Estrogen disruptors and neuroimmune signaling in obesity: focus on bisphenol A

Research output: Contribution to journalReview article

Abstract

Investigations of the obesity epidemic implicate environmental toxins that affect hormone systems, including the estrogen disruptor bisphenol acetate (BPA). This review concentrates on effects of BPA exposure on central nervous system areas involved in the control of feeding and body weight, drawing parallels between central nervous system effects of estrogens and of BPA. Conflicting findings abound because of methodological differences in species and sex, as well as BPA dose, timing of exposure, and specific model systems used. Nonetheless, common factors include the hypothalamic feeding-inhibitory peptide, pro-opiomelanocortin, and neuroimmune signaling in the hypothalamus, which may involve neuronal and non-neuronal cells. Receptor and intracellular mechanisms remain elusive but likely involve nuclear factor-kappa B signaling via interactions between nuclear estrogen receptors and peroxisome proliferator–activated receptor gamma.

Original languageEnglish
Pages (from-to)15-20
Number of pages6
JournalCurrent Opinion in Toxicology
Volume19
DOIs
StatePublished - Feb 2020

Fingerprint

Estrogens
Acetates
Obesity
Neurology
Central Nervous System
Pro-Opiomelanocortin
Peroxisomes
NF-kappa B
Estrogen Receptors
Hypothalamus
Body Weight
Hormones
Peptides
bisphenol A

Keywords

  • Arcuate nucleus
  • Estrogen receptor
  • IL-6
  • NF-κB
  • POMC
  • PPARγ

Cite this

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title = "Estrogen disruptors and neuroimmune signaling in obesity: focus on bisphenol A",
abstract = "Investigations of the obesity epidemic implicate environmental toxins that affect hormone systems, including the estrogen disruptor bisphenol acetate (BPA). This review concentrates on effects of BPA exposure on central nervous system areas involved in the control of feeding and body weight, drawing parallels between central nervous system effects of estrogens and of BPA. Conflicting findings abound because of methodological differences in species and sex, as well as BPA dose, timing of exposure, and specific model systems used. Nonetheless, common factors include the hypothalamic feeding-inhibitory peptide, pro-opiomelanocortin, and neuroimmune signaling in the hypothalamus, which may involve neuronal and non-neuronal cells. Receptor and intracellular mechanisms remain elusive but likely involve nuclear factor-kappa B signaling via interactions between nuclear estrogen receptors and peroxisome proliferator–activated receptor gamma.",
keywords = "Arcuate nucleus, Estrogen receptor, IL-6, NF-κB, POMC, PPARγ",
author = "Davis, {Randall L.} and Curtis, {Kathleen S.}",
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language = "English",
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AU - Davis, Randall L.

AU - Curtis, Kathleen S.

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N2 - Investigations of the obesity epidemic implicate environmental toxins that affect hormone systems, including the estrogen disruptor bisphenol acetate (BPA). This review concentrates on effects of BPA exposure on central nervous system areas involved in the control of feeding and body weight, drawing parallels between central nervous system effects of estrogens and of BPA. Conflicting findings abound because of methodological differences in species and sex, as well as BPA dose, timing of exposure, and specific model systems used. Nonetheless, common factors include the hypothalamic feeding-inhibitory peptide, pro-opiomelanocortin, and neuroimmune signaling in the hypothalamus, which may involve neuronal and non-neuronal cells. Receptor and intracellular mechanisms remain elusive but likely involve nuclear factor-kappa B signaling via interactions between nuclear estrogen receptors and peroxisome proliferator–activated receptor gamma.

AB - Investigations of the obesity epidemic implicate environmental toxins that affect hormone systems, including the estrogen disruptor bisphenol acetate (BPA). This review concentrates on effects of BPA exposure on central nervous system areas involved in the control of feeding and body weight, drawing parallels between central nervous system effects of estrogens and of BPA. Conflicting findings abound because of methodological differences in species and sex, as well as BPA dose, timing of exposure, and specific model systems used. Nonetheless, common factors include the hypothalamic feeding-inhibitory peptide, pro-opiomelanocortin, and neuroimmune signaling in the hypothalamus, which may involve neuronal and non-neuronal cells. Receptor and intracellular mechanisms remain elusive but likely involve nuclear factor-kappa B signaling via interactions between nuclear estrogen receptors and peroxisome proliferator–activated receptor gamma.

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