5 research outputs found
Effects of Bisphenol A and its substitutes on the proliferation and differentiation in Caco-2 intestine cell model: MELBA project.
National audienc
P019: Effet obésogène des bisphénols A et S chez la souris C57Bl/6
International audienceIntroduction et but de l’étudeLe Bisphénol A (BPA) est un composé utilisé dans la fabrication de plastique de type polycarbonate ou dans la composition de résines époxy tapissant l’intérieur des conserves alimentaires et canettes. Il est capable de migrer de l’emballage vers l’aliment. Son utilisation est remise en cause car il a été reconnu comme étant un perturbateur endocrinien mais également un reprotoxique, cancérogène et perturbateur de la balance énergétique (« obésogène») chez les rongeurs. En 2015, l’interdiction totale du BPA dans les emballages à contact alimentaire a conduit les fabricants à utiliser des substituts tels que le bisphénol S (BPS) pour lequel il existe peu d’études sur sa toxicité..
Obesogen effects after perinatal exposure of 4,4′-sulfonyldiphenol (Bisphenol S) in C57BL/6 mice
International audienceBisphenol A were removed from consumer products and replaced by chemical substitutes such as Bisphenol S (BPS). Based on their structural similarity, BPS may be obesogen like Bisphenol A in mice. Our objective was to determine the impact of BPS on lipid homeostasis in C57B1/6 mice after perinatal and chronic exposure. Pregnant mice were exposed to BPS via the drinking water (0.2; 1.5; 50 mu g/kg bw/d). Treatment began at gestational day 0 and continued in offspring up to 23-weeks old. Then, offspring mice were fed with a standard or high fat diet. The body weight, food consumption, fat mass and energy expenditure were measured. A lipid load test was performed to check the postprandial triglyceridemia. Plasma parameters and mRNA gene expression in adipose tissues were also analysed. BPS induced overweight in male mice offspring fed with a HFD at the two highest doses. There was no change in food intake and energy expenditure. The overweight was correlated to the fat mass, hyperinsulinemia and hyperleptinemia. The plasma triglyceride clearance was significantly increased with BPS and tyloxapol (R) (triglyceride clearance inhibitor) reversed this phenomenon. BPS induced alteration in mRNA expression of marker genes involved in adipose tissue homeostasis: hormone sensitive lipase, PPAR gamma, insulin receptor, SOCS3 and adiponectin. This is the first time that BPS is described as obesogenic at low doses and after perinatal and chronic exposure in male mice. BPS potentiated the obesity induced by a HFD by inducing the lipid storage linked to faster lipid plasma clearance. (C) 2016 Elsevier Ireland Ltd. All rights reserved