University of Monastir, High Institute of Biotechnology of Monastir, Laboratory of Bioresources: Integrative Biology and Valorisation BIOLIVAL, Tunisia.
Institut National de la Santé et de la Recherche Médicale (INSERM), U1220, Université Paul Sabatier, UPS, Institut de Recherche en Santé Digestive et Nutrition (IRSD), CHU Purpan, Place du Docteur Baylac, CS 60039, 31024 Toulouse Cedex 3; NeuroMicrobiota, European Associated Laboratory (EAL) INSERM/UCL, France.
Ecotoxicol Environ Saf. 2018 Oct;161:459-466. doi: 10.1016/j.ecoenv.2018.06.001. Epub 2018 Jun 14.
Since 2010, Bisphenol A (BPA), an endocrine disruptor has been restricted and replaced by analogues like Bisphenol S (BPS). However, little is known about BPS effects and growing concern have suspected the "BPA-free" Label. Several recent studies suggest that BPS is associated with increased risk of diabetes and obesity. However, the underlying mechanisms remain unidentified. The current study investigates investigate BPS effects on hypothalamic neuropeptides regulating feeding behavior, either orexigenic or anorexigenic in Swiss Albino mice. We also studied the effect of BPS on the apelinergic system (apelin/apelin receptor (APJ)) as an original physiological system with pleiotropic actions. Bisphenol S at 25, 50, 100 µg/kg was administered to mice in water drink for 10 weeks started after weaning. Our results showed that BPS exposure alters orexigenic hypothalamic neuropeptide (AgRP) regulating feeding behavior but not anorexigenic neuropeptides (POMC, CART). Such orexigenic alterations may underlay appetite disorders leading to a concomitant food intake and body weight gain increase. In addition, data show that BPS affects the hypothalamic apelinergic system. We found a significant decrease in APJ mRNA but not in apelin expression. Based on hypothalamic APJ distribution, we suggested a potent specific physiological alteration of this receptor in mediating neuroendocrine responses in hypothalamus. Thus, our findings provide that BPS exposure could contribute to the development of obesity and metabolic disorders.
自 2010 年以来,内分泌干扰物双酚 A(BPA)被限制使用并被类似物双酚 S(BPS)所取代。然而,人们对 BPS 的影响知之甚少,而且人们越来越担心“不含 BPA”的标签。最近的几项研究表明,BPS 与糖尿病和肥胖风险增加有关。然而,其潜在机制仍未确定。本研究旨在探讨 BPS 对调节摄食行为的下丘脑神经肽的影响,这些神经肽既有食欲促进作用,也有食欲抑制作用。我们还研究了 BPS 对食欲肽系统(apelin/apelin 受体(APJ))的影响,因为它是一种具有多种作用的原始生理系统。BPS 以 25、50、100μg/kg 的剂量添加到饮用水中,在断奶后开始给小鼠饮用 10 周。我们的结果表明,BPS 暴露会改变调节摄食行为的食欲促进型下丘脑神经肽(AgRP),但不会改变食欲抑制型神经肽(POMC、CART)。这种食欲促进型的改变可能是导致食欲紊乱、食物摄入增加和体重增加的原因。此外,数据表明 BPS 会影响下丘脑食欲肽系统。我们发现 APJ mRNA 显著下降,但 apelin 表达没有变化。基于下丘脑 APJ 的分布,我们推测该受体在介导下丘脑神经内分泌反应方面存在特定的、强烈的生理改变。因此,我们的研究结果表明,BPS 暴露可能导致肥胖和代谢紊乱的发生。