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Perinatal exposure to maternal obesity: Lasting cardiometabolic impact on offspring
Author(s) -
Kislal Sezen,
Shook Lydia L.,
Edlow Andrea G.
Publication year - 2020
Publication title -
prenatal diagnosis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.956
H-Index - 97
eISSN - 1097-0223
pISSN - 0197-3851
DOI - 10.1002/pd.5784
Subject(s) - offspring , obesity , medicine , pregnancy , insulin resistance , endocrinology , metabolic syndrome , fatty liver , adipose tissue , hyperlipidemia , animal studies , physiology , diabetes mellitus , disease , biology , genetics
Evidence from epidemiological, clinical, and animal model studies clearly demonstrates that prenatal and lactational maternal obesity and high‐fat diet consumption are associated with cardiometabolic morbidity in offspring. Fetal and offspring sex may be an important effect modifier. Adverse offspring cardiometabolic outcomes observed in the setting of maternal obesity include an increased risk for obesity, features of metabolic syndrome (hypertension, hyperglycemia and insulin resistance, hyperlipidemia, increased adiposity), and non‐alcoholic fatty liver disease. This review article synthesizes human and animal data linking maternal obesity and high‐fat diet consumption in pregnancy and lactation to adverse cardiometabolic outcomes in offspring. We review key mechanisms underlying skeletal muscle, adipose tissue, pancreatic, liver, and central brain reward programming in obesity‐exposed offspring, and how such malprogramming contributes to offspring cardiometabolic morbidity.