Obesity, not a high fat, high sucrose diet alone, induced glucose intolerance and cardiac dysfunction during pregnancy and postpartum

Eunhee Chung,Kassandra Gonzalez,Masataka Umeda,Sarah L. Ullevig,John Zhang

doi:10.1038/s41598-021-97336-x

Eunhee Chung, Kassandra Gonzalez + Show 3 more

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https://doi.org/10.1038/s41598-021-97336-x

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Journal: Scientific Reports	Publication Date: Sep 10, 2021
Citations: 3	License type: open-access

Affiliation: The University of Texas at San Antonio

Abstract

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.

Highlights

Cardiovascular disease is the leading cause of death in women during pregnancy and the postpartum period
While initial body weight (BW) was similar, we found significant differences in weight gain after diet intervention, but with divergent phenotypes in the HFHS-fed mice resulting in obese-prone (HFHS/OP) and obese resistance (HFHS/OR) mice
A significant weight gain was observed after 4 weeks of diet intervention in the HFHS/OP group until gestational day 16 compared to control diet (CON) (Fig. 1a)

Summary

Introduction

Cardiovascular disease is the leading cause of death in women during pregnancy and the postpartum period. Our results suggested that obesity, not the diet alone, negatively affected cardiac adaptation during pregnancy and postpartum. Pregnancy-induced cardiac hypertrophy serves as an adaptive response as it enables the heart to increase its contractile power and to minimize the wall stress to meet maternal and fetal growth[4]. There is a lack of studies examining how pre-pregnancy obesity and early gestational weight gain influence maternal cardiac adaptation to the increasing cardiovascular demands of pregnancy, lactation, and following pregnancy with persistent nutritional challenges. The objective of this study was to evaluate cardiac adaptation at term, at weaning, and postpartum in response to an obesogenic diet. We hypothesized that maternal obesity would challenge pregnancy-induced cardiac adaptation during pregnancy and persistent dietary challenges would be detrimental to the cardiometabolic health of postpartum female mice

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