According to a recent mouse study, maternal obesity reduces the fetus’s ability to function and maintain cardiac health. The study, which was published in The Journal of Physiology, discovered that maternal obesity raises the chance of offspring developing cardiac issues later in life by altering the expression of genes involved in nutrition metabolism and causing molecular alterations in the developing fetus’s heart.
This is the first study to demonstrate how the nutrients the heart receives throughout embryonic life “programmed” it. Gene expression changes affect how the heart typically metabolizes lipids and carbs. They cause the heart’s inclination for fat and away from sugar to change.
Because of this, the hearts of obese female mouse fetuses were bigger, heavier, had thicker walls, and displayed symptoms of inflammation. This reduces the heart’s ability to contract and circulate blood effectively.
Researchers from the University of Colorado employed A mouse model that matches human maternal physiology and placental nutrition transfer in obese women in the US.
Female mice (n=31) were given a high-fat meal along with a sugary beverage, simulating a person frequently ingesting a burger, chips, and fizzy drink (1500kcal). The female mice consumed this diet up until the point at which they developed obesity and gained roughly 25% of their initial body weight. A control diet was given to 50 female mice.
Imaging methods, such as echocardiogram and positron emission tomography (PET) scans, were used to examine mouse pups (n=187) during pregnancy as well as 3, 6, and 9 months after delivery. Researchers examined the offspring’s DNA, proteins, and mitochondria.
Our research indicates a mechanism linking maternal obesity with cardiometabolic illness in the next generation. This is important because obesity is increasing rapidly in the human population and affects almost one-third of women of childbearing age. By improving our understanding of the mechanisms involved, this research paves the way for treatments that could be used in early life to prevent later-life cardiometabolic illnesses, which are costly for health services and affect many people’s quality of life.
Dr. Owen Vaughan
Sex had a significant impact on changes in the heart metabolism of the progeny. Less than 10% of genes were often altered in both sexes, however, 841 genes in the hearts of female fetuses and 764 genes in the hearts of male fetuses had altered expression.
It’s interesting to note that, despite the fact that both male and female offspring of obese mothers had impaired cardiac function, there were differences in the course of the impairment between the sexes; males’ cardiac function was impaired from the beginning, whereas females’ cardiac function progressively deteriorated with age.
Oestrogen may be the cause of the sex difference in the long-term impairments of cardiovascular health and function. Higher amounts in young girls may preserve cardiovascular health, but the benefit decreases as the females age and their oestrogen levels fall. It is still unclear what causes the sex difference at the molecular level.
Lead author, Dr. Owen Vaughan, University of Colorado, US said:
“Our research indicates a mechanism linking maternal obesity with cardiometabolic illness in the next generation. This is important because obesity is increasing rapidly in the human population and affects almost one-third of women of childbearing age. By improving our understanding of the mechanisms involved, this research paves the way for treatments that could be used in early life to prevent later-life cardiometabolic illnesses, which are costly for health services and affect many people’s quality of life.”
“For example, we could offer more tailored advice on nutrition to mothers or children based on their body mass index or sex, or develop new drugs that target metabolism in the heart of the fetus.”
To extend the findings to women’s health, further research in human volunteers is needed because mice have shorter gestations, more children, and different diets than humans. In order to establish this link between maternal obesity and offspring heart function and identify the precise molecules at fault, loss-of-function experiments must also be conducted.
