Knockout of the predominant conventional PKC isoform, PKCalpha, in mouse skeletal muscle does not affect contraction-stimulated glucose uptake

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Knockout of the predominant conventional PKC isoform, PKCalpha, in mouse skeletal muscle does not affect contraction-stimulated glucose uptake. / Jensen, Thomas Elbenhardt; Maarbjerg, Stine Just; Rose, Adam John; Leitges, Michael; Richter, Erik A.

I: American Journal of Physiology: Endocrinology and Metabolism, Bind 297, Nr. 2, 2009, s. E340-E348.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Jensen, TE, Maarbjerg, SJ, Rose, AJ, Leitges, M & Richter, EA 2009, 'Knockout of the predominant conventional PKC isoform, PKCalpha, in mouse skeletal muscle does not affect contraction-stimulated glucose uptake', American Journal of Physiology: Endocrinology and Metabolism, bind 297, nr. 2, s. E340-E348. https://doi.org/10.1152/ajpendo.90610.2008

APA

Jensen, T. E., Maarbjerg, S. J., Rose, A. J., Leitges, M., & Richter, E. A. (2009). Knockout of the predominant conventional PKC isoform, PKCalpha, in mouse skeletal muscle does not affect contraction-stimulated glucose uptake. American Journal of Physiology: Endocrinology and Metabolism, 297(2), E340-E348. https://doi.org/10.1152/ajpendo.90610.2008

Vancouver

Jensen TE, Maarbjerg SJ, Rose AJ, Leitges M, Richter EA. Knockout of the predominant conventional PKC isoform, PKCalpha, in mouse skeletal muscle does not affect contraction-stimulated glucose uptake. American Journal of Physiology: Endocrinology and Metabolism. 2009;297(2):E340-E348. https://doi.org/10.1152/ajpendo.90610.2008

Author

Jensen, Thomas Elbenhardt ; Maarbjerg, Stine Just ; Rose, Adam John ; Leitges, Michael ; Richter, Erik A. / Knockout of the predominant conventional PKC isoform, PKCalpha, in mouse skeletal muscle does not affect contraction-stimulated glucose uptake. I: American Journal of Physiology: Endocrinology and Metabolism. 2009 ; Bind 297, Nr. 2. s. E340-E348.

Bibtex

@article{74be91608e4411de8bc9000ea68e967b,
title = "Knockout of the predominant conventional PKC isoform, PKCalpha, in mouse skeletal muscle does not affect contraction-stimulated glucose uptake",
abstract = "Conventional (c) protein kinase C (PKC) activity has been shown to increase with skeletal muscle contraction, and numerous studies using primarily pharmacological inhibitors have implicated cPKCs in contraction-stimulated glucose uptake. Here, to confirm that cPKC activity is required for contraction-stimulated glucose uptake in mouse muscles, contraction-stimulated glucose uptake ex vivo was first evaluated in the presence of three commonly used cPKC inhibitors (calphostin C, G{\"o}-6976, and G{\"o}-6983) in incubated mouse soleus and extensor digitorum longus (EDL) muscles. All potently inhibited contraction-stimulated glucose uptake by 50-100{\%}, whereas both G{\"o} compounds, but not calphostin C, inhibited insulin-stimulated glucose uptake modestly. AMP-activated protein kinase (AMPK) and eukaryotic elongation factor 2 phosphorylation was unaffected by the blockers. PKCalpha was estimated to account for approximately 97{\%} of total cPKC protein expression in skeletal muscle. However, in muscles from PKCalpha knockout (KO) mice, neither contraction- nor phorbol ester-stimulated glucose uptake ex vivo differed compared with the wild type. Furthermore, the effects of calphostin C and G{\"o}-6983 on contraction-induced glucose uptake were similar in muscles lacking PKCalpha and in the wild type. It can be concluded that PKCalpha, representing approximately 97{\%} of cPKC in skeletal muscle, is not required for contraction-stimulated glucose uptake. Thus the effect of the PKC blockers on glucose uptake is either nonspecific working on other parts of contraction-induced signaling or the remaining cPKC isoforms are sufficient for stimulating glucose uptake during contractions.",
author = "Jensen, {Thomas Elbenhardt} and Maarbjerg, {Stine Just} and Rose, {Adam John} and Michael Leitges and Richter, {Erik A.}",
note = "Keywords: Animals; Biological Transport; Carbazoles; Enzyme Inhibitors; Glucose; Isoenzymes; Male; Mice; Mice, Knockout; Muscle Contraction; Muscle, Skeletal; Naphthalenes; Phosphorylation; Protein Kinase C-alpha",
year = "2009",
doi = "10.1152/ajpendo.90610.2008",
language = "English",
volume = "297",
pages = "E340--E348",
journal = "American Journal of Physiology: Endocrinology and Metabolism",
issn = "0193-1849",
publisher = "American Physiological Society",
number = "2",

}

RIS

TY - JOUR

T1 - Knockout of the predominant conventional PKC isoform, PKCalpha, in mouse skeletal muscle does not affect contraction-stimulated glucose uptake

AU - Jensen, Thomas Elbenhardt

AU - Maarbjerg, Stine Just

AU - Rose, Adam John

AU - Leitges, Michael

AU - Richter, Erik A.

