Abstract
The prevalence of obesity among children, adolescents and adults has been dramatically increasing worldwide during the last several decades. The obesity epidemic has been recognized as one of the major global health problems, because its health hazard is linked to a number of common diseases including breast and prostate cancers. Obesity is caused by combination of genetic and environmental factors. While genetic contribution to obesity has been known to be significant, the genetic factors remain relatively unchanged. Recent studies have highlighted the involvement of environmental "obesogens", i.e. the xenobiotic chemicals that can disrupt the normal development and homeostatic control over adipogenesis and energy balance. Several lines of evidence suggest that increasing exposure to chemicals with endocrine-disrupting activities (endocrine-disrupting chemicals, EDCs) contributes to the increased obesity. The cellular and molecular mechanisms underlying obesogen-associated obesity are just now being appreciated. In this paper, we comprehensively reviewed current knowledge about the role of estrogen receptors alpha and beta (ERα and ERβ) in regulation of energy metabolism pathways, including glucose transport, glycolysis, tricarboxylic acid (TCA) cycle, mitochondrial respiratory chain (MRC), adenosine nucleotide translocator (ANT) and fatty acid β-oxidation and synthesis, by estrogens; and then examined the disturbance of E2/ER-mediated energy metabolism pathways by environmental obesogens; and finally, we discussed the potential implications of disturbance of energy metabolism pathways by obesogens in obesity and pointed out several key aspects of this area that need to be further explored. A better understanding of the cellular and molecular mechanisms underlying obesogen-associated obesity will lead to new approaches for slow down and/or prevention of the increased trend of obesity associated with exposure to obesogens.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1128-1143 |
| Number of pages | 16 |
| Journal | Biochimica et Biophysica Acta - Molecular Cell Research |
| Volume | 1793 |
| Issue number | 7 |
| DOIs | |
| State | Published - Jul 2009 |
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Keywords
- Adenosine nucleotide translocase (ANT)
- Endocrine-disrupting chemicals
- Estrogen receptor-alpha and beta
- Estrogens
- Glucose transport
- Glycolysis
- Mitochondrial respiratory chain
- Obesity
- Tricarboxylic acid cycle
ASJC Scopus subject areas
- Cell Biology
- Molecular Biology
Cite this
Regulation of energy metabolism pathways by estrogens and estrogenic chemicals and potential implications in obesity associated with increased exposure to endocrine disruptors. / Chen, Jin Qiang; Brown, Terry R.; Russo, Jose.
In: Biochimica et Biophysica Acta - Molecular Cell Research, Vol. 1793, No. 7, 07.2009, p. 1128-1143.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Regulation of energy metabolism pathways by estrogens and estrogenic chemicals and potential implications in obesity associated with increased exposure to endocrine disruptors
AU - Chen, Jin Qiang
AU - Brown, Terry R.
AU - Russo, Jose
PY - 2009/7
Y1 - 2009/7
N2 - The prevalence of obesity among children, adolescents and adults has been dramatically increasing worldwide during the last several decades. The obesity epidemic has been recognized as one of the major global health problems, because its health hazard is linked to a number of common diseases including breast and prostate cancers. Obesity is caused by combination of genetic and environmental factors. While genetic contribution to obesity has been known to be significant, the genetic factors remain relatively unchanged. Recent studies have highlighted the involvement of environmental "obesogens", i.e. the xenobiotic chemicals that can disrupt the normal development and homeostatic control over adipogenesis and energy balance. Several lines of evidence suggest that increasing exposure to chemicals with endocrine-disrupting activities (endocrine-disrupting chemicals, EDCs) contributes to the increased obesity. The cellular and molecular mechanisms underlying obesogen-associated obesity are just now being appreciated. In this paper, we comprehensively reviewed current knowledge about the role of estrogen receptors alpha and beta (ERα and ERβ) in regulation of energy metabolism pathways, including glucose transport, glycolysis, tricarboxylic acid (TCA) cycle, mitochondrial respiratory chain (MRC), adenosine nucleotide translocator (ANT) and fatty acid β-oxidation and synthesis, by estrogens; and then examined the disturbance of E2/ER-mediated energy metabolism pathways by environmental obesogens; and finally, we discussed the potential implications of disturbance of energy metabolism pathways by obesogens in obesity and pointed out several key aspects of this area that need to be further explored. A better understanding of the cellular and molecular mechanisms underlying obesogen-associated obesity will lead to new approaches for slow down and/or prevention of the increased trend of obesity associated with exposure to obesogens.
AB - The prevalence of obesity among children, adolescents and adults has been dramatically increasing worldwide during the last several decades. The obesity epidemic has been recognized as one of the major global health problems, because its health hazard is linked to a number of common diseases including breast and prostate cancers. Obesity is caused by combination of genetic and environmental factors. While genetic contribution to obesity has been known to be significant, the genetic factors remain relatively unchanged. Recent studies have highlighted the involvement of environmental "obesogens", i.e. the xenobiotic chemicals that can disrupt the normal development and homeostatic control over adipogenesis and energy balance. Several lines of evidence suggest that increasing exposure to chemicals with endocrine-disrupting activities (endocrine-disrupting chemicals, EDCs) contributes to the increased obesity. The cellular and molecular mechanisms underlying obesogen-associated obesity are just now being appreciated. In this paper, we comprehensively reviewed current knowledge about the role of estrogen receptors alpha and beta (ERα and ERβ) in regulation of energy metabolism pathways, including glucose transport, glycolysis, tricarboxylic acid (TCA) cycle, mitochondrial respiratory chain (MRC), adenosine nucleotide translocator (ANT) and fatty acid β-oxidation and synthesis, by estrogens; and then examined the disturbance of E2/ER-mediated energy metabolism pathways by environmental obesogens; and finally, we discussed the potential implications of disturbance of energy metabolism pathways by obesogens in obesity and pointed out several key aspects of this area that need to be further explored. A better understanding of the cellular and molecular mechanisms underlying obesogen-associated obesity will lead to new approaches for slow down and/or prevention of the increased trend of obesity associated with exposure to obesogens.
KW - Adenosine nucleotide translocase (ANT)
KW - Endocrine-disrupting chemicals
KW - Estrogen receptor-alpha and beta
KW - Estrogens
KW - Glucose transport
KW - Glycolysis
KW - Mitochondrial respiratory chain
KW - Obesity
KW - Tricarboxylic acid cycle
UR - http://www.scopus.com/inward/record.url?scp=67649398814&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=67649398814&partnerID=8YFLogxK
U2 - 10.1016/j.bbamcr.2009.03.009
DO - 10.1016/j.bbamcr.2009.03.009
M3 - Article
C2 - 19348861
AN - SCOPUS:67649398814
VL - 1793
SP - 1128
EP - 1143
JO - Biochimica et Biophysica Acta - Molecular Cell Research
JF - Biochimica et Biophysica Acta - Molecular Cell Research
SN - 0167-4889
IS - 7
ER -