Potentiation of epinephrine-induced lipolysis by catechol estrogens and their methoxy derivatives

G. E. Ackerman, P. C. MacDonald, G. Gudelsky, C. R. Mendelson, E. R. Simpson

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

The role of catechol estrogens or methoxy derivatives of these compounds in the regulation of lipolysis was evaluated using adipocytes prepared from rat epididymal fat pads. Glycerol released into the incubation medium was measured as ab index of lipolysis. When adipocytes were incubated with epinephrine alone (5 x 10-7 M), glycerol formation was increased 2- to 5-fold over that in untreated cells. Incubation of cells in the presence of 2-hydroxyestrone, 2-hydroxyestradiol, 2-methoxyestrone, 2-methoxyestradiol, estrone, or 17β-estradiol did not increase triglyceride hydrolysis over that in untreated cells. However, when cells were incubated with epinephrine together with either 2-hydroxyestrone, 2-hydroxyestradiol, or 2-methoxyestradiol glycerol formation was increased 2- to 3-fold over the rate in cells treated with epinephrine alone. Estrone 17β-estradiol, and 2-methoxyestradiol did not affect the rate of epinephrine-induced lipolysis in adipocytes. To define whether catechol estrogens were potentiating the lipolytic effect of epinephrine by competition for catechol-O-methyltransferase (COMT), adipocytes were incubated with epinephrine in the presence of a number of COMT inhibitors. Each of these COMT inhibitors potentiated the lipolytic effect of epinephrine, but did not potentiate further the stimulatory effect of catechol estrogens on epinephrine-induced lipolysis. 2-Hydroxyestrone, 2-hydroxyestradiol, or 2-methoxyestradiol did not potentiate the lipolytic effect of soterenol, a β-adrenergic agonist that is not a substrate for COMT. The steroids that potentiated the epinephrine-induced lipolytic response also inhibited the formation of [3H]methanephrine from [3H]epinephrine in rat adipocytes. These data suggest that catechol estrogens compete with epinephrine for binding to COMT and thereby enhance the lypolytic effect of epinephrine.

Original languageEnglish (US)
Pages (from-to)2084-2088
Number of pages5
JournalEndocrinology
Volume109
Issue number6
StatePublished - 1981

Fingerprint

Catechol Estrogens
Lipolysis
Epinephrine
Adipocytes
Catechol O-Methyltransferase
Glycerol
Estrone
Estradiol
Adrenergic Agonists

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Potentiation of epinephrine-induced lipolysis by catechol estrogens and their methoxy derivatives. / Ackerman, G. E.; MacDonald, P. C.; Gudelsky, G.; Mendelson, C. R.; Simpson, E. R.

In: Endocrinology, Vol. 109, No. 6, 1981, p. 2084-2088.

Research output: Contribution to journalArticle

Ackerman, G. E. ; MacDonald, P. C. ; Gudelsky, G. ; Mendelson, C. R. ; Simpson, E. R. / Potentiation of epinephrine-induced lipolysis by catechol estrogens and their methoxy derivatives. In: Endocrinology. 1981 ; Vol. 109, No. 6. pp. 2084-2088.
@article{3ab5a94109854d428f29006ed6d66f59,
title = "Potentiation of epinephrine-induced lipolysis by catechol estrogens and their methoxy derivatives",
abstract = "The role of catechol estrogens or methoxy derivatives of these compounds in the regulation of lipolysis was evaluated using adipocytes prepared from rat epididymal fat pads. Glycerol released into the incubation medium was measured as ab index of lipolysis. When adipocytes were incubated with epinephrine alone (5 x 10-7 M), glycerol formation was increased 2- to 5-fold over that in untreated cells. Incubation of cells in the presence of 2-hydroxyestrone, 2-hydroxyestradiol, 2-methoxyestrone, 2-methoxyestradiol, estrone, or 17β-estradiol did not increase triglyceride hydrolysis over that in untreated cells. However, when cells were incubated with epinephrine together with either 2-hydroxyestrone, 2-hydroxyestradiol, or 2-methoxyestradiol glycerol formation was increased 2- to 3-fold over the rate in cells treated with epinephrine alone. Estrone 17β-estradiol, and 2-methoxyestradiol did not affect the rate of epinephrine-induced lipolysis in adipocytes. To define whether catechol estrogens were potentiating the lipolytic effect of epinephrine by competition for catechol-O-methyltransferase (COMT), adipocytes were incubated with epinephrine in the presence of a number of COMT inhibitors. Each of these COMT inhibitors potentiated the lipolytic effect of epinephrine, but did not potentiate further the stimulatory effect of catechol estrogens on epinephrine-induced lipolysis. 2-Hydroxyestrone, 2-hydroxyestradiol, or 2-methoxyestradiol did not potentiate the lipolytic effect of soterenol, a β-adrenergic agonist that is not a substrate for COMT. The steroids that potentiated the epinephrine-induced lipolytic response also inhibited the formation of [3H]methanephrine from [3H]epinephrine in rat adipocytes. These data suggest that catechol estrogens compete with epinephrine for binding to COMT and thereby enhance the lypolytic effect of epinephrine.",
author = "Ackerman, {G. E.} and MacDonald, {P. C.} and G. Gudelsky and Mendelson, {C. R.} and Simpson, {E. R.}",
year = "1981",
language = "English (US)",
volume = "109",
pages = "2084--2088",
journal = "Endocrinology",
issn = "0013-7227",
publisher = "The Endocrine Society",
number = "6",

