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Titolo:
Mitochondrial adaptation to in vivo polyunsaturated fatty acid deficiency:Increase in phosphorylation efficiency
Autore:
Nogueira, V; Piquet, MA; Devin, A; Fiore, C; Fontaine, E; Brandolin, G; Rigoulet, M; Leverve, XM;
Indirizzi:
Univ Grenoble 1, Lab Bioenerget Fondamentale & Applique, F-38041 Grenoble,France Univ Grenoble 1 Grenoble France F-38041 pplique, F-38041 Grenoble,France Univ Bordeaux 2, CNRS, Inst Biochim & Genet Cellulaires, F-33077 Bordeaux,France Univ Bordeaux 2 Bordeaux France F-33077 ulaires, F-33077 Bordeaux,France CEA Grenoble, Dept Biol Mol & Struct, CNRS, UMR 314, F-38054 Grenoble, France CEA Grenoble Grenoble France F-38054 , UMR 314, F-38054 Grenoble, France
Titolo Testata:
JOURNAL OF BIOENERGETICS AND BIOMEMBRANES
fascicolo: 1, volume: 33, anno: 2001,
pagine: 53 - 61
SICI:
0145-479X(200102)33:1<53:MATIVP>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT-LIVER MITOCHONDRIA; ADENINE-NUCLEOTIDE TRANSLOCATOR; INNER MEMBRANE PHOSPHOLIPIDS; OHMIC PROTON CONDUCTANCE; OXIDATIVE-PHOSPHORYLATION; THYROID-HORMONES; HEPATOCYTES; PERMEABILITY; CARRIER; RESPIRATION;
Keywords:
respiratory chain; ATP synthesis; PUFA; uncoupler; hepatocyte; mitochondria; proton motive force;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
56
Recensione:
Indirizzi per estratti:
Indirizzo: Leverve, XM Univ Grenoble 1, Lab Bioenerget Fondamentale & Applique, BP 53X, F-38041 Grenoble, France Univ Grenoble 1 BP 53X Grenoble France F-38041enoble, France
Citazione:
V. Nogueira et al., "Mitochondrial adaptation to in vivo polyunsaturated fatty acid deficiency:Increase in phosphorylation efficiency", J BIOENER B, 33(1), 2001, pp. 53-61

Abstract

Polyunsaturated fatty acid (PUFA) deficiency affects respiratory rate bothin isolated mitochondria and in hepatocytes, an effect that is normally ascribed to major changes in membrane composition causing, in turn, protonophoriclike effects. In this study, we have compared the properties of hepatocytes isolated from PUFA-deficient rats with those from control animals treated with concentrations of the protonophoric uncoupler 2,3-dinitrophenol (DNP). Despite identical respiratory rate and in situ mitochondrial membrane potential (Delta Psi), mitochondrial and cytosolic ATP/ADP-P-i ratios were significantly higher in PUFA-deficient cells than in control cells treated with DNP. We show that PUFA-deficient cells display an increase of phosphorylation efficiency, a higher mitochondrial ATP/ADP-P-i ratio being maintained despite the lower Delta Psi. This is achieved by (1) decreasing mitochondrial P-i accumulation, (2) increasing ATP synthase activity, and (3) by increasing the flux control coefficient of adenine nucleotide translocation. As a consequence, oxidative phosphorylation efficiency was only slightly affected in PUFA-deficient animals as compared to protonophoric uncoupling (DNP). Thus, the energy waste induced by PUFA deficiency on the processes that generate the proton motive force (pmf) is compensated in vivo by powerfuladaptive mechanisms that act on the processes that use the pmf to synthesize ATP.

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Documento generato il 10/07/20 alle ore 14:37:46