Non-alcoholic fatty liver disease is a serious and growing problem. Previously linked with obesity, a new study also connects it to maternal obesity – meaning that what your mother ate during pregnancy may affect your future liver health.
Non-alcoholic fatty liver disease (NAFLD) is characterized by a buildup of fat within the cells of the liver. Although having fat in the liver is normal, if there is an excessive amount, it can lead to liver scarring and cirrhosis.
Cirrhosis describes a process during which liver cells are gradually replaced by scar tissue, hindering the liver’s capacity to work effectively.
NAFLD is estimated to affect 20 to 30 percent of people in the Western world, and this level appears to be on the rise.
Although some of the risk factors are understood, it is not always clear why one person develops NAFLD while another, similar person, does not. Because of the rising prevalence of NAFLD, a great deal of research is currently under way that attempts to generate an understanding of the pathways behind the condition.
The latest research comes from a team headed up by Dr. Michael Thompson, Ph.D., a pediatric endocrinology fellow at Nationwide Children’s Hospital in Ohio. The results are presented today at the Experimental Biology 2017 meeting, held in Chicago, IL.
Using a mouse model, the research explores the effect, if any, of a maternal high-fat diet on the offspring’s liver health.
Dr. Thompson explains the reasons for his decision to embark on the current project: “Complications of obesity are a significant cost burden for the medical system, especially given the prevalence of obesity. Understanding how maternal exposures impact obesity-related disease such as non-alcoholic fatty liver disease will allow us to develop lower-cost preventative therapies to utilize up front rather than awaiting complications down the road.”
Once the data had been analyzed, they found that exposure to a high-fat diet during development produced changes in the liver that persisted through to adulthood. These changes remained even if the offspring were fed a low-fat diet after birth.
If this effect is confirmed in humans, it would mean that someone of a healthy weight could still be at risk for NAFLD if their mother had been obese during pregnancy.
When the team looked further into the data, they found that levels of bile acid and the genes involved in its regulation were altered in the offspring of obese mothers. This suggests that the offspring might have cholestasis, a condition in which the normal flow of bile is interrupted.
“If human offspring from obese mothers have a similar risk for developing fibrosis as we see in mice, we may be able to predict who is going to develop more serious disease.
Knowing who is most at risk for more serious disease will guide us on which patients should be treated more aggressively. Furthermore, understanding the biological mechanisms involved in this increased risk could lead to preventative therapies.”
Dr. Michael Thompson
The results will need to be confirmed, but they open the door to a raft of new questions. Thompson and his team are now planning research to further investigate the risk of disease progression. Using the same mouse model, they are also designing studies that will examine preventative therapies able to be administered during pregnancy or shortly after birth.
Due to the rising rates of NAFLD, research in this vein is likely to continue at breakneck pace. Preventing or slowing this condition could have huge health benefits for the population at large.