A specific bacterial gut microbiota profile with increased extraction of energy has recently been associated with obesity, which has been shown to be a transmissible phenotype by microbiota transplantation. At the same time, there is now increasing evidence that gut microbiota plays a role in the development of hepatic steatosis and its progression to nonalcoholic steatohepatitis. This review summarizes well known and unexpected interacting factors leading to obesity and its related hepatic diseases, including intestinal mucosal permeability and its regulation, gut microbiota and translocation of its biological products, and gut-associated lymphoid tissue. These intestinal factors dictate also the balance between tolerance and immune response, which are critical for most of the complications in near and far organs or systems. We review novel mechanisms involving the development of gut permeability and adipose tissue plasticity, for example, the cross-talk between the gut microbiota, lipopolysaccharide, high-fat diet, and the endocannabinoid system tone, which have not been fully explored. Interactions between gut microbiota and other factors (eg, inflammasome deficiency) also are reviewed as emerging but far from being completely elucidated mechanisms influencing the onset of obesity and nonalcoholic fatty liver disease.
*University of Salerno Medical School, Salerno, and ELFID, Naples, Italy
†Mucosal Immunology and Biology Research Center, Massachusetts General Hospital, Boston.
Address correspondence and reprint requests to Prof Pietro Vajro, Chair of Pediatrics, Department of Medicine and Surgery, University of Salerno, Baronissi (Sa) 84081, Italy (e-mail email@example.com).
Received 1 October, 2012
Accepted 17 December, 2012
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This article was partially supported by the National Institutes of Health grant DK-48373 to A.F. and FARB-ex 60% 2012 grant to P.V.
The authors report no conflicts of interest.