Perinatal and Postnatal Exposure to Bisphenol A Increases Adipose Tissue Mass and Serum Cholesterol Level in Mice

Department of Bone and Joint Surgery, Ehime University Graduate School of Medicine, Ehime, Japan.
Journal of atherosclerosis and thrombosis (Impact Factor: 2.73). 11/2007; 14(5):245-52. DOI: 10.5551/jat.E486
Source: PubMed


To investigate whether the perinatal and postnatal exposure of mice to bisphenol A (BPA) caused the development of obesity and/or hyperlipidemia.
Pregnant mice were exposed to BPA in drinking water at concentrations of either 1 microg/mL (LD group) or 10 microg/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.
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).
The continuous exposure of mice to BPA during the perinatal and postnatal periods caused the development of obesity and hyperlipidemia.

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    • "Offspring from rats exposed to BPA 0.1 mg/kg or 1.2 mg/kg from day 6 of pregnancy through the period of lactation showed an increase in body weight that resulted evident soon after birth and seemed to continue into adulthood (Rubin et al., 2001). Also, the BPA exposure from day 10 of gestation throughout the lactation period, but at lower doses (1 mg/mL or 10 mg/mL), resulted in an increment of adipose tissue and body weight (Miyawaki et al., 2007). Changes in the expression of some important adipogenic genes including PPAR-g (peroxisome proliferator activated receptor gamma), SREBP-1C (sterol regulatory element binding protein-1C), SCD-1 (stearoyl-CoA desaturase 1) and C/EBP-a (CCAAT/enhancer-binding protein alpha) have been also observed in female offspring at 21 days of age after perinatal exposure to 1 mg/L BPA (Somm et al., 2009). "
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    • "This profile included measurements of plasma glucose, cholesterol, and triglycerides . Obesity has been associated with hyperlipidemia in mice (Miyawaki et al., 2007). The fact that tail girth was increased in BPAtreated alligators relative to controls at weeks 3 and 5 suggests that BPA-treated neonates had more adipose tissue shortly after hatching "
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    • "Additionally, the presence of such synthetic chemicals in humans has been associated with elevated triglycerides and cholesterol, impaired fasting glucose and diabetes (Meeker, 2012; Tang-Péronard et al., 2011), factors that are all related to the body's natural weight control mechanisms potentially leading to obesity. Exposure to EDCs, such as BPA and phthalates, has already been linked to obesity in animal studies (Miyawaki et al., 2007; R.R. Newbold et al., 2007). Such compounds are widely used as plasticizers and stabilizers in the manufacture of consumer products including children's toys and food-packaging materials (Koch and Calafat, 2009). "
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