Developmental programming: interaction between prenatal BPA exposure and postnatal adiposity on metabolic variables in female sheep
| Autor: | Vasantha Padmanabhan, Almudena Veiga-Lopez, Anthony Pease, Rohit Sreedharan, Carey N. Lumeng, Kanakadurga Singer, Jacob Moeller, Wen Ye |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
endocrine system medicine.medical_specialty Physiology Endocrinology Diabetes and Metabolism Adipocytes White Subcutaneous Fat Antigens Differentiation Myelomonocytic Inflammation Intra-Abdominal Fat Biology 03 medical and health sciences Overnutrition Insulin resistance Phenols Antigens CD Pregnancy Physiology (medical) Internal medicine medicine Animals Genetic Predisposition to Disease Estrogens Non-Steroidal Obesity Benzhydryl Compounds Adiposity Sheep urogenital system Macrophages Incidence (epidemiology) Hypertrophy Articles medicine.disease 030104 developmental biology Endocrinology Prenatal Exposure Delayed Effects Female Insulin Resistance medicine.symptom Developmental programming hormones hormone substitutes and hormone antagonists |
| Zdroj: | American Journal of Physiology-Endocrinology and Metabolism. 310:E238-E247 |
| ISSN: | 1522-1555 0193-1849 |
| Popis: | Among potential contributors for the increased incidence of metabolic diseases is the developmental exposure to endocrine-disrupting chemicals such as bisphenol A (BPA). BPA is an estrogenic chemical used in a variety of consumer products. Evidence points to interactions of BPA with the prevailing environment. The aim of this study was to assess the effects of prenatal exposure to BPA on postnatal metabolic outcomes, including insulin resistance, adipose tissue distribution, adipocyte morphometry, and expression of inflammatory markers in adipose tissue as well as to assess whether postnatal overfeeding would exacerbate these effects. Findings indicate that prenatal BPA exposure leads to insulin resistance in adulthood in the first breeder cohort ( study 1), but not in the second cohort ( study 2), which is suggestive of potential differences in genetic susceptibility. BPA exposure induced adipocyte hypertrophy in the visceral fat depot without an accompanying increase in visceral fat mass or increased CD68, a marker of macrophage infiltration, in the subcutaneous fat depot. Cohens effect size analysis found the ratio of visceral to subcutanous fat depot in the prenatal BPA-treated overfed group to be higher compared with the control-overfed group. Altogether, these results suggest that exposure to BPA during fetal life at levels found in humans can program metabolic outcomes that lead to insulin resistance, a forerunner of type 2 diabetes, with postnatal obesity failing to manifest any interaction with prenatal BPA relative to insulin resistance and adipocyte hypertrophy. |
| Databáze: | OpenAIRE |
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