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Intestinal Microbiota During Infancy and Its Implications for Obesity

Reinhardt, Christoph; Reigstad, Christopher S; Bäckhed, Fredrik

Journal of Pediatric Gastroenterology & Nutrition:
doi: 10.1097/MPG.0b013e318183187c
Invited Review
Abstract

Obesity is a worldwide epidemic, threatening both industrialized and developing countries, and is accompanied by a dramatic increase in obesity-related disorders, including type 2 diabetes mellitus, hypertension, cardiovascular diseases, and nonalcoholic fatty liver disease. Recent studies have shown that the gut microbial community (microbiota) is an environmental factor that regulates obesity by increasing energy harvest from the diet and by regulating peripheral metabolism. However, there are no data on how obesogenic microbiotas are established and whether this process is determined during infancy. The sterile fetus is born into a microbial world and is immediately colonized by numerous species originating from the surrounding ecosystems, especially the maternal vaginal and fecal microflora. This initial microbiota develops into a complex ecosystem in a predictable fashion determined by internal (eg, oxygen depletion) and external (eg, mode of birth, impact of environment, diet, hospitalization, application of antibiotics) factors. We discuss how the gut microbiota regulates obesity and how environmental factors that affect the establishment of the gut microbiota during infancy may contribute to obesity later in life.

Author Information

Sahlgrenska Center for Cardiovascular and Metabolic Research/Wallenberg Laboratory, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden

Received 17 January, 2008

Accepted 8 June, 2008

Address correspondence and reprint requests to Fredrik Bäckhed, PhD, Wallenberg Laboratory, Sahlgrenska University Hospital, S-413 45 Gothenburg, Sweden (e-mail: Fredrik.Backhed@wlab.gu.se).

Supported by the Swedish Research Council, Swedish Foundation for Strategic Research, Wenner-Gren Foundation, Petrus and Augusta Hedlund Foundation, the Novo Nordisk Foundation, Harald Jeansson Foundation, and a LUA-ALF grant from Västra Götalandsregionen.

The authors report no conflicts of interest.

© 2009 Lippincott Williams & Wilkins, Inc.