The estrogenic endocrine disrupting chemical bisphenol A (BPA) and obesity

► Estrogenic EDC exposure may lead to obesity via genetic programming. ► Estrogens and EDCs directly regulate adipocyte function. ► Developmental EDC exposure influences adult body weight and metabolism. ► Effects of EDCs on body weight and on glucose homeostasis are seen at low doses. There is incr...

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Bibliographic Details
Published inMolecular and cellular endocrinology Vol. 354; no. 1-2; pp. 74 - 84
Main Authors vom Saal, Frederick S., Nagel, Susan C., Coe, Benjamin L., Angle, Brittany M., Taylor, Julia A.
Format Journal Article
LanguageEnglish
Published Ireland Elsevier Ireland Ltd 06.05.2012
Subjects
adipocytes
Adipocytes - drug effects
Adipocytes - metabolism
Adipocytes - physiology
adults
Animals
Benzhydryl Compounds
Bisphenol A
blood flow
Endocrine disrupting chemicals
Endocrine Disruptors - toxicity
Environmental Exposure
Environmental Pollutants - toxicity
epigenetics
Estrogens - toxicity
fetal development
Fetal Development - drug effects
fetus
Gene Expression Regulation - drug effects
Humans
Metabolic syndrome
nutrient transport
Obesity
Obesity - chemically induced
Obesity - genetics
Obesity - pathology
Phenols - toxicity
Phenotype
reproductive performance
C/EBPβ
C/EBPα
Obesity
DOHaD
DGAT1
ERβ
ERα
LPL
Cyp19
GLP
Metabolic syndrome
PPARγ
Endocrine disrupting chemicals
Bisphenol A
BPA
SERMs
IUGR
GLUT4
GnRH
GPAT
HPLC
Online AccessGet full text
ISSN0303-7207
1872-8057
1872-8057
DOI10.1016/j.mce.2012.01.001

