Obesity during pregnancy increases the risk of lifelong heart disease in offspring.
Obesity is defined as an abnormal or excessive buildup of fat that poses a health risk. A BMI of 30 or above is considered obese. Obesity has become increasingly prevalent in America. Recent estimates suggest that more than 42% of adults in the United States are obese. Health risks of obesity include type 2 diabetes, high blood pressure, heart disease, and sleep apnea. New research has found it might even have an impact on your children too.
According to a recent study, maternal obesity impacts the fetus, heart health and function.
The research, which was published in The Journal of Physiology, discovered that maternal obesity produces molecular changes in the fetus heart and modifies the expression of genes involved in nutrition metabolism, dramatically increasing the likelihood of cardiac problems in the child later in life. This is the first study to demonstrate that the heart is programmed by the nutrition it receives throughout the birth.
Gene expression changes affect how carbs and fats are metabolized in the heart. They change the heart?s nutritional preference away from sugar and toward fat. As a result, the hearts of obese female mice?s fetuses were bigger, heavier, had thicker walls, and displayed signs of inflammation. The heart?s ability to contract and circulate blood throughout the body is impaired as a result.
A mouse model that replicates human maternal physiology and placental nutrient transfer in obese women was used by researchers from the University of Colorado, US. Thirty-one female mice were given a high-fat diet along with a sugary drink, which is roughly equal to a person eating a burger, chips, and a soft drink daily (1500kcal). Female mice were fed this diet until they became obese, gaining roughly 25% of their initial body weight. A control diet was fed to 50 female mice. Mouse pups (n=187) were studied in utero, as well as after birth at 3, 6, 9, and 24 months using imaging techniques, including echocardiography and positron emission tomography (PET) scan. Researchers analyzed the genes, proteins, and mitochondria of the offspring. The changes in offspring cardiac metabolism strongly depended on sex. The expression of 841 genes was altered in the hearts of female fetuses and 764 genes were altered in male fetuses, but less than 10% of genes were commonly altered in both sexes.
Interestingly, although both male and female offspring from mothers with obesity had impaired cardiac function, there were differences in the progression between sexes; males were impaired from the start, whereas females? cardiac function got progressively worse with age. The sex difference in the lasting impairments of cardiovascular health and function could be due to estrogen. Higher levels in young females may protect cardiovascular health, the protection diminishes as estrogen levels deplete as the females age.
The molecular cause for the sex difference is not yet understood.
The research indicates a mechanism linking maternal obesity with cardiometabolic illness in the next generation. The 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.
Mice have shorter pregnancies, more offspring, and different diets than humans so further studies on human volunteers would be required to extrapolate the findings to women?s health. Loss-of-function studies also need to be carried out to prove this mechanism linking maternal obesity and offspring heart function and pinpoint the exact molecules responsible.
Parvathy Sukumaran 
