Intestinal microbiota and host metabolism — A complex relationship.

Thus, although the gut microbiota undoubtedly plays a key role in the development of obesity, several studies have challenged the view that diet-induced obesity is causally related to intestinal microbiota. In the current issue of I Acta Physiologica, i Lundberg and co-workers publish a paper entitled "Germ-free mice are not protected against diet-induced obesity and metabolic dysfunction" in which the authors show that feeding a Western diet to both conventionally raised and germ-free mice results in weight gain, increased fat mass, fatty liver, glucose intolerance and adipose tissue inflammation.1 This indicates that the development of obesity and components of the metabolic syndrome is not dependent on the presence of gut microbiota and adds to the ongoing discussion regarding the causal role of intestinal microbiota in the development of obesity.2 More than 15 years ago, pioneering gnotobiotic studies were conducted by Bäckhed and co-workers providing compelling evidence that germ-free mice are protected against diet-induced obesity.3 This original concept, which considers the gut microbiota as a hub between environmental factors, mostly diet, and the host metabolism has been extensively developed by the Bäckhed group and successfully translated to humans. Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice. [Extracted from the article]