Fuel utilization in patients with very long-chain acyl-coa dehydrogenase deficiency

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Standard

Fuel utilization in patients with very long-chain acyl-coa dehydrogenase deficiency. / ØRngreen, Mette C; Nørgaard, Mette; Sacchetti, Massimo; van Engelen, Baziel G M; Vissing, John; Charlot, Mette Gitz.

I: Annals of Neurology, Bind 56, Nr. 2, 01.08.2004, s. 279-83.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

ØRngreen, MC, Nørgaard, M, Sacchetti, M, van Engelen, BGM, Vissing, J & Charlot, MG 2004, 'Fuel utilization in patients with very long-chain acyl-coa dehydrogenase deficiency', Annals of Neurology, bind 56, nr. 2, s. 279-83. https://doi.org/10.1002/ana.20168

APA

ØRngreen, M. C., Nørgaard, M., Sacchetti, M., van Engelen, B. G. M., Vissing, J., & Charlot, M. G. (2004). Fuel utilization in patients with very long-chain acyl-coa dehydrogenase deficiency. Annals of Neurology, 56(2), 279-83. https://doi.org/10.1002/ana.20168

Vancouver

ØRngreen MC, Nørgaard M, Sacchetti M, van Engelen BGM, Vissing J, Charlot MG. Fuel utilization in patients with very long-chain acyl-coa dehydrogenase deficiency. Annals of Neurology. 2004 aug. 1;56(2):279-83. https://doi.org/10.1002/ana.20168

Author

ØRngreen, Mette C ; Nørgaard, Mette ; Sacchetti, Massimo ; van Engelen, Baziel G M ; Vissing, John ; Charlot, Mette Gitz. / Fuel utilization in patients with very long-chain acyl-coa dehydrogenase deficiency. I: Annals of Neurology. 2004 ; Bind 56, Nr. 2. s. 279-83.

Bibtex

@article{e68c593cc8ab41d49fb79f1360057bd0,

title = "Fuel utilization in patients with very long-chain acyl-coa dehydrogenase deficiency",

abstract = "Fuel utilization in two adult patients with the myopathic form of very long-chain acyl-CoA dehydrogenase (VLCAD) deficiency and five healthy subjects was investigated with stable isotopes during exercise at 50% of VO2max. The findings indicate that residual VLCAD activity in the patients is sufficient to maintain normal oxidation of fat at rest, but that fat oxidation rate cannot increase above basal levels during exercise. This can cause an energy deficit and intramuscular accumulation of fat intermediates that may induce the exercise-induced symptoms.",

author = "{\O}Rngreen, {Mette C} and Mette N{\o}rgaard and Massimo Sacchetti and {van Engelen}, {Baziel G M} and John Vissing and Charlot, {Mette Gitz}",

year = "2004",

month = aug,

day = "1",

doi = "http://dx.doi.org/10.1002/ana.20168",

language = "English",

volume = "56",

pages = "279--83",

journal = "Annals of Neurology",

issn = "0364-5134",

publisher = "JohnWiley & Sons, Inc.",

number = "2",

}

RIS

TY - JOUR

T1 - Fuel utilization in patients with very long-chain acyl-coa dehydrogenase deficiency

AU - ØRngreen, Mette C

AU - Nørgaard, Mette

AU - Sacchetti, Massimo

AU - van Engelen, Baziel G M

AU - Vissing, John

AU - Charlot, Mette Gitz

PY - 2004/8/1

Y1 - 2004/8/1

N2 - Fuel utilization in two adult patients with the myopathic form of very long-chain acyl-CoA dehydrogenase (VLCAD) deficiency and five healthy subjects was investigated with stable isotopes during exercise at 50% of VO2max. The findings indicate that residual VLCAD activity in the patients is sufficient to maintain normal oxidation of fat at rest, but that fat oxidation rate cannot increase above basal levels during exercise. This can cause an energy deficit and intramuscular accumulation of fat intermediates that may induce the exercise-induced symptoms.

AB - Fuel utilization in two adult patients with the myopathic form of very long-chain acyl-CoA dehydrogenase (VLCAD) deficiency and five healthy subjects was investigated with stable isotopes during exercise at 50% of VO2max. The findings indicate that residual VLCAD activity in the patients is sufficient to maintain normal oxidation of fat at rest, but that fat oxidation rate cannot increase above basal levels during exercise. This can cause an energy deficit and intramuscular accumulation of fat intermediates that may induce the exercise-induced symptoms.

U2 - http://dx.doi.org/10.1002/ana.20168

DO - http://dx.doi.org/10.1002/ana.20168

M3 - Journal article

VL - 56

SP - 279

EP - 283

JO - Annals of Neurology

JF - Annals of Neurology

SN - 0364-5134

IS - 2

ER -

ID: 34085619

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