Hormone-disrupting chemicals may cause fatty liver
Exposure to even low doses of hormone-disrupting chemicals called endocrine disruptors early in life may alter gene expression in liver and its function, a new study said.
Washington: Exposure to even low doses of hormone-disrupting chemicals called endocrine disruptors early in life may alter gene expression in liver and its function, a new study said.
Brief exposure in infancy to several industrial chemicals that are common in the human environment, particularly bisphenol A (BPA), caused fatty liver disease in adulthood.
"Even a short exposure to these endocrine disruptors at the wrong time of development has a life-long effect on the individual," said Cheryl Lyn Walker from the Texas A&M Health Science Centre's Institute of Biosciences and Technology.
During the study, Walker and her colleagues focused on liver, which plays a central role in fat metabolism and obesity.
The researchers gave groups of newborn rats low doses of one of four different endocrine disruptors during the three days immediately after birth, a critical period of liver development.
The liver tissues from these chemically-exposed animals were examined later.
The endocrine disruptors induced developmental reprogramming of the animals' epigenomes.
In both rodents and humans, the epigenome programmes the genome - our complete set of DNA.
These chemical exposures interfere with the epigenetic 'programmers' to do their job.
This reprogramming of the liver could potentially drive obesity.
Unlike genetic defects, however, epigenetic programming can be reversed.
"It may be possible to reset the malprogramming, or 'malware', to reduce the risk of obesity and associated diseases," Walker stressed.
"With additional research and knowledge, it may also be possible one day to use these epigenetic changes as markers, which can tell that a child is at risk of obesity and other diseases," Walker concluded.
The results were presented at the Endocrine Society's annual meeting in San Diego, California, this week.