Gene expression modifications affect how carbohydrates and fats are metabolized in the heart. As an outcome, the hearts of obese female mices fetuses were bigger, heavier, had thicker walls, and showed indications of inflammation.
A mouse design that replicates human maternal physiology and placental nutrient transfer in obese women was used by researchers from the University of Colorado, United States. Female mice (n= 31) were given a high-fat diet along with a sugary beverage, which is roughly equal to a person eating a burger, chips, and a soft drink every day (1500kcal). Female mice were fed this diet till they ended up being overweight, getting approximately 25% of their initial body weight. A control diet was fed to 50 female mice.
Mouse puppies (n= 187) were studied in utero, along with after birth at 3, 6, 9, and 24 months utilizing imaging techniques, including echocardiography and positron emission tomography (PET) scans. Researchers evaluated the genes, proteins, and mitochondria of the offspring.
The changes in offspring heart metabolic process highly depended on sex. The expression of 841 genes was modified in the hearts of female fetuses and 764 genes were modified in male fetuses, however less than 10% of genes were commonly changed in both sexes. Interestingly, although both male and female offspring from moms with weight problems had impaired heart function, there were differences in the progression in between sexes; males were impaired from the start, whereas women heart function got gradually even worse with age.
The sex distinction in the long lasting disabilities of cardiovascular health and function could be due to estrogen. Greater levels in young females might protect cardiovascular health, the security lessens as estrogen levels deplete as the women age. The molecular cause for the sex distinction is not yet understood.
Lead author, Dr. Owen Vaughan, University of Colorado, United States said:
” Our research suggests a mechanism linking maternal obesity with cardiometabolic disease in the next generation. We could use more tailored suggestions on nutrition to moms or children based on their body mass index or sex, or establish new drugs that target metabolic process in the heart of the fetus.”
Mice have much shorter pregnancies, more offspring, and various diets than humans so further studies on human volunteers would be needed to theorize the findings to ladiess health. Loss-of-function research studies likewise require to be performed to show this mechanism linking maternal obesity and offspring heart function and identify the precise particles responsible.
Reference: “Maternal weight problems triggers fetal cardiac hypertrophy and modifies adult offspring myocardial metabolism in mice” by Owen R. Vaughan, Fredrick J. Rosario, Jeannie Chan, Laura A. Cox, Veronique Ferchaud-Roucher, Karin A. Zemski-Berry, Jane E. B. Reusch, Amy C. Keller, Theresa L. Powell and Thomas Jansson, 11 May 2022, The Journal of Physiology.DOI: 10.1113/ JP282462.
According to a recent research study in mice, maternal obesity affects the fetus heart health and function.
Obesity during pregnancy increases the danger of lifelong heart disease in offspring
Weight problems is defined as a unusual or extreme accumulation of fat that positions a health risk. A BMI of 30 or above is considered obese.
Weight problems has actually ended up being significantly common in America. Health dangers of weight problems consist of type 2 diabetes, high blood pressure, heart illness, and sleep apnea.
According to a current research study, maternal obesity impacts the fetus heart health and function. The research study, which was published in The Journal of Physiology, discovered that maternal obesity produces molecular changes in the fetuss heart and modifies the expression of genes associated with nutrition metabolism, drastically increasing the probability of cardiac issues in the child later on in life.
Health dangers of weight problems include type 2 diabetes, high blood pressure, heart illness, and sleep apnea. As an outcome, the hearts of obese female mices fetuses were bigger, much heavier, had thicker walls, and displayed signs of swelling. The expression of 841 genes was modified in the hearts of female fetuses and 764 genes were modified in male fetuses, but less than 10% of genes were frequently changed in both sexes. Interestingly, although both female and male offspring from mothers with obesity had impaired cardiac function, there were differences in the development in between sexes; males were impaired from the start, whereas females heart function got progressively worse with age.
We might offer more customized guidance on nutrition to children or moms based on their body mass index or sex, or establish new drugs that target metabolic process in the heart of the fetus.”
