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Pharmacol Res. 2016 Nov;113(Pt A):376-383. doi: 10.1016/j.phrs.2016.09.005. Epub 2016 Sep 15.

Bisphenol A induces hypothalamic down-regulation of the the cannabinoid receptor 1 and anorexigenic effects in male mice.

Author information

1
Department of Experimental Medicine, Sez. Bottazzi, II University of Naples, 80138, Napoli, Italy.
2
Department of Science and Technology University of Sannio, Via Port'Arsa 11, 82100, Benevento, Italy; IRGS, Biogem, Via Camporeale, 83031, Ariano Irpino, Avellino, Italy.
3
Department of Experimental Medicine, Sez. Bottazzi, II University of Naples, 80138, Napoli, Italy. Electronic address: riccardo.pierantoni@unina2.it.

Abstract

Bisphenol A is an environment-polluting industrial chemical able to interfere with the endocrine system. An obesogenic effect in perinatally exposed rodents has been described as estrogenic activity. We exposed male mice to Bisphenol A during fetal-perinatal period (from 10 days post coitum to 31 days post partum) and investigated the effects of this early-life exposure at 78 days of age. Body weight, food intake, fat mass, and hypothalamic signals related to anorexigenic control of food intake were analyzed. Results show that Bisphenol A exposure reduced body weight and food intake. In addition, the exposure decreased epididymal fat mass and adiposity, acting negatively on adipocyte volume. At hypothalamic level, Bisphenol A exposure reduced the expression of the cannabinoid receptor 1 and induced gene expression of cocaine and amphetamine-regulated transcript-1. This observation suggests that Bisphenol A induces activation of anorexigenic signals via down-regulation of the hypothalamic cannabinoid receptor 1 with negative impact on food intake.

KEYWORDS:

BPA; CB1 receptor; Estrogens; Food intake; Hypothalamus; POMC/CART anorexigenic signals

PMID:
27641926
DOI:
10.1016/j.phrs.2016.09.005
[Indexed for MEDLINE]

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