Key result
Pre-pregnancy obesity, but not a high-fat high-sucrose diet alone, induced glucose intolerance and transiently decreased systolic function during pregnancy that resolved by 6 weeks postpartum.
Why the study?
Cardiovascular disease is the leading cause of death in women during pregnancy and postpartum, with obesity being an independent risk factor, motivating investigation into the effects of an obesogenic diet on cardiometabolic health during these periods.
Does an obesogenic diet induce glucose intolerance and cardiac dysfunction during pregnancy and postpartum in female mice?
Does an obesogenic diet induce glucose intolerance and cardiac dysfunction during pregnancy and postpartum in female mice?
Maternal obesity, rather than an obesogenic diet alone, impairs glucose tolerance and transiently reduces cardiac systolic function during pregnancy, though cardiac function normalizes postpartum.
Pre-pregnancy obesity may warrant closer monitoring in pregnancy; animal data leave human cardiac implications open.
Cardiovascular disease is the leading cause of death in women during pregnancy and the postpartum period. Obesity is an independent risk factor for cardiovascular diseases. Nearly 60% of women of reproductive age are considered overweight or obese, cardiovascular disease morbidity and mortality continue to be pervasive. The objective of this study was to determine the effects of an obesogenic diet on the cardiometabolic health of dams during pregnancy and postpartum. Female mice were fed either a high-fat, high-sucrose diet (HFHS) or a refined control diet (CON) for 8 weeks before initiation of pregnancy and throughout the study period. Mice in the HFHS showed two distinct phenotypes, obesity-prone (HFHS/OP) and obesity resistance (HFHS/OR). Pre-pregnancy obesity (HFHS/OP) induced glucose intolerance before pregnancy and during postpartum. Systolic function indicated by the percent fractional shortening (%FS) was significantly decreased in the HFHS/OP at late pregnancy (vs. HFHS/OR) and weaning (vs. CON), but no differences were found at 6 weeks of postpartum among groups. No induction of pathological cardiac hypertrophy markers was found during postpartum. Plasma adiponectin was decreased while total cholesterol was increased in the HFHS/OP. Our results suggested that obesity, not the diet alone, negatively affected cardiac adaptation during pregnancy and postpartum.
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Chung et al. (2021) studied Pregnancy and postpartum cardiometabolic health (n=32). High-fat, high-sucrose diet vs. Refined control diet was evaluated on Percent fractional shortening (%FS) at 6 weeks postpartum. Pre-pregnancy obesity, but not a high-fat high-sucrose diet alone, induced glucose intolerance and transiently decreased systolic function during pregnancy that resolved by 6 weeks postpartum.
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