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JPEN J Parenter Enteral Nutr. 2013 Nov;37(6):787-93. doi: 10.1177/0148607113481623. Epub 2013 Mar 28.

Nonalcoholic fatty liver disease: for better or worse, blame the gut microbiota?

Author information

1
Division of Gastroenterology, Children's Mercy Hospital, University of Missouri School of Medicine, Kansas City, Missouri.

Abstract

Nonalcoholic fatty liver disease (NAFLD) is a major clinical consequence for people with obesity and metabolic syndrome and is also associated with enteral and parenteral nutrition. Early studies suggested that altered gut microbiota might contribute to obesity by affecting energy harvest from the diet and energy storage in the host. Recent evidence in humans as well as in animal models has linked gut microbiota to the development of NAFLD through the gut-liver axis. With bacterial overgrowth and increased intestinal permeability observed in patients with NAFLD and in animal models, gut-derived bacterial products such as endotoxin (lipopolysaccharide) and bacterial DNA are being delivered to the liver through the portal vein and then activate Toll-like receptors (TLRs), mainly TLR4 and TLR9, and their downstream cytokines and chemokines, leading to the development and progression of NAFLD. Given the limited data in humans, the role of gut microbiota in the pathogenesis of NAFLD is still open to discussion. Prebiotics and probiotics have been attempted to modify the microbiota as preventive or therapeutic strategies on this pathological condition. Their beneficial effects on NALFD have been demonstrated in animal models and limited human studies. However, prospective, appropriately powered, randomized, controlled clinical trials are needed to determine whether prebiotics and probiotics and other integrated strategies to modify intestinal microbiota are efficacious therapeutic modalities to treat NALFD.

KEYWORDS:

gut microbiota; microbiome; nonalcoholic fatty liver disease; obesity

PMID:
23538296
DOI:
10.1177/0148607113481623
[Indexed for MEDLINE]

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