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Abstract ► Estrogenic EDC exposure may lead to obesity via genetic programming. ► Estrogens and EDCs directly regulate adipocyte function. ► Developmental EDC exposure influences adult body weight and metabolism. ► Effects of EDCs on body weight and on glucose homeostasis are seen at low doses. There is increasing experimental and epidemiological evidence that fetal programming of genetic systems is a contributing factor in the recent increase in adult obesity and other components of metabolic syndrome. In particular, there is evidence that epigenetic changes associated with the use of manmade chemicals may interact with other factors that influence fetal and postnatal growth in contributing to the current obesity epidemic. The focus of this review is on the developmental effects of estrogenic endocrine disrupting chemicals (EDCs), and more specifically on effects of exposure to the estrogenic EDC bisphenol A (BPA), on adipocytes and their function, and the ultimate impact on adult obesity; BPA exposure also results in impaired reproductive capacity. We discuss the interaction of EDCs with other factors that impact growth during fetal and neonatal life, such as placental blood flow and nutrient transport to fetuses, and how these influence fetal growth and abnormalities in homeostatic control systems required to maintain normal body weight throughout life.
AbstractList There is increasing experimental and epidemiological evidence that fetal programming of genetic systems is a contributing factor in the recent increase in adult obesity and other components of metabolic syndrome. In particular, there is evidence that epigenetic changes associated with the use of manmade chemicals may interact with other factors that influence fetal and postnatal growth in contributing to the current obesity epidemic. The focus of this review is on the developmental effects of estrogenic endocrine disrupting chemicals (EDCs), and more specifically on effects of exposure to the estrogenic EDC bisphenol A (BPA), on adipocytes and their function, and the ultimate impact on adult obesity; BPA exposure also results in impaired reproductive capacity. We discuss the interaction of EDCs with other factors that impact growth during fetal and neonatal life, such as placental blood flow and nutrient transport to fetuses, and how these influence fetal growth and abnormalities in homeostatic control systems required to maintain normal body weight throughout life.There is increasing experimental and epidemiological evidence that fetal programming of genetic systems is a contributing factor in the recent increase in adult obesity and other components of metabolic syndrome. In particular, there is evidence that epigenetic changes associated with the use of manmade chemicals may interact with other factors that influence fetal and postnatal growth in contributing to the current obesity epidemic. The focus of this review is on the developmental effects of estrogenic endocrine disrupting chemicals (EDCs), and more specifically on effects of exposure to the estrogenic EDC bisphenol A (BPA), on adipocytes and their function, and the ultimate impact on adult obesity; BPA exposure also results in impaired reproductive capacity. We discuss the interaction of EDCs with other factors that impact growth during fetal and neonatal life, such as placental blood flow and nutrient transport to fetuses, and how these influence fetal growth and abnormalities in homeostatic control systems required to maintain normal body weight throughout life.
There is increasing experimental and epidemiological evidence that fetal programming of genetic systems is a contributing factor in the recent increase in adult obesity and other components of metabolic syndrome. In particular, there is evidence that epigenetic changes associated with the use of manmade chemicals may interact with other factors that influence fetal and postnatal growth in contributing to the current obesity epidemic. The focus of this review is on the developmental effects of estrogenic endocrine disrupting chemicals (EDCs), and more specifically on effects of exposure to the estrogenic EDC bisphenol A (BPA), on adipocytes and their function, and the ultimate impact on adult obesity; BPA exposure also results in impaired reproductive capacity. We discuss the interaction of EDCs with other factors that impact growth during fetal and neonatal life, such as placental blood flow and nutrient transport to fetuses, and how these influence fetal growth and abnormalities in homeostatic control systems required to maintain normal body weight throughout life.
► Estrogenic EDC exposure may lead to obesity via genetic programming. ► Estrogens and EDCs directly regulate adipocyte function. ► Developmental EDC exposure influences adult body weight and metabolism. ► Effects of EDCs on body weight and on glucose homeostasis are seen at low doses. There is increasing experimental and epidemiological evidence that fetal programming of genetic systems is a contributing factor in the recent increase in adult obesity and other components of metabolic syndrome. In particular, there is evidence that epigenetic changes associated with the use of manmade chemicals may interact with other factors that influence fetal and postnatal growth in contributing to the current obesity epidemic. The focus of this review is on the developmental effects of estrogenic endocrine disrupting chemicals (EDCs), and more specifically on effects of exposure to the estrogenic EDC bisphenol A (BPA), on adipocytes and their function, and the ultimate impact on adult obesity; BPA exposure also results in impaired reproductive capacity. We discuss the interaction of EDCs with other factors that impact growth during fetal and neonatal life, such as placental blood flow and nutrient transport to fetuses, and how these influence fetal growth and abnormalities in homeostatic control systems required to maintain normal body weight throughout life.
Author Coe, Benjamin L.
Angle, Brittany M.
vom Saal, Frederick S.
Taylor, Julia A.
Nagel, Susan C.
AuthorAffiliation 1 Division of Biological Sciences, University of Missouri-Columbia, Columbia, MO, 65211 USA
2 Department of Obstetrics, Gynecology and Women's Health, University of Missouri-Columbia, Columbia, MO, 65211 USA
AuthorAffiliation_xml – name: 2 Department of Obstetrics, Gynecology and Women's Health, University of Missouri-Columbia, Columbia, MO, 65211 USA
– name: 1 Division of Biological Sciences, University of Missouri-Columbia, Columbia, MO, 65211 USA
Author_xml – sequence: 1
  givenname: Frederick S.
  surname: vom Saal
  fullname: vom Saal, Frederick S.
  organization: Division of Biological Sciences, University of Missouri – Columbia, Columbia, MO 65211, USA
– sequence: 2
  givenname: Susan C.
  surname: Nagel
  fullname: Nagel, Susan C.
  organization: Department of Obstetrics, Gynecology and Women’s Health, University of Missouri – Columbia, Columbia, MO 65211, USA
– sequence: 3
  givenname: Benjamin L.
  surname: Coe
  fullname: Coe, Benjamin L.
  organization: Division of Biological Sciences, University of Missouri – Columbia, Columbia, MO 65211, USA
– sequence: 4
  givenname: Brittany M.
  surname: Angle
  fullname: Angle, Brittany M.
  organization: Division of Biological Sciences, University of Missouri – Columbia, Columbia, MO 65211, USA
– sequence: 5
  givenname: Julia A.
  surname: Taylor
  fullname: Taylor, Julia A.
  email: taylorja@missouri.edu
  organization: Division of Biological Sciences, University of Missouri – Columbia, Columbia, MO 65211, USA
BackLink https://www.ncbi.nlm.nih.gov/pubmed/22249005$$D View this record in MEDLINE/PubMed
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Issue 1-2
Keywords C/EBPβ
C/EBPα
Obesity
DOHaD
DGAT1
ERβ
ERα
LPL
Cyp19
GLP
Metabolic syndrome
PPARγ
Endocrine disrupting chemicals
Bisphenol A
BPA
SERMs
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GnRH
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HPLC
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Snippet ► Estrogenic EDC exposure may lead to obesity via genetic programming. ► Estrogens and EDCs directly regulate adipocyte function. ► Developmental EDC exposure...
There is increasing experimental and epidemiological evidence that fetal programming of genetic systems is a contributing factor in the recent increase in...
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SubjectTerms adipocytes
Adipocytes - drug effects
Adipocytes - metabolism
Adipocytes - physiology
adults
Animals
Benzhydryl Compounds
Bisphenol A
blood flow
Endocrine disrupting chemicals
Endocrine Disruptors - toxicity
Environmental Exposure
Environmental Pollutants - toxicity
epigenetics
Estrogens - toxicity
fetal development
Fetal Development - drug effects
fetus
Gene Expression Regulation - drug effects
Humans
Metabolic syndrome
nutrient transport
Obesity
Obesity - chemically induced
Obesity - genetics
Obesity - pathology
Phenols - toxicity
Phenotype
reproductive performance
Title The estrogenic endocrine disrupting chemical bisphenol A (BPA) and obesity
URI https://dx.doi.org/10.1016/j.mce.2012.01.001
https://www.ncbi.nlm.nih.gov/pubmed/22249005
https://www.proquest.com/docview/1022893357
https://www.proquest.com/docview/1694479022
https://www.proquest.com/docview/928910359
https://pubmed.ncbi.nlm.nih.gov/PMC3306519
Volume 354
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