Effects of ethanol or ethylene glycol exposure on PPARγ and aromatase expression in adipose tissue

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Effects of ethanol or ethylene glycol exposure on PPARγ and aromatase expression in adipose tissue. / Ardenkjær-Skinnerup, Jacob; Saar, Daniel; Christiansen, Sofie; Svingen, Terje; Hadrup, Niels; Brown, Kristy A.; Emanuelli, Brice; Kragelund, Birthe B.; Ravn-Haren, Gitte; Vogel, Ulla.

In: Biochemistry and Biophysics Reports, Vol. 38, 101742, 2024.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Ardenkjær-Skinnerup, J, Saar, D, Christiansen, S, Svingen, T, Hadrup, N, Brown, KA, Emanuelli, B, Kragelund, BB, Ravn-Haren, G & Vogel, U 2024, 'Effects of ethanol or ethylene glycol exposure on PPARγ and aromatase expression in adipose tissue', Biochemistry and Biophysics Reports, vol. 38, 101742. https://doi.org/10.1016/j.bbrep.2024.101742

APA

Ardenkjær-Skinnerup, J., Saar, D., Christiansen, S., Svingen, T., Hadrup, N., Brown, K. A., Emanuelli, B., Kragelund, B. B., Ravn-Haren, G., & Vogel, U. (2024). Effects of ethanol or ethylene glycol exposure on PPARγ and aromatase expression in adipose tissue. Biochemistry and Biophysics Reports, 38, [101742]. https://doi.org/10.1016/j.bbrep.2024.101742

Vancouver

Ardenkjær-Skinnerup J, Saar D, Christiansen S, Svingen T, Hadrup N, Brown KA et al. Effects of ethanol or ethylene glycol exposure on PPARγ and aromatase expression in adipose tissue. Biochemistry and Biophysics Reports. 2024;38. 101742. https://doi.org/10.1016/j.bbrep.2024.101742

Author

Ardenkjær-Skinnerup, Jacob ; Saar, Daniel ; Christiansen, Sofie ; Svingen, Terje ; Hadrup, Niels ; Brown, Kristy A. ; Emanuelli, Brice ; Kragelund, Birthe B. ; Ravn-Haren, Gitte ; Vogel, Ulla. / Effects of ethanol or ethylene glycol exposure on PPARγ and aromatase expression in adipose tissue. In: Biochemistry and Biophysics Reports. 2024 ; Vol. 38.

Bibtex

@article{9bc7404aeccd4788a077fafcc2d683d1,
title = "Effects of ethanol or ethylene glycol exposure on PPARγ and aromatase expression in adipose tissue",
abstract = "The estrogen-synthesizing enzyme aromatase is expressed in adipose tissue where it controls the local concentration of estrogen. It has been suggested that the organic solvents ethanol and ethylene glycol can induce estrogen synthesis by inhibiting PPARγ activity. Since elevated estrogen synthesis in adipose tissue is a risk factor for breast cancer development, it is of interest to further characterize the mechanisms regulating aromatase expression. Here, we explored the mechanisms by which ethanol and ethylene glycol modulate aromatase mRNA expression and the ultimate conversion of androgens into estrogens. NMR spectroscopy revealed that ethanol and ethylene glycol influence the active state of PPARγ. An inhibitory effect on PPARγ was confirmed by adipogenesis assays and PPARγ target gene expression analysis in adipocytes. However, only ethanol increased aromatase mRNA in differentiated human adipocytes. In contrast, ethylene glycol downregulated aromatase in a PPARγ-independent manner. An animal study using female Wistar rats was conducted to assess the acute effects of ethanol and ethylene glycol on aromatase expression in adipose tissue within a physiological context. No changes in aromatase or PPARγ target gene (Adipoq and Fabp4) levels were observed in adipose tissue or ovary in response to the chemical exposures, suggesting an absence of acute PPARγ-mediated effects in these organs. The results suggest that ethanol and ethylene glycol are weak PPARγ antagonists in mouse and human adipocytes as well as in cell-free NMR spectroscopy. Both compounds seem to affect adipocyte aromatase expression in vitro, where ethanol increased aromatase expression PPARγ-dependently and ethylene glycol decreased aromatase expression independently of PPARγ. No acute effects on aromatase expression or PPARγ activity were observed in adipose tissue or ovary in rats in this study design.",
keywords = "Adipogenesis, Adipose tissue, Alcohol, Aromatase, Breast cancer, PPARγ",
author = "Jacob Ardenkj{\ae}r-Skinnerup and Daniel Saar and Sofie Christiansen and Terje Svingen and Niels Hadrup and Brown, {Kristy A.} and Brice Emanuelli and Kragelund, {Birthe B.} and Gitte Ravn-Haren and Ulla Vogel",
note = "Publisher Copyright: {\textcopyright} 2024 The Authors",
year = "2024",
doi = "10.1016/j.bbrep.2024.101742",
language = "English",
volume = "38",
journal = "Biochemistry and Biophysics Reports",
issn = "2405-5808",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Effects of ethanol or ethylene glycol exposure on PPARγ and aromatase expression in adipose tissue

AU - Ardenkjær-Skinnerup, Jacob

AU - Saar, Daniel

AU - Christiansen, Sofie

AU - Svingen, Terje

AU - Hadrup, Niels

AU - Brown, Kristy A.

