Induction and degradation of the uncoupling protein thermogenin in brown adipocytes in vitro and in vivo. Evidence for a rapidly degradable pool

P. Puigserver, D. Herron, M. Gianotti, A. Palou, B. Cannon, J. Nedergaard

Research output: Contribution to journalArticle

Abstract

The induction and degradation of the brown-fat-specific uncoupling protein thermogenin in brown fat cell cultures was investigated. Cultures were initiated with undifferentiated precursor cells from young mice and the amount of thermogenin was determined by immunoblotting. High levels of thermogenin could be induced by noradrenaline treatment in cells grown for more than 5 days in culture, and in such cell cultures continuously stimulated with noradrenaline, the thermogenin level continued to increase for at least a further 5 days. In cell cultures stimulated for only 24 h, the induced thermogenin was subsequently specifically and rapidly degraded, with a half-life of 20 h. As the half-life was prolonged by cycloheximide treatment, the degradation was apparently due to the induction of specific proteins after cessation of adrenergic stimulation. In cell cultures continuously stimulated with noradrenaline for 5 days, the induced thermogenin was degraded much more slowly after noradrenaline removal, with a half-life of 70 h. This half-life was unchanged by cycloheximide treatment, and the degradation after cycloheximide was in parallel with the degradation of protein in general, and was therefore non-specific. The prolongation of the half-life of thermogenin after the chronic treatment may be related to mitochondrial incorporation of thermogenin and consequent stabilization of the protein. The half-life of thermogenin in an in vivo situation of similar experimental design (the reacclimation of mice to warm after 5 days in the cold), was also long (about 7 days), and the loss was also non-specific, as it parallelled the loss of protein. Thus different molecular events arc involved in thermogenin degradation when the protein is found in different functional pools.

Original languageEnglish (US)
Pages (from-to)393-398
Number of pages6
JournalBiochemical Journal
Volume284
Issue number2
StatePublished - 1992
Externally publishedYes

Fingerprint

Brown Adipocytes
Cell culture
Degradation
Norepinephrine
Half-Life
Cycloheximide
Proteins
Cell Culture Techniques
Fats
Proteolysis
Adrenergic Agents
Design of experiments
Uncoupling Protein 1
Mitochondrial Uncoupling Proteins
In Vitro Techniques
Life Support Care
Stabilization
Cells
Brown Adipose Tissue
Therapeutics

ASJC Scopus subject areas

  • Biochemistry

Cite this

Puigserver, P., Herron, D., Gianotti, M., Palou, A., Cannon, B., & Nedergaard, J. (1992). Induction and degradation of the uncoupling protein thermogenin in brown adipocytes in vitro and in vivo. Evidence for a rapidly degradable pool. Biochemical Journal, 284(2), 393-398.

Induction and degradation of the uncoupling protein thermogenin in brown adipocytes in vitro and in vivo. Evidence for a rapidly degradable pool. / Puigserver, P.; Herron, D.; Gianotti, M.; Palou, A.; Cannon, B.; Nedergaard, J.

In: Biochemical Journal, Vol. 284, No. 2, 1992, p. 393-398.

Research output: Contribution to journalArticle

Puigserver, P, Herron, D, Gianotti, M, Palou, A, Cannon, B & Nedergaard, J 1992, 'Induction and degradation of the uncoupling protein thermogenin in brown adipocytes in vitro and in vivo. Evidence for a rapidly degradable pool', Biochemical Journal, vol. 284, no. 2, pp. 393-398.
Puigserver, P. ; Herron, D. ; Gianotti, M. ; Palou, A. ; Cannon, B. ; Nedergaard, J. / Induction and degradation of the uncoupling protein thermogenin in brown adipocytes in vitro and in vivo. Evidence for a rapidly degradable pool. In: Biochemical Journal. 1992 ; Vol. 284, No. 2. pp. 393-398.
@article{621c92c7bb9a41f7a426f24b2b4d6546,
title = "Induction and degradation of the uncoupling protein thermogenin in brown adipocytes in vitro and in vivo. Evidence for a rapidly degradable pool",
abstract = "The induction and degradation of the brown-fat-specific uncoupling protein thermogenin in brown fat cell cultures was investigated. Cultures were initiated with undifferentiated precursor cells from young mice and the amount of thermogenin was determined by immunoblotting. High levels of thermogenin could be induced by noradrenaline treatment in cells grown for more than 5 days in culture, and in such cell cultures continuously stimulated with noradrenaline, the thermogenin level continued to increase for at least a further 5 days. In cell cultures stimulated for only 24 h, the induced thermogenin was subsequently specifically and rapidly degraded, with a half-life of 20 h. As the half-life was prolonged by cycloheximide treatment, the degradation was apparently due to the induction of specific proteins after cessation of adrenergic stimulation. In cell cultures continuously stimulated with noradrenaline for 5 days, the induced thermogenin was degraded much more slowly after noradrenaline removal, with a half-life of 70 h. This half-life was unchanged by cycloheximide treatment, and the degradation after cycloheximide was in parallel with the degradation of protein in general, and was therefore non-specific. The prolongation of the half-life of thermogenin after the chronic treatment may be related to mitochondrial incorporation of thermogenin and consequent stabilization of the protein. The half-life of thermogenin in an in vivo situation of similar experimental design (the reacclimation of mice to warm after 5 days in the cold), was also long (about 7 days), and the loss was also non-specific, as it parallelled the loss of protein. Thus different molecular events arc involved in thermogenin degradation when the protein is found in different functional pools.",
author = "P. Puigserver and D. Herron and M. Gianotti and A. Palou and B. Cannon and J. Nedergaard",
year = "1992",
language = "English (US)",
volume = "284",
pages = "393--398",
journal = "Biochemical Journal",
issn = "0264-6021",
publisher = "Portland Press Ltd.",
number = "2",

