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• W2143248519 abstract "Therapidincreaseinobesityinmanycountriesinrecent years has been associated with an increase in the prevalence of associated cardiovascular disorders, including type 2 diabetes, hypertension, and dyslipidaemia. Although genetic factors are likely to play a role in an individual’s susceptibility to these disorders (1), this increase indiseaseprevalencehasoccurredtoorapidlytobearesult of a genetic change within a population, and there is general acceptance that the combination of reduced exercise and increased consumption of calorie-rich food are important factors in the development of the conditions. Although it is attractive to believe that it is simply lifestyle changes during childhood/adulthood that are fuelling this epidemic, it is now recognized that the environment experienced in early life can influence susceptibility to cardiovascular and metabolic disorders in later life, including an increased risk of obesity and the “metabolic syndrome” (2). There is widespread acceptance of the “developmental origins hypothesis,” which suggests that the action of a stimulus or insult during a specific critical period of in utero or early postnatal development can lead to “programmed” alterations in tissue structure and function, predisposingtheindividualtolaterdisease(2).Inthiscontext, therefore, metabolic syndrome disorders in adults may represent a complex interaction between early developmental influences on disease susceptibility and later lifestyle, which builds on the level of predisposition, therefore, more of a “lifetime” than simply a “lifestyle”disorder.Giventhewidespreadexposureofhumans to environmental chemicals, is it possible that early life exposure to one or more of these substances during fetal and early postnatal life might underpin the current epidemic of obesity and related metabolic disorders? Ryanet al. (3) report in the present issue on their use of a mouse model system to test whether perinatal exposure tohuman-relevantlevelsofbisphenolA,anenvironmental chemical to which we are all exposed, might provide a predisposing trigger to obesity and glucose intolerance in adulthood.Theirresultsshowcategoricallythatbisphenol A affects neither of these endpoints, even when exposed offspring were fed a high-fat (Western style) diet. This makes it unlikely that bisphenol A exposure in early life in humans is a factor in predisposing to metabolic syndrome disordersinadulthood.Negativeresultssuchasthisrarely stir the passions of scientists (and especially reviewers), but in this case, it is arguably a landmark study with importantimplications.Beforeevaluatingthisinmoredetail, some more background is necessary to place these new results in their full context. Initial studies in the area of early life programming focusedontheroleofpoorfetalgrowthintheprogramming" @default.
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• W2143248519 date "2010-06-01" @default.
• W2143248519 modified "2023-09-27" @default.
• W2143248519 title "Bisphenol A and Metabolic Syndrome" @default.
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• W2143248519 doi "https://doi.org/10.1210/en.2010-0445" @default.
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