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Titolo:
Lipid oxidation is reduced in obese human skeletal muscle
Autore:
Kim, JY; Hickner, RC; Cortright, RL; Dohm, GL; Houmard, JA;
Indirizzi:
E Carolina Univ, Human Performance Lab, Greenville, NC 27858 USA E Carolina Univ Greenville NC USA 27858 nce Lab, Greenville, NC 27858 USA E Carolina Univ, Dept Biochem, Greenville, NC 27858 USA E Carolina Univ Greenville NC USA 27858 Biochem, Greenville, NC 27858 USA E Carolina Univ, Dept Physiol, Greenville, NC 27858 USA E Carolina Univ Greenville NC USA 27858 Physiol, Greenville, NC 27858 USA E Carolina Univ, Dept Exercise & Sport Sci, Greenville, NC 27858 USA E Carolina Univ Greenville NC USA 27858 ort Sci, Greenville, NC 27858 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
fascicolo: 5, volume: 279, anno: 2000,
pagine: E1039 - E1044
SICI:
0193-1849(200011)279:5<E1039:LOIRIO>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
CARNITINE PALMITOYLTRANSFERASE SYSTEM; FATTY-ACID OXIDATION; MALONYL-COA; INSULIN SENSITIVITY; WEIGHT-LOSS; METABOLISM; TRIGLYCERIDE; RESISTANCE; CAPACITIES; CHAIN;
Keywords:
carnitine palmitoyltransferase; fatty acids; malonyl-coenzyme A;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Houmard, JA E Carolina Univ, Human Performance Lab, Rm 371,Ward Sports MedBldg, Greenville, NC 27858 USA E Carolina Univ Rm 371,Ward Sports Med BldgGreenville NC USA 27858
Citazione:
J.Y. Kim et al., "Lipid oxidation is reduced in obese human skeletal muscle", AM J P-ENDO, 279(5), 2000, pp. E1039-E1044

Abstract

The purpose of this study was to discern cellular mechanisms that contribute to the suppression of lipid oxidation in the skeletal muscle of obese individuals. Muscle was obtained from obese [body mass index (BMI), 38.3 +/- 3.1 kg/m(2)] and lean (BMI, 23.8 +/- 0.9 kg/m(2)) women, and fatty acid oxidation was studied by measuring (CO2)-C-14 production from C-14-labeled fatty acids. Palmitate oxidation, which is at least partially dependent on carnitine palmitoyltransferase-1 (CPT-1) activity, was depressed (P < 0.05) by<approximate to>50% with obesity (6.8 +/- 2.2 vs. 13.7 +/- 1.4 nmole CO2.g(-1).h(-1)). The CPT-1-independent event of palmitoyl carnitine oxidation was also depressed (P < 0.01) by <approximate to>45%. There were significantnegative relationships (P < 0.05) for adiposity with palmitate (r = -0.76)and palmitoyl carnitine (r = 0.82) oxidation. Muscle CPT-1 and citrate synthase activity, an index of mitochondrial content, were also significantly (P < 0.05) reduced (approximate to 35%) with obesity. CPT-1 (r = -0.48) andcitrate synthase (r = -0.65) activities were significantly (P < 0.05) related to adiposity. These data suggest that lesions at CPT-1 and post-CPT-1 events, such as mitochondrial content, contribute to the reduced reliance onfat oxidation evident in human skeletal muscle with obesity.

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Documento generato il 27/11/20 alle ore 01:30:47