}

TY - JOUR

T1 - Potentiation of epinephrine-induced lipolysis by catechol estrogens and their methoxy derivatives

AU - Ackerman, G. E.

AU - MacDonald, P. C.

AU - Gudelsky, G.

AU - Mendelson, C. R.

AU - Simpson, E. R.

PY - 1981

Y1 - 1981

N2 - The role of catechol estrogens or methoxy derivatives of these compounds in the regulation of lipolysis was evaluated using adipocytes prepared from rat epididymal fat pads. Glycerol released into the incubation medium was measured as ab index of lipolysis. When adipocytes were incubated with epinephrine alone (5 x 10-7 M), glycerol formation was increased 2- to 5-fold over that in untreated cells. Incubation of cells in the presence of 2-hydroxyestrone, 2-hydroxyestradiol, 2-methoxyestrone, 2-methoxyestradiol, estrone, or 17β-estradiol did not increase triglyceride hydrolysis over that in untreated cells. However, when cells were incubated with epinephrine together with either 2-hydroxyestrone, 2-hydroxyestradiol, or 2-methoxyestradiol glycerol formation was increased 2- to 3-fold over the rate in cells treated with epinephrine alone. Estrone 17β-estradiol, and 2-methoxyestradiol did not affect the rate of epinephrine-induced lipolysis in adipocytes. To define whether catechol estrogens were potentiating the lipolytic effect of epinephrine by competition for catechol-O-methyltransferase (COMT), adipocytes were incubated with epinephrine in the presence of a number of COMT inhibitors. Each of these COMT inhibitors potentiated the lipolytic effect of epinephrine, but did not potentiate further the stimulatory effect of catechol estrogens on epinephrine-induced lipolysis. 2-Hydroxyestrone, 2-hydroxyestradiol, or 2-methoxyestradiol did not potentiate the lipolytic effect of soterenol, a β-adrenergic agonist that is not a substrate for COMT. The steroids that potentiated the epinephrine-induced lipolytic response also inhibited the formation of [3H]methanephrine from [3H]epinephrine in rat adipocytes. These data suggest that catechol estrogens compete with epinephrine for binding to COMT and thereby enhance the lypolytic effect of epinephrine.

AB - The role of catechol estrogens or methoxy derivatives of these compounds in the regulation of lipolysis was evaluated using adipocytes prepared from rat epididymal fat pads. Glycerol released into the incubation medium was measured as ab index of lipolysis. When adipocytes were incubated with epinephrine alone (5 x 10-7 M), glycerol formation was increased 2- to 5-fold over that in untreated cells. Incubation of cells in the presence of 2-hydroxyestrone, 2-hydroxyestradiol, 2-methoxyestrone, 2-methoxyestradiol, estrone, or 17β-estradiol did not increase triglyceride hydrolysis over that in untreated cells. However, when cells were incubated with epinephrine together with either 2-hydroxyestrone, 2-hydroxyestradiol, or 2-methoxyestradiol glycerol formation was increased 2- to 3-fold over the rate in cells treated with epinephrine alone. Estrone 17β-estradiol, and 2-methoxyestradiol did not affect the rate of epinephrine-induced lipolysis in adipocytes. To define whether catechol estrogens were potentiating the lipolytic effect of epinephrine by competition for catechol-O-methyltransferase (COMT), adipocytes were incubated with epinephrine in the presence of a number of COMT inhibitors. Each of these COMT inhibitors potentiated the lipolytic effect of epinephrine, but did not potentiate further the stimulatory effect of catechol estrogens on epinephrine-induced lipolysis. 2-Hydroxyestrone, 2-hydroxyestradiol, or 2-methoxyestradiol did not potentiate the lipolytic effect of soterenol, a β-adrenergic agonist that is not a substrate for COMT. The steroids that potentiated the epinephrine-induced lipolytic response also inhibited the formation of [3H]methanephrine from [3H]epinephrine in rat adipocytes. These data suggest that catechol estrogens compete with epinephrine for binding to COMT and thereby enhance the lypolytic effect of epinephrine.

UR - http://www.scopus.com/inward/record.url?scp=0019850380&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0019850380&partnerID=8YFLogxK

M3 - Article

VL - 109

SP - 2084

EP - 2088

JO - Endocrinology

JF - Endocrinology

SN - 0013-7227

IS - 6

ER -