CHICAGO, March 25 (Xinhua) -- Researchers at Washington University School of Medicine in St. Louis have found that a high-fat, high-sugar diet in mouse mothers before and during pregnancy causes problems in the hearts of their offspring.
The study also found that diet-induced heart changes in offspring are not only transmitted to offspring by their mothers. Obese mothers' male offspring that mated with healthy females fed a normal diet also passed on the same heart problems.
Notably, the researchers found multi-generational heart problems, even when the mouse offspring were not obese and ate a normal diet throughout their lives.
The researchers also used in-vitro fertilization to implant fertilized eggs from obese mice into normal-weight mice to carry the pregnancies. These offspring also showed the heart defects, demonstrating that the problems are specific to the original egg from the mother fed the high-fat, high-sugar diet, and not the gestational environment during the pregnancy or nursing afterward.
The researchers suspect that the defects in heart mitochondria are likely caused by so-called epigenetic changes in the DNA of the original obese mother's eggs. The epigenome is an important layer of genetic regulation that governs how DNA instructions are read and executed. In theory, these epigenetic changes in the egg would be present in every cell of the offspring, including in their male or female reproductive systems.
Previous study by the researchers confirmed that mitochondrial problems also exist in the skeletal muscle, leading to whole-body metabolic abnormalities, such as insulin resistance, in the offspring of obese mouse mothers and in two subsequent generations.
The researchers plan to study the epigenetic changes in the eggs of obese mothers and tissues of the offspring in an effort to understand what is happening to the mitochondria. In the meantime, they emphasize the importance of maintaining a healthy weight before and during pregnancy.
The heart abnormalities induced by maternal obesity included cardiac mitochondria that appeared small and fragmented and that consumed less oxygen than their normal counterparts. The hearts of most of the offspring, though not all, also showed an increase in the weight of the left ventricle, the main pumping chamber of the heart.
In people, increased left ventricle weight is often a marker of poor heart muscle quality that predisposes one to heart failure, a potentially fatal condition in which the heart does not pump blood as well as it should.
The study was published on March 22 in the journal AJP-Heart and Circulatory Physiology.
