Abstract
One of the leading global public-health burdens is metabolic syndrome (MetS), despite the many advances in pharmacotherapies. MetS, now known as “developmental origins of health and disease” (DOHaD), can have its origins in early life. Offspring MetS can be programmed by various adverse early-life conditions, such as nutrition imbalance, maternal conditions or diseases, maternal chemical exposure, and medication use. Conversely, early interventions have shown potential to revoke programming processes to prevent MetS of developmental origins, namely reprogramming. In this review, we summarize what is currently known about adverse environmental insults implicated in MetS of developmental origins, including the fundamental underlying mechanisms. We also describe animal models that have been developed to study the developmental programming of MetS. This review extends previous research reviews by addressing implementation of reprogramming strategies to prevent the programming of MetS. These mechanism-targeted strategies include antioxidants, melatonin, resveratrol, probiotics/prebiotics, and amino acids. Much work remains to be accomplished to determine the insults that could induce MetS, to identify the mechanisms behind MetS programming, and to develop potential reprogramming strategies for clinical translation.
Highlights
Metabolic syndrome (MetS) is not a single disease but a collection of medical conditions that occur together and increase the risk of cardiovascular disease (CVD)
We previously reported that AMPK activation by resveratrol prevented the elevation of offspring hypertension programmed by a high-fructose diet [150] and a high-fat diet [151]
branched chain amino acids (BCAAs) supplementation in pregnancy is able to prevent maternal caloric restriction-induced programmed hypertension [189], another study revealed that supplementation of BCAAs in rats fed with a high-fat diet contributes to development of obesity-associated insulin resistance [193]
Summary
Metabolic syndrome (MetS) is not a single disease but a collection of medical conditions that occur together and increase the risk of cardiovascular disease (CVD). The establishment of various adverse environmental conditions, which takes place during pregnancy and lactation, could be involved in the early-life programming of health This concept is known as the developmental origin of health and disease (DOHaD) [5], which is supported by evidence coming from a large number of epidemiological and experimental observations. There is evidence for the programming of some similar features of MetS from different early-life insults, possibly suggesting a commonality of mechanism and highlighting that identifying underlying mechanistic pathways is vital to develop ideal prevention interventions [6]. We first highlight epidemiological studies that link early-life factors to MetS of developmental origins. This is followed by a summary of the potential developmental mechanisms behind the origin of MetS. Additional papers were selected and evaluated on the basis of fitting references in eligible literature
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