Interaction between prenatal bpa exposure and postnatal adiposity on metabolic variables in female sheep. The University of Michigan. TY - JOURT1 - Developmental programming. T2 - American Journal of Physiology - Cell Physiology. AU - Veiga- Lopez,Almudena. AU - Moeller,Jacob. AU - Sreedharan,Rohit. AU - Singer,Kanakadurga. AU - Lumeng,Carey. AU - Ye,Wen. AU - Pease,Anthony. AU - Padmanabhan,Vasantha. PY - 2. 01. 6Y1 - 2. N2 - < p> 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 CD6. 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.< /p> AB - < p> 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. Developmental Interaction Approach Monday. The program creates a curriculum that coincides with the capacities and the needs of children at various stages of. 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. Bank Street College of Education. Apple; Facebook; Twitter; LinkedIn; You Tube; Support Us; Directory; Alumni. Graduate School Alumni; School for Children Alumni. National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention. RESEARCH ARTICLE Open Access Effects of a dolphin interaction program on children with autism spectrum disorders – an exploratory research Em Theory & Practice. The Developmental-Interaction approach is the basis for much of Bank Street’s work with children and for the education of our. Explorations: A Developmental-Interaction Educational Center, Mandaluyong, Philippines. Early childhood education. The Developmental Interaction Approach is based on the. BPA exposure induced adipocyte hypertrophy in the visceral fat depot without an accompanying increase in visceral fat mass or increased CD6. 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.< /p> KW - Adipocytes. KW - Bisphenol AKW - Development origins and toxicology. KW - Inflammation. KW - Insulin resistance. UR - http: //www. ID=8. YFLogx. KUR - http: //www. ID=8. YFLogx. KU2 - 1. DO - 1. 0. 1. 15. M3 - Article. VL - 3. SP - E2. 38- E2. 47. JO - American Journal of Physiology - Cell Physiology. JF - American Journal of Physiology - Cell Physiology. SN - 0. 36. 3- 6.
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