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Over the past 30 years, the worldwide prevalence of obesity has nearly doubled. In addition, more and more women in their child-bearing years are overweight or obese, which increases the risk of gestational diabetes mellitus (GDM). It is increasingly accepted by the scientific community that early life exposure to environmental stress influences the long-term health of an individual, which has been termed the Developmental Origins of Health and Disease theory. Evidence from human cohorts and epidemiological and animal studies has shown that maternal obesity and GDM condition the offspring for cardiometabolic disease development. These effects are most likely regulated by epigenetic mechanisms; however, biological sex is an important factor in defining the risk of the development of several metabolic health disorders. The aim of this review is to describe the current evidence from human cohort and animal model studies that implicates sex differences in the developmental origins of cardiometabolic disease following exposure to maternal obesity and GDM. In addition, this review addresses the potential mechanisms involved in these sex differences. In many studies, sex is ignored as an important variable in disease development; however, the results presented in this review highlight important differences between sexes in the developmental programming of biological responses to exposures during the fetal stage. This knowledge will ultimately help in the development of effective therapeutic strategies for the treatment of cardiometabolic diseases that exhibit sexual dimorphism.

ScopeChocolate consumption lowers cardiovascular disease risk, which might be attributed to the methylxanthine theobromine. These effects may be mediated through effects on HDL‐mediated cholesterol efflux, which may be affected by microRNA (miRNA) levels in the HDL particles. Therefore, the aim of this study is to investigate effects of theobromine consumption on fasting and postprandial cholesterol efflux and miRNAs levels.Methods and resultsThirty overweight and 14 obese healthy men and women participated in this randomized, double‐blind crossover study. Participants consumed 500 mg d−1 of theobromine or placebo for 4 weeks. ABCA1‐mediated cholesterol efflux was measured using J774 macrophages. MiRNAs levels (miR‐92a, miR‐223, miR‐135a*) were quantified in apolipoprotein B‐depleted serum. Theobromine consumption did not affect fasting and postprandial cholesterol efflux. Fasting miR‐223 and miR‐135a levels were unchanged, while miR‐92a levels were decreased (−0.21; p < 0.05). The high‐fat meal increased postprandial cholesterol efflux capacity (+4.3 percentage points; p ≤ 0.001), miR‐92a (+1.21; p < 0.001), and miR‐223 (+1.79; p < 0.001) levels, while a trend was found for miR‐135a (+1.08; p = 0.06).ConclusionTheobromine did not improve fasting and postprandial ABCA1‐mediated cholesterol efflux capacity, but decreased fasting miR‐92a levels. High‐fat meal intake increased postprandial cholesterol efflux and the three selected miRNAs levels.

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