Nonalcoholic fatty liver disease may be reversed

Scientists at Columbia University Medical Center have identified a factor in liver cells responsible for turning a relatively benign liver condition, present in 30 percent of U.S. adults, into a serious disease that can lead to liver failure.
The serious consequences of nonalcoholic fatty liver disease may be prevented when the factor, known as TAZ, is shut down, according to Xiaobo Wang, PhD, an associate research scientist at Columbia.
With the rise of obesity in the United States, the incidence of nonalcoholic fatty liver disease — in which excess fat fills the liver — has risen to epidemic levels. The extra liver fat is generally benign, but in one in five people, the disease evolves into a more serious condition, called nonalcoholic steatohepatitis, or NASH.
In NASH, the liver becomes inflamed and criss-crossed by fibrous scar tissue, and liver cells start dying. Patients are at risk of liver failure and liver cancer, but there are no drugs on the market that can slow or stop the disease.
Because the amount of fibrosis in the liver is associated with a greater risk of death, Wang, working in the lab of Ira Tabas, MD, looked for ways to stop fibrosis in a mouse model. He found that in liver cells, TAZ plays a critical role in initiating fibrosis, which stops in mice when TAZ is inactivated in liver cells. With TAZ shut down, existing fibers in the liver also dissolved, essentially reversing the disease.
Two other critical features of NASH, inflammation and cell death, were also reduced when TAZ was turned off. Fat accumulation in the liver was unaffected.
Based on their examination of liver biopsies from patients, Qang and Tabas believe that TAZ works in the same way in people.
“We think that by stopping fibrosis through TAZ and its partners, we may be able to prevent the serious consequences of NASH, including liver failure and liver cancer,” said Tabas, the Richard J. Stock Professor and vice chair of research in the Department of Medicine and professor of pathology and cell biology (in physiology and cellular biophysics) at Columbia.
Wang and Tabas and Columbia University have filed a patent for the use of TAZ pathway inhibitors in treating nonalcoholic fatty liver disease.
Source: Columbia University Medical Center: newsroom.cumc.columbia.edu