作者: Chanjuan Hao , Xuejia Cheng , Hongfei Xia , Xu Ma
DOI: 10.1042/BSR20120042
关键词: Endocrine disruptor 、 Adipogenesis 、 Receptor 、 Endocrinology 、 Obesogen 、 Adipocyte 、 Offspring 、 Phthalate 、 Internal medicine 、 Adipose tissue 、 Biology
摘要: The environmental obesogen hypothesis proposes that exposure to endocrine disruptors during developmental ‘window’ contributes adipogenesis and the development of obesity. MEHP [mono-(2-ethylhexyl) phthalate], a metabolite widespread plasticizer DEHP [di-(2-ethylhexyl) has been found in exposed organisms identified as selective PPARγ (peroxisome-proliferator-activated receptor γ) modulator. However, implication on adipose tissue poorly investigated. In present study, we show dose-dependent effects adipocyte differentiation GPDH (glycerol-3-phosphate dehydrogenase) activity murine 3T3-L1 cell model. induced expression well its target genes required for in vitro. Moreover, perturbed key regulators lipogenic pathway in vivo. utero low dose significantly increased b.w. (body weight) fat pad weight male offspring at PND (postnatal day) 60. addition, serum cholesterol, TAG (triacylglycerol) glucose levels were also elevated. These results suggest perinatal may be expected increase incidence obesity sex-dependent manner can act potential chemical stressor obesity-related disorders.