title: Perinatal exposure to bisphenol A at reference dose predisposes offspring to metabolic syndrome in adult rats on a high-fat diet.
abstract: Bisphenol A (BPA), a widely used environmental endocrine disruptor, has been reported to disrupt glucose homeostasis. BPA exposure may be a risk factor for type 2 diabetes. In this study, we investigated the effects of early-life BPA exposure on metabolic syndrome in rat offspring fed a normal diet and a high-fat diet. Pregnant Wistar rats were exposed to BPA (50, 250, or 1250 μg/kg · d) or corn oil throughout gestation and lactation by oral gavage. Offspring were fed a normal diet or a high-fat diet after weaning. Body weight, parameters of glucose and lipid metabolism, morphology, and function of β-cells were measured in offspring. On a normal diet, perinatal exposure to 50 μg/kg · d BPA resulted in increased body weight, elevated serum insulin, and impaired glucose tolerance in adult offspring. On a high-fat diet, such detrimental effects were accelerated and exacerbated. Furthermore, severe metabolic syndrome, including obesity, dyslipidemia, hyperleptindemia, hyperglycemia, hyperinsulinemia, and glucose intolerance, was observed in high-fat-fed offspring perinatally exposed to 50 μg/kg · d BPA. No adverse effect of perinatal BPA exposure at 250 and 1250 μg/kg · d was observed no matter on a normal diet or a high-fat diet. These results suggest that perinatal exposure to BPA at reference dose, but not at high dose, impairs glucose tolerance in adult rat offspring on a normal diet and predisposes offspring to metabolic syndrome at adult on a high-fat diet. High-fat diet intake is a trigger that initiates adverse metabolic effects of BPA.
authors.affiliation: Ministry of Education Key Laboratory of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Wei
authors.forename: Yi
authors.initials: Y
authors.lastname: Lin
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Li
authors.forename: Chenjiang
authors.initials: C
authors.lastname: Ying
authors.forename: Jun
authors.initials: J
authors.lastname: Chen
authors.forename: Liqiong
authors.initials: L
authors.lastname: Song
authors.forename: Zhao
authors.initials: Z
authors.lastname: Zhou
authors.forename: Ziquan
authors.initials: Z
authors.lastname: Lv
authors.forename: Wei
authors.initials: W
authors.lastname: Xia
authors.forename: Xi
authors.initials: X
authors.lastname: Chen
authors.forename: Shunqing
authors.initials: S
authors.lastname: Xu
mesh_terms: D000375:Aging; D000818:Animals; D001559:Benzhydryl Compounds; D001835:Body Weight / Q000187:drug effects; D004041:Dietary Fats / Q000008:administration & dosage*; D002149:Energy Intake; D005260:Female; D005333:Fetus / Q000187:drug effects*; D005947:Glucose / Q000378:metabolism; D006706:Homeostasis; D050417:Insulin-Secreting Cells / Q000187:drug effects / Q000473:pathology / Q000502:physiology; D020738:Leptin / Q000097:blood; D050356:Lipid Metabolism / Q000187:drug effects; D008297:Male; D024821:Metabolic Syndrome / Q000139:chemically induced*; D008928:Mitochondria / Q000187:drug effects; D010636:Phenols / Q000633:toxicity*; D011247:Pregnancy; D051381:Rats; D017208:Rats, Wistar; D000098826:Bisphenol A Compounds
chemical_list: D001559:Benzhydryl Compounds; D004041:Dietary Fats; D005947:Glucose; D020738:Leptin; D010636:Phenols; C006780:bisphenol A; D000098826:Bisphenol A Compounds