This morning, presenters discussed how some environmental chemicals may lead to steatosis—fatty liver disease—during the session “Does This Chemical Make My Liver Look Fat? (Environmental Exposures and Steatosis).”
The session co-chairs, Charlene A. McQueen, PhD, ATS, US EPA, and Nathan J. Cherrington, PhD, University of Arizona, told me prior to the presentations that this session was focused on two main ideas: the “how” and “what” of environmental exposure. The “how” references how changes in liver cells caused by environmental chemicals can lead to the development of fatty liver disease and how the disease may progress and cause further damage. The “what” references what chemicals are currently known to cause these molecular changes.
The team assembled to help them accomplish these objectives were:
- Saurabh Chatterjee, PhD, University of South Carolina;
- Wen Xie, MD, PhD, University of Pittsburgh;
- Angela L. Slitt, PhD, University of Rhode Island; and
- Bruce Blumberg, PhD, University of California Irvine.
Dr. Chatterjee discussed his lab’s hypothesis that the drinking water disinfection byproduct bromodichloromethane (BDCM) can aid in the progression of fatty liver disease. The results showed that BDCM exposure caused more fat deposition in the liver of exposed rodents, more circulating insulin levels, insulin resistance, and metabolic disturbances where the liver was reprogrammed to produce more fat at the expense of carbohydrates.
Dr. Xie presented research that showed an endobiotic role for AhR in hepatic steatosis and steatohepatitis. The results convey that the activation of the AhR sensitizes mice to fatty liver disease.
Describing her lab’s research into anti-stick components found in household goods, Dr. Slitt shared the results of a study testing the hypothesis that PFOS interfere with the beneficial effects of caloric restriction on hepatic lipid utilization and glucose homeostasis. She found that a relatively low sub-chronic administration of PFOS had some disruptive effects for lipid and glucose homeostasis under ad libitum and caloric restriction conditions.
Finally, Dr. Blumberg shared his research in the “obesogen hypothesis,” or how chemicals reprogram our bodies to store more calories as fat. He discussed his tests of the hypothesis that organotin exposure during prenatal adipose tissue development favors the subsequent development of adipocytes. The results show that exposure to xenobiotics can have a lasting effect on generations of offspring.