Obesity in pregnancy and risk of cardiovascular disease in offspring
Maternal obesity impairs heart health and function of the fetus according to a new study in mice.
The study, published in The Journal of Physiology, found that maternal obesity causes molecular changes in the heart of the fetus and alters expression of genes related to nutrient metabolism, which greatly increases an offspring’s risk of cardiac problems in later life.
This is the first study to show that the heart is ‘programmed’ by the nutrients it receives in fetal life. Changes in the expression of genes alter how the heart normally metabolises carbohydrates and fats. They shift the heart’s nutrient preference further toward fat and away from sugar. As a result, the hearts of fetuses of obese female mice were larger, weighed more, had thicker walls and showed signs of inflammation. This impairs how efficiently the heart contracts and pumps blood around the body.
The researchers from University of Colorado, USA, used a mouse model that replicates human maternal physiology and placental nutrient transport in obese women. Female mice (n=31) were fed a diet with a high fat content together with a sugary drink, which is equivalent to a human regularly consuming a burger, chips and a fizzy drink (1500 kcal). The female mice ate this diet until they developed obesity, putting on about 25% of their original body weight. 50 female mice were fed a control diet.
Mice have shorter pregnancies, more offspring and different diets to humans so further studies in 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.