}

TY - JOUR

T1 - Induction and degradation of the uncoupling protein thermogenin in brown adipocytes in vitro and in vivo. Evidence for a rapidly degradable pool

AU - Puigserver, P.

AU - Herron, D.

AU - Gianotti, M.

AU - Palou, A.

AU - Cannon, B.

AU - Nedergaard, J.

PY - 1992

Y1 - 1992

N2 - The induction and degradation of the brown-fat-specific uncoupling protein thermogenin in brown fat cell cultures was investigated. Cultures were initiated with undifferentiated precursor cells from young mice and the amount of thermogenin was determined by immunoblotting. High levels of thermogenin could be induced by noradrenaline treatment in cells grown for more than 5 days in culture, and in such cell cultures continuously stimulated with noradrenaline, the thermogenin level continued to increase for at least a further 5 days. In cell cultures stimulated for only 24 h, the induced thermogenin was subsequently specifically and rapidly degraded, with a half-life of 20 h. As the half-life was prolonged by cycloheximide treatment, the degradation was apparently due to the induction of specific proteins after cessation of adrenergic stimulation. In cell cultures continuously stimulated with noradrenaline for 5 days, the induced thermogenin was degraded much more slowly after noradrenaline removal, with a half-life of 70 h. This half-life was unchanged by cycloheximide treatment, and the degradation after cycloheximide was in parallel with the degradation of protein in general, and was therefore non-specific. The prolongation of the half-life of thermogenin after the chronic treatment may be related to mitochondrial incorporation of thermogenin and consequent stabilization of the protein. The half-life of thermogenin in an in vivo situation of similar experimental design (the reacclimation of mice to warm after 5 days in the cold), was also long (about 7 days), and the loss was also non-specific, as it parallelled the loss of protein. Thus different molecular events arc involved in thermogenin degradation when the protein is found in different functional pools.

AB - The induction and degradation of the brown-fat-specific uncoupling protein thermogenin in brown fat cell cultures was investigated. Cultures were initiated with undifferentiated precursor cells from young mice and the amount of thermogenin was determined by immunoblotting. High levels of thermogenin could be induced by noradrenaline treatment in cells grown for more than 5 days in culture, and in such cell cultures continuously stimulated with noradrenaline, the thermogenin level continued to increase for at least a further 5 days. In cell cultures stimulated for only 24 h, the induced thermogenin was subsequently specifically and rapidly degraded, with a half-life of 20 h. As the half-life was prolonged by cycloheximide treatment, the degradation was apparently due to the induction of specific proteins after cessation of adrenergic stimulation. In cell cultures continuously stimulated with noradrenaline for 5 days, the induced thermogenin was degraded much more slowly after noradrenaline removal, with a half-life of 70 h. This half-life was unchanged by cycloheximide treatment, and the degradation after cycloheximide was in parallel with the degradation of protein in general, and was therefore non-specific. The prolongation of the half-life of thermogenin after the chronic treatment may be related to mitochondrial incorporation of thermogenin and consequent stabilization of the protein. The half-life of thermogenin in an in vivo situation of similar experimental design (the reacclimation of mice to warm after 5 days in the cold), was also long (about 7 days), and the loss was also non-specific, as it parallelled the loss of protein. Thus different molecular events arc involved in thermogenin degradation when the protein is found in different functional pools.

UR - http://www.scopus.com/inward/record.url?scp=0026642858&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026642858&partnerID=8YFLogxK

M3 - Article

VL - 284

SP - 393

EP - 398

JO - Biochemical Journal

JF - Biochemical Journal

SN - 0264-6021

IS - 2

ER -