RIVERSIDE, Calif. A team of scientists at the University of California, Riverside has found that even second-hand tobacco smoke exposure can result in nonalcoholic fatty liver disease (NAFLD), a common disease and rising cause of chronic liver injury in which fat accumulates in the liver of people who drink little or no alcohol.
The researchers found fat accumulated in liver cells of mice exposed to second-hand cigarette smoke for a year in the lab. Such fat buildup is a sign of NAFLD, leading eventually to liver dysfunction.
In their study, the researchers focused on two key regulators of lipid (fat) metabolism that are found in many human cells as well: SREBP (sterol regulatory element-binding protein) that stimulates synthesis of fatty acids in the liver, and AMPK (adenosine monophosphate kinase) that turns SREBP on and off.
They found that second-hand smoke exposure inhibits AMPK activity, which, in turn, causes an increase in activity of SREBP. When SREBP is more active, more fatty acids get synthesized. The result is NAFLD induced by second-hand smoke.
"Our study provides compelling experimental evidence in support of tobacco smoke exposure playing a major role in NAFLD development," said Manuela Martins-Green, a professor of cell biology, who led the study. "Our work points to SREBP and AMPK as new molecular targets for drug therapy that can reverse NAFLD development resulting from second-hand smoke. Drugs could now be developed that stimulate AMPK activity, and thereby inhibit SREBP, leading to reduced fatty acid production in the liver."
Results of the study appear in the September issue of the Journal of Hepatology.
The study emphasizes that discouraging cigarette smoki
|Contact: Iqbal Pittalwala|
University of California - Riverside