N1 - Keywords: Animals; Biological Transport; Carbazoles; Enzyme Inhibitors; Glucose; Isoenzymes; Male; Mice; Mice, Knockout; Muscle Contraction; Muscle, Skeletal; Naphthalenes; Phosphorylation; Protein Kinase C-alpha

PY - 2009

Y1 - 2009

N2 - Conventional (c) protein kinase C (PKC) activity has been shown to increase with skeletal muscle contraction, and numerous studies using primarily pharmacological inhibitors have implicated cPKCs in contraction-stimulated glucose uptake. Here, to confirm that cPKC activity is required for contraction-stimulated glucose uptake in mouse muscles, contraction-stimulated glucose uptake ex vivo was first evaluated in the presence of three commonly used cPKC inhibitors (calphostin C, Gö-6976, and Gö-6983) in incubated mouse soleus and extensor digitorum longus (EDL) muscles. All potently inhibited contraction-stimulated glucose uptake by 50-100%, whereas both Gö compounds, but not calphostin C, inhibited insulin-stimulated glucose uptake modestly. AMP-activated protein kinase (AMPK) and eukaryotic elongation factor 2 phosphorylation was unaffected by the blockers. PKCalpha was estimated to account for approximately 97% of total cPKC protein expression in skeletal muscle. However, in muscles from PKCalpha knockout (KO) mice, neither contraction- nor phorbol ester-stimulated glucose uptake ex vivo differed compared with the wild type. Furthermore, the effects of calphostin C and Gö-6983 on contraction-induced glucose uptake were similar in muscles lacking PKCalpha and in the wild type. It can be concluded that PKCalpha, representing approximately 97% of cPKC in skeletal muscle, is not required for contraction-stimulated glucose uptake. Thus the effect of the PKC blockers on glucose uptake is either nonspecific working on other parts of contraction-induced signaling or the remaining cPKC isoforms are sufficient for stimulating glucose uptake during contractions.

AB - Conventional (c) protein kinase C (PKC) activity has been shown to increase with skeletal muscle contraction, and numerous studies using primarily pharmacological inhibitors have implicated cPKCs in contraction-stimulated glucose uptake. Here, to confirm that cPKC activity is required for contraction-stimulated glucose uptake in mouse muscles, contraction-stimulated glucose uptake ex vivo was first evaluated in the presence of three commonly used cPKC inhibitors (calphostin C, Gö-6976, and Gö-6983) in incubated mouse soleus and extensor digitorum longus (EDL) muscles. All potently inhibited contraction-stimulated glucose uptake by 50-100%, whereas both Gö compounds, but not calphostin C, inhibited insulin-stimulated glucose uptake modestly. AMP-activated protein kinase (AMPK) and eukaryotic elongation factor 2 phosphorylation was unaffected by the blockers. PKCalpha was estimated to account for approximately 97% of total cPKC protein expression in skeletal muscle. However, in muscles from PKCalpha knockout (KO) mice, neither contraction- nor phorbol ester-stimulated glucose uptake ex vivo differed compared with the wild type. Furthermore, the effects of calphostin C and Gö-6983 on contraction-induced glucose uptake were similar in muscles lacking PKCalpha and in the wild type. It can be concluded that PKCalpha, representing approximately 97% of cPKC in skeletal muscle, is not required for contraction-stimulated glucose uptake. Thus the effect of the PKC blockers on glucose uptake is either nonspecific working on other parts of contraction-induced signaling or the remaining cPKC isoforms are sufficient for stimulating glucose uptake during contractions.

U2 - 10.1152/ajpendo.90610.2008

DO - 10.1152/ajpendo.90610.2008

M3 - Journal article

C2 - 19458061

VL - 297

SP - E340-E348

JO - American Journal of Physiology: Endocrinology and Metabolism

JF - American Journal of Physiology: Endocrinology and Metabolism

SN - 0193-1849

IS - 2

ER -

ID: 13916589