Insulin resistance and mitochondrial function in skeletal muscle

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Insulin resistance and mitochondrial function in skeletal muscle. / Dela, Flemming; Helge, Jørn Wulff.

I: International Journal of Biochemistry & Cell Biology, Bind 45, Nr. 1, 01.2013, s. 11-5.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Dela, F & Helge, JW 2013, 'Insulin resistance and mitochondrial function in skeletal muscle', International Journal of Biochemistry & Cell Biology, bind 45, nr. 1, s. 11-5. https://doi.org/10.1016/j.biocel.2012.09.019

APA

Dela, F., & Helge, J. W. (2013). Insulin resistance and mitochondrial function in skeletal muscle. International Journal of Biochemistry & Cell Biology, 45(1), 11-5. https://doi.org/10.1016/j.biocel.2012.09.019

Vancouver

Dela F, Helge JW. Insulin resistance and mitochondrial function in skeletal muscle. International Journal of Biochemistry & Cell Biology. 2013 jan;45(1):11-5. https://doi.org/10.1016/j.biocel.2012.09.019

Author

Dela, Flemming ; Helge, Jørn Wulff. / Insulin resistance and mitochondrial function in skeletal muscle. I: International Journal of Biochemistry & Cell Biology. 2013 ; Bind 45, Nr. 1. s. 11-5.

Bibtex

@article{acb406254f19435b9290a2e0896b5023,
title = "Insulin resistance and mitochondrial function in skeletal muscle",
abstract = "The mechanism(s) behind the decreased ability of insulin to facilitate glucose uptake in insulin sensitive tissues as seen in type 2 diabetes is not resolved. With the rapidly increasing prevalence of this disease world-wide, and the many complications that follow the disease, large resources are used in the attempt to resolve the mechanisms of insulin resistance. In this context, a dysfunction of mitochondria in the skeletal muscle has been suggested to play a pivotal role. It has been postulated that a decrease in the content of mitochondria in the skeletal muscle can explain the insulin resistance. Complementary to this also specific defects of components in the respiratory chain in the mitochondria have been suggested to play a role in insulin resistance. A key element in these mechanistic suggestions is inability to handle substrate fluxes and subsequently an accumulation of ectopic intramyocellular lipids, interfering with insulin signaling. In this review we will present the prevailing view-points and argue for the unlikelihood of this scenario being instrumental in human insulin resistance. This article is part of a Directed Issue entitled: Bioenergetic dysfunction.",
author = "Flemming Dela and Helge, {J{\o}rn Wulff}",
note = "Copyright {\circledC} 2012 Elsevier Ltd. All rights reserved.",
year = "2013",
month = "1",
doi = "10.1016/j.biocel.2012.09.019",
language = "English",
volume = "45",
pages = "11--5",
journal = "International Journal of Biochemistry & Cell Biology",
issn = "1357-2725",
publisher = "Elsevier",
number = "1",

}

RIS

TY - JOUR

T1 - Insulin resistance and mitochondrial function in skeletal muscle

AU - Dela, Flemming

AU - Helge, Jørn Wulff

N1 - Copyright © 2012 Elsevier Ltd. All rights reserved.

PY - 2013/1

Y1 - 2013/1

N2 - The mechanism(s) behind the decreased ability of insulin to facilitate glucose uptake in insulin sensitive tissues as seen in type 2 diabetes is not resolved. With the rapidly increasing prevalence of this disease world-wide, and the many complications that follow the disease, large resources are used in the attempt to resolve the mechanisms of insulin resistance. In this context, a dysfunction of mitochondria in the skeletal muscle has been suggested to play a pivotal role. It has been postulated that a decrease in the content of mitochondria in the skeletal muscle can explain the insulin resistance. Complementary to this also specific defects of components in the respiratory chain in the mitochondria have been suggested to play a role in insulin resistance. A key element in these mechanistic suggestions is inability to handle substrate fluxes and subsequently an accumulation of ectopic intramyocellular lipids, interfering with insulin signaling. In this review we will present the prevailing view-points and argue for the unlikelihood of this scenario being instrumental in human insulin resistance. This article is part of a Directed Issue entitled: Bioenergetic dysfunction.

AB - The mechanism(s) behind the decreased ability of insulin to facilitate glucose uptake in insulin sensitive tissues as seen in type 2 diabetes is not resolved. With the rapidly increasing prevalence of this disease world-wide, and the many complications that follow the disease, large resources are used in the attempt to resolve the mechanisms of insulin resistance. In this context, a dysfunction of mitochondria in the skeletal muscle has been suggested to play a pivotal role. It has been postulated that a decrease in the content of mitochondria in the skeletal muscle can explain the insulin resistance. Complementary to this also specific defects of components in the respiratory chain in the mitochondria have been suggested to play a role in insulin resistance. A key element in these mechanistic suggestions is inability to handle substrate fluxes and subsequently an accumulation of ectopic intramyocellular lipids, interfering with insulin signaling. In this review we will present the prevailing view-points and argue for the unlikelihood of this scenario being instrumental in human insulin resistance. This article is part of a Directed Issue entitled: Bioenergetic dysfunction.

U2 - 10.1016/j.biocel.2012.09.019

DO - 10.1016/j.biocel.2012.09.019

M3 - Journal article

VL - 45

SP - 11

EP - 15

JO - International Journal of Biochemistry & Cell Biology

JF - International Journal of Biochemistry & Cell Biology

SN - 1357-2725

IS - 1

ER -

ID: 44914748