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High-fat diet makes mice susceptible to liver injury
Date:11/1/2007

A high fat diet may kill regulatory T cells in the liver, allowing steatosis (simple fatty liver) to develop into steatohepatitis (fatty liver with inflammation), according to the results of a new study in the November issue of Hepatology, a journal published by John Wiley & Sons on behalf of the American Association for the Study of Liver Diseases (AASLD). The article is also available online at Wiley Interscience (http://www.interscience.wiley.com/journal/hepatology).

Nonalcoholic fatty liver disease (NAFLD), a condition related to obesity, can range in severity from simple hepatic steatosis to nonalcoholic steatohepatitis (NASH) to cirrhosis which can lead to death. However, the progression of the disease is not well understood. The prevailing hypothesis suggests two-hits are necessary. The first is prolonged over-nutrition which causes the accumulation of fat in the liver. The second hit has been hypothesized to involve oxidative stress, mitochondrial injury or inflammatory cytokine production involving regulatory T cells (Tregs).

Tregs have recently emerged as a key player in hepatic immune regulation, so researchers, led by Xiong Ma of Johns Hopkins University in Baltimore, sought to determine their role in the pathogenesis of NASH. They hypothesized that regulation by Tregs is decreased in a fatty liver, which makes inflammation worse when the organ is exposed to secondary injury.

To test this hypothesis, they fed adult mice a high-fat diet to induce obesity, steatosis, and insulin resistance similar to that seen in humans. (Mice in the control group were fed a normal diet.) They examined the mices hepatic lymphocyte population by flow cytometry. The researchers then injected the mice with liver inflammation-causing exogenous lipopolysaccarhide (LPS, a bacterial toxin usually presented in the normal intestine and carried to the liver by blood flow), and examined serum and liver tissue of the sacrificed mice.

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Contact: Amy Molnar
amolnar@wiley.com
John Wiley & Sons, Inc.
Source:Eurekalert

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