AU - Emanuelli, Brice

AU - Kragelund, Birthe B.

AU - Ravn-Haren, Gitte

AU - Vogel, Ulla

N1 - Publisher Copyright: © 2024 The Authors

PY - 2024

Y1 - 2024

N2 - The estrogen-synthesizing enzyme aromatase is expressed in adipose tissue where it controls the local concentration of estrogen. It has been suggested that the organic solvents ethanol and ethylene glycol can induce estrogen synthesis by inhibiting PPARγ activity. Since elevated estrogen synthesis in adipose tissue is a risk factor for breast cancer development, it is of interest to further characterize the mechanisms regulating aromatase expression. Here, we explored the mechanisms by which ethanol and ethylene glycol modulate aromatase mRNA expression and the ultimate conversion of androgens into estrogens. NMR spectroscopy revealed that ethanol and ethylene glycol influence the active state of PPARγ. An inhibitory effect on PPARγ was confirmed by adipogenesis assays and PPARγ target gene expression analysis in adipocytes. However, only ethanol increased aromatase mRNA in differentiated human adipocytes. In contrast, ethylene glycol downregulated aromatase in a PPARγ-independent manner. An animal study using female Wistar rats was conducted to assess the acute effects of ethanol and ethylene glycol on aromatase expression in adipose tissue within a physiological context. No changes in aromatase or PPARγ target gene (Adipoq and Fabp4) levels were observed in adipose tissue or ovary in response to the chemical exposures, suggesting an absence of acute PPARγ-mediated effects in these organs. The results suggest that ethanol and ethylene glycol are weak PPARγ antagonists in mouse and human adipocytes as well as in cell-free NMR spectroscopy. Both compounds seem to affect adipocyte aromatase expression in vitro, where ethanol increased aromatase expression PPARγ-dependently and ethylene glycol decreased aromatase expression independently of PPARγ. No acute effects on aromatase expression or PPARγ activity were observed in adipose tissue or ovary in rats in this study design.

AB - The estrogen-synthesizing enzyme aromatase is expressed in adipose tissue where it controls the local concentration of estrogen. It has been suggested that the organic solvents ethanol and ethylene glycol can induce estrogen synthesis by inhibiting PPARγ activity. Since elevated estrogen synthesis in adipose tissue is a risk factor for breast cancer development, it is of interest to further characterize the mechanisms regulating aromatase expression. Here, we explored the mechanisms by which ethanol and ethylene glycol modulate aromatase mRNA expression and the ultimate conversion of androgens into estrogens. NMR spectroscopy revealed that ethanol and ethylene glycol influence the active state of PPARγ. An inhibitory effect on PPARγ was confirmed by adipogenesis assays and PPARγ target gene expression analysis in adipocytes. However, only ethanol increased aromatase mRNA in differentiated human adipocytes. In contrast, ethylene glycol downregulated aromatase in a PPARγ-independent manner. An animal study using female Wistar rats was conducted to assess the acute effects of ethanol and ethylene glycol on aromatase expression in adipose tissue within a physiological context. No changes in aromatase or PPARγ target gene (Adipoq and Fabp4) levels were observed in adipose tissue or ovary in response to the chemical exposures, suggesting an absence of acute PPARγ-mediated effects in these organs. The results suggest that ethanol and ethylene glycol are weak PPARγ antagonists in mouse and human adipocytes as well as in cell-free NMR spectroscopy. Both compounds seem to affect adipocyte aromatase expression in vitro, where ethanol increased aromatase expression PPARγ-dependently and ethylene glycol decreased aromatase expression independently of PPARγ. No acute effects on aromatase expression or PPARγ activity were observed in adipose tissue or ovary in rats in this study design.

KW - Adipogenesis

KW - Adipose tissue

KW - Alcohol

KW - Aromatase

KW - Breast cancer

KW - PPARγ

U2 - 10.1016/j.bbrep.2024.101742

DO - 10.1016/j.bbrep.2024.101742

M3 - Journal article

AN - SCOPUS:85194430085

VL - 38

JO - Biochemistry and Biophysics Reports

JF - Biochemistry and Biophysics Reports

SN - 2405-5808

M1 - 101742

ER -

ID: 393842851