脂肪组织
内分泌学
内科学
高脂血症
断奶
妊娠期
肥胖
医学
后代
怀孕
生物
糖尿病
遗传学
作者
Joji Miyawaki,Kenshi Sakayama,Hideo Kato,Haruyasu Yamamoto,Hiroshi Masuno
出处
期刊:Journal of Atherosclerosis and Thrombosis
[Japan Atherosclerosis Society]
日期:2007-01-01
卷期号:14 (5): 245-252
被引量:263
摘要
Aim: To investigate whether the perinatal and postnatal exposure of mice to bisphenol A (BPA) caused the development of obesity and/or hyperlipidemia.Methods: Pregnant mice were exposed to BPA in drinking water at concentrations of either 1 µg/mL (LD group) or 10 µg/mL (HD group) from gestation day 10 and throughout the lactating period. After weaning, the pups were allowed free access to drinking water containing the appropriate concentrations of BPA. The body weight, adipose tissue weight, and serum lipid levels were measured in the offspring at postnatal day 31.Results: In females, the mean body weight increased by 13% in the LD group (p<0.05) and 11% in the HD group (p<0.05) compared with the control group. The mean adipose tissue weight increased by 132% in the LD group (p<0.01). The mean total cholesterol level increased by 33% in the LD group (p<0.01) and 17% in the HD group (p<0.05). In males, the mean body weight and mean adipose tissue weight increased by 22% (p<0.01) and 59% (p<0.01), respectively, in the HD group compared with the control group. The mean triacylglycerol level increased by 34% in the LD group (p<0.05).Conclusions: The continuous exposure of mice to BPA during the perinatal and postnatal periods caused the development of obesity and hyperlipidemia.
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