Molecular regulation of fatty acid oxidation in skeletal muscle during aerobic exercise

Research output: Contribution to journal › Review › Research › peer-review

Standard

Molecular regulation of fatty acid oxidation in skeletal muscle during aerobic exercise. / Lundsgaard, Annemarie; Fritzen, Andreas Mæchel; Kiens, Bente.

In: Trends in Endocrinology and Metabolism, Vol. 29, No. 1, 2018, p. 18-30.

Research output: Contribution to journal › Review › Research › peer-review

Harvard

Lundsgaard, A, Fritzen, AM & Kiens, B 2018, 'Molecular regulation of fatty acid oxidation in skeletal muscle during aerobic exercise', Trends in Endocrinology and Metabolism, vol. 29, no. 1, pp. 18-30. https://doi.org/10.1016/j.tem.2017.10.011

APA

Lundsgaard, A., Fritzen, A. M., & Kiens, B. (2018). Molecular regulation of fatty acid oxidation in skeletal muscle during aerobic exercise. Trends in Endocrinology and Metabolism, 29(1), 18-30. https://doi.org/10.1016/j.tem.2017.10.011

Vancouver

Lundsgaard A, Fritzen AM, Kiens B. Molecular regulation of fatty acid oxidation in skeletal muscle during aerobic exercise. Trends in Endocrinology and Metabolism. 2018;29(1):18-30. https://doi.org/10.1016/j.tem.2017.10.011

Author

Lundsgaard, Annemarie ; Fritzen, Andreas Mæchel ; Kiens, Bente. / Molecular regulation of fatty acid oxidation in skeletal muscle during aerobic exercise. In: Trends in Endocrinology and Metabolism. 2018 ; Vol. 29, No. 1. pp. 18-30.

Bibtex

@article{6313cb42c20a41919379eef35feada17,
title = "Molecular regulation of fatty acid oxidation in skeletal muscle during aerobic exercise",
abstract = "This review summarizes how fatty acid (FA) oxidation is regulated in skeletal muscle during exercise. From the available evidence it seems that acetyl-CoA availability in the mitochondrial matrix adjusts FA oxidation to exercise intensity and duration. This is executed at the step of mitochondrial fatty acyl import, as the extent of acetyl group sequestration by carnitine determines the availability of carnitine for the carnitine palmitoyltransferase 1 (CPT1) reaction. The rate of glycolysis seems therefore to be central to the amount of β-oxidation-derived acetyl-CoA that is oxidized in the tricarboxylic acid (TCA) cycle. FA oxidation during exercise is also determined by FA availability to mitochondria, dependent on trans-sarcolemmal FA uptake via cluster of differentiation 36/SR-B2 (CD36) and FAs mobilized from myocellular lipid droplets.",
keywords = "Glycolysis, Pyruvate dehydrogenase, Acetyl-CoA, Carnitine palmitoyltransferase 1, Carnitine acyltransferase",
author = "Annemarie Lundsgaard and Fritzen, {Andreas M{\ae}chel} and Bente Kiens",
note = "CURIS 2018 NEXS 010",
year = "2018",
doi = "10.1016/j.tem.2017.10.011",
language = "English",
volume = "29",
pages = "18--30",
journal = "Trends in Endocrinology and Metabolism",
issn = "1043-2760",
publisher = "Elsevier Ltd. * Trends Journals",
number = "1",

}

RIS

TY - JOUR

T1 - Molecular regulation of fatty acid oxidation in skeletal muscle during aerobic exercise

AU - Lundsgaard, Annemarie

AU - Fritzen, Andreas Mæchel

AU - Kiens, Bente

N1 - CURIS 2018 NEXS 010

PY - 2018

Y1 - 2018

N2 - This review summarizes how fatty acid (FA) oxidation is regulated in skeletal muscle during exercise. From the available evidence it seems that acetyl-CoA availability in the mitochondrial matrix adjusts FA oxidation to exercise intensity and duration. This is executed at the step of mitochondrial fatty acyl import, as the extent of acetyl group sequestration by carnitine determines the availability of carnitine for the carnitine palmitoyltransferase 1 (CPT1) reaction. The rate of glycolysis seems therefore to be central to the amount of β-oxidation-derived acetyl-CoA that is oxidized in the tricarboxylic acid (TCA) cycle. FA oxidation during exercise is also determined by FA availability to mitochondria, dependent on trans-sarcolemmal FA uptake via cluster of differentiation 36/SR-B2 (CD36) and FAs mobilized from myocellular lipid droplets.

AB - This review summarizes how fatty acid (FA) oxidation is regulated in skeletal muscle during exercise. From the available evidence it seems that acetyl-CoA availability in the mitochondrial matrix adjusts FA oxidation to exercise intensity and duration. This is executed at the step of mitochondrial fatty acyl import, as the extent of acetyl group sequestration by carnitine determines the availability of carnitine for the carnitine palmitoyltransferase 1 (CPT1) reaction. The rate of glycolysis seems therefore to be central to the amount of β-oxidation-derived acetyl-CoA that is oxidized in the tricarboxylic acid (TCA) cycle. FA oxidation during exercise is also determined by FA availability to mitochondria, dependent on trans-sarcolemmal FA uptake via cluster of differentiation 36/SR-B2 (CD36) and FAs mobilized from myocellular lipid droplets.

KW - Glycolysis

KW - Pyruvate dehydrogenase

KW - Acetyl-CoA

KW - Carnitine palmitoyltransferase 1

KW - Carnitine acyltransferase

U2 - 10.1016/j.tem.2017.10.011

DO - 10.1016/j.tem.2017.10.011

M3 - Review

C2 - 29221849

VL - 29

SP - 18

EP - 30

JO - Trends in Endocrinology and Metabolism

JF - Trends in Endocrinology and Metabolism

SN - 1043-2760

IS - 1

ER -

ID: 186648654