Abstract
The metabolism-disrupting chemicals (MDCs) are molecules (largely belonging to the category of endocrine disrupting chemicals, EDCs) that can cause important diseases as the metabolic syndrome, obesity, Type 2 Diabetes Mellitus or fatty liver. MDCs act on fat tissue and liver, may regulate gut functions (influencing absorption), but they may also alter the hypothalamic peptidergic circuits that control food intake and energy metabolism. These circuits are normally regulated by several factors, including estrogens, therefore those EDCs that are able to bind estrogen receptors may promote metabolic changes through their action on the same hypothalamic circuits. Here, we discuss data showing how the exposure to some MDCs can alter the expression of neuropeptides within the hypothalamic circuits involved in food intake and energy metabolism. In particular, in this review we have described the effects at hypothalamic level of three known EDCs: Genistein, an isoflavone (phytoestrogen) abundant in soy-based food (a possible new not-synthetic MDC), Bisphenol A (compound involved in the manufacturing of many consumer plastic products), and Tributyltin chloride (one of the most dangerous and toxic endocrine disruptor, used in antifouling paint for boats).
Highlights
metabolism-disrupting chemicals (MDCs) and Circuits Controlling Food IntakeThese systems are sensitive to peripheral signals of energetic balance (for example leptin, insulin, and GHrelin)
Reviewed by: Luis Miguel Garcia-Segura, Spanish National Research Council (CSIC), Spain Tanja Adam, Maastricht University, Netherlands
In this review we have described the effects at hypothalamic level of three known EDCs: Genistein, an isoflavone abundant in soy-based food, Bisphenol A, and Tributyltin chloride
Summary
These systems are sensitive to peripheral signals of energetic balance (for example leptin, insulin, and GHrelin). An anti-obesogenic effect of GEN is reported for many obese mouse models [43, 44], in juvenile and adult ovariectomized [45, 46] and intact mice [34] This effect is dose dependent [42]: GEN inhibits adipogenesis at low concentrations and enhances it at high concentrations [47, 48]. Our ongoing study in male and female mice demonstrates that early postnatal exposure to GEN, in a dose comparable to exposure level in babies fed with soy-based formula, determines an obesogenic phenotype in adult females and a long-term sex specific effects on hypothalamic kiss, POMC and Orexin systems [55]. The contradictory experimental data underline the importance of considering the timing of exposure, the dose/concentration, the sex, and the species-specificity when establishing safety recommendations for dietary GEN intake, especially if in early-life
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