energy Metabolism; D000069196:Gastrointestinal Microbiome / Q000502:physiology*; D006801:Humans; D061148:Hygiene Hypothesis; D006967:Hypersensitivity / Q000382:microbiology; D007249:Inflammation; D007333:Insulin Resistance; D008659:Metabolic Diseases / Q000382:microbiology; D009765:Obesity / Q000453:epidemiology / Q000382:microbiology* / Q000517:prevention & control; D012307:Risk Factors