Cited by 190Effects and risks of endocrine disrupting chemicalsEstrogen and related hormone effectsPeroxisome Proliferator-Activated Receptors

Regulation of energy metabolism pathways by estrogens and estrogenic chemicals and potential implications in obesity associated with increased exposure to endocrine disruptors

Open access
Chen, Jin-Qiang, Brown, Terry R., Russo, Jose·2009·Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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 (ERalpha and ERbeta) 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 beta-oxidation and synthesis, by estrogens; and then examined the disturbance of E(2)/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.

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Crossref · 10.1016/j.bbamcr.2009.03.009

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  • Estrogen actions in pancreatic islet β-cells regulate insulin secretion, nutrient homeostasis, and survival.

    “Estrogen actions in pancreatic islet β-cells also regulate insulin secretion, nutrient homeostasis, and survival [66,69,70].”

    From International society of sports nutrition position stand: nutritional concerns of the female athlete (2023) · cites this paper as [69]

    Section 4.1 (page unavailable) says estrogens influence glucose homeostasis, predominantly through effects in the liver, and discusses insulin sensitivity in muscle and liver. It does not support the more specific attribution to pancreatic islet β-cells or address their insulin secretion or survival. (LLM, conf=0.78)

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Research works printed but not linked: 3

  1. [102]Chen JQ Yager JD Russo J Regulation of mitochondrial respiratory chain structure and function by estrogens/estrogen receptors and potential physiological/pathophysiological implications Biochim Biophys Acta 2005 16169101
  2. [135]Chen JQ Eshete M Alworth WL Yager JD Binding of MCF-7 cell mitochondrial proteins and recombinant human estrogen receptors alpha and beta to human mitochondrial DNA estrogen response elements J Cell Biochem 2004 93 358 373 15368362
  3. [136]Stirone C Duckles SP Krause DN V. Procaccio, Estrogen increases mitochondrial efficiency and reduces oxidative stress in cerebral blood vessels Mol Pharmacol 2005 15994367

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Authors
Chen, J.-Q., Brown, T. R., & Russo, J.
Affiliations
  • Fox Chase Cancer Center (US)
  • Johns Hopkins University (US)
Corresponding author
Chen, Jin-Qiang
Venue
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research
Publisher
Elsevier BV
Published
2009-07
Volume
1793
Issue
7
Pages
1128-1143
ISSN
0167-4889 (ISSN-L)
OpenAlex
W2104940203
Cited by
190
References
190
Citations by year
2026: 5 · 2025: 9 · 2024: 13 · 2023: 8 · 2022: 10 · 2021: 8 · 2020: 16 · 2019: 11 · 2018: 9 · 2017: 9 · 2016: 12 · 2015: 16 · 2014: 13 · 2013: 9 · 2012: 15
FWCI
1.68
Type
journal article
Language
en
Open access
Locations
  • Biochimica et Biophysica Acta (BBA) - Molecular Cell Research (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • U.S. Department of Health and Human Services
  • Johns Hopkins University
  • National Institutes of Health
  • National Cancer Institute (U01 ES/CA12771)
  • National Institute of Environmental Health Sciences (U01ES012771)
Topics
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
Keywords
obesity, obesogens, endocrine disruptors, estrogen, estrogen receptor alpha, estrogen receptor beta, energy metabolism, glucose transport, glycolysis, TCA cycle, mitochondrial respiratory chain, fatty acid beta-oxidation, fatty acid synthesis, adipogenesis, energy balance
MeSH terms
Animals, Energy Metabolism, Environmental Exposure, Estrogens, Humans, Obesity, Signal Transduction, Endocrine Disruptors

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