AMPK and insulin action: Responses to ageing and high fat diet

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Standard

AMPK and insulin action : Responses to ageing and high fat diet. / Frøsig, Christian; Jensen, Thomas Elbenhardt; Jeppesen, Jacob; Pehmøller, Christian; Treebak, Jonas Thue; Maarbjerg, Stine Just; Kristensen, Jonas Møller; Sylow, Lykke; Alsted, Thomas Junker; Schjerling, Peter; Kiens, Bente; Wojtaszewski, Jørgen; Richter, Erik.

I: P L o S One, Bind 8, Nr. 5, 2013, s. e62338.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Frøsig, C, Jensen, TE, Jeppesen, J, Pehmøller, C, Treebak, JT, Maarbjerg, SJ, Kristensen, JM, Sylow, L, Alsted, TJ, Schjerling, P, Kiens, B, Wojtaszewski, J & Richter, E 2013, 'AMPK and insulin action: Responses to ageing and high fat diet', P L o S One, bind 8, nr. 5, s. e62338. https://doi.org/10.1371/journal.pone.0062338

APA

Frøsig, C., Jensen, T. E., Jeppesen, J., Pehmøller, C., Treebak, J. T., Maarbjerg, S. J., ... Richter, E. (2013). AMPK and insulin action: Responses to ageing and high fat diet. P L o S One, 8(5), e62338. https://doi.org/10.1371/journal.pone.0062338

Vancouver

Frøsig C, Jensen TE, Jeppesen J, Pehmøller C, Treebak JT, Maarbjerg SJ o.a. AMPK and insulin action: Responses to ageing and high fat diet. P L o S One. 2013;8(5):e62338. https://doi.org/10.1371/journal.pone.0062338

Author

Frøsig, Christian ; Jensen, Thomas Elbenhardt ; Jeppesen, Jacob ; Pehmøller, Christian ; Treebak, Jonas Thue ; Maarbjerg, Stine Just ; Kristensen, Jonas Møller ; Sylow, Lykke ; Alsted, Thomas Junker ; Schjerling, Peter ; Kiens, Bente ; Wojtaszewski, Jørgen ; Richter, Erik. / AMPK and insulin action : Responses to ageing and high fat diet. I: P L o S One. 2013 ; Bind 8, Nr. 5. s. e62338.

Bibtex

@article{41f014cba3794682b890af29dc483793,
title = "AMPK and insulin action: Responses to ageing and high fat diet",
abstract = "The 5'-AMP-activated protein kinase (AMPK) is considered {"}a metabolic master-switch{"} in skeletal muscle reducing ATP- consuming processes whilst stimulating ATP regeneration. Within recent years, AMPK has also been proposed as a potential target to attenuate insulin resistance, although the exact role of AMPK is not well understood. Here we hypothesized that mice lacking a2AMPK activity in muscle would be more susceptible to develop insulin resistance associated with ageing alone or in combination with high fat diet. Young (~4 month) or old (~18 month) wild type and muscle specific a2AMPK kinase-dead mice on chow diet as well as old mice on 17 weeks of high fat diet were studied for whole body glucose homeostasis (OGTT, ITT and HOMA-IR), insulin signaling and insulin-stimulated glucose uptake in muscle. We demonstrate that high fat diet in old mice results in impaired glucose homeostasis and insulin stimulated glucose uptake in both the soleus and extensor digitorum longus muscle, coinciding with reduced insulin signaling at the level of Akt (pSer473 and pThr308), TBC1D1 (pThr590) and TBC1D4 (pThr642). In contrast to our hypothesis, the impact of ageing and high fat diet on insulin action was not worsened in mice lacking functional a2AMPK in muscle. It is concluded that a2AMPK deficiency in mouse skeletal muscle does not cause muscle insulin resistance in young and old mice and does not exacerbate obesity-induced insulin resistance in old mice suggesting that decreased a2AMPK activity does not increase susceptibility for insulin resistance in skeletal muscle.",
author = "Christian Fr{\o}sig and Jensen, {Thomas Elbenhardt} and Jacob Jeppesen and Christian Pehm{\o}ller and Treebak, {Jonas Thue} and Maarbjerg, {Stine Just} and Kristensen, {Jonas M{\o}ller} and Lykke Sylow and Alsted, {Thomas Junker} and Peter Schjerling and Bente Kiens and J{\o}rgen Wojtaszewski and Erik Richter",
note = "CURIS 2013 NEXS 104",
year = "2013",
doi = "10.1371/journal.pone.0062338",
language = "English",
volume = "8",
pages = "e62338",
journal = "P L o S One",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "5",

}

RIS

TY - JOUR

T1 - AMPK and insulin action

T2 - Responses to ageing and high fat diet

AU - Frøsig, Christian

AU - Jensen, Thomas Elbenhardt

AU - Jeppesen, Jacob

AU - Pehmøller, Christian

AU - Treebak, Jonas Thue

AU - Maarbjerg, Stine Just

AU - Kristensen, Jonas Møller

AU - Sylow, Lykke

AU - Alsted, Thomas Junker

AU - Schjerling, Peter

AU - Kiens, Bente

AU - Wojtaszewski, Jørgen

AU - Richter, Erik

N1 - CURIS 2013 NEXS 104

PY - 2013

Y1 - 2013

N2 - The 5'-AMP-activated protein kinase (AMPK) is considered "a metabolic master-switch" in skeletal muscle reducing ATP- consuming processes whilst stimulating ATP regeneration. Within recent years, AMPK has also been proposed as a potential target to attenuate insulin resistance, although the exact role of AMPK is not well understood. Here we hypothesized that mice lacking a2AMPK activity in muscle would be more susceptible to develop insulin resistance associated with ageing alone or in combination with high fat diet. Young (~4 month) or old (~18 month) wild type and muscle specific a2AMPK kinase-dead mice on chow diet as well as old mice on 17 weeks of high fat diet were studied for whole body glucose homeostasis (OGTT, ITT and HOMA-IR), insulin signaling and insulin-stimulated glucose uptake in muscle. We demonstrate that high fat diet in old mice results in impaired glucose homeostasis and insulin stimulated glucose uptake in both the soleus and extensor digitorum longus muscle, coinciding with reduced insulin signaling at the level of Akt (pSer473 and pThr308), TBC1D1 (pThr590) and TBC1D4 (pThr642). In contrast to our hypothesis, the impact of ageing and high fat diet on insulin action was not worsened in mice lacking functional a2AMPK in muscle. It is concluded that a2AMPK deficiency in mouse skeletal muscle does not cause muscle insulin resistance in young and old mice and does not exacerbate obesity-induced insulin resistance in old mice suggesting that decreased a2AMPK activity does not increase susceptibility for insulin resistance in skeletal muscle.

AB - The 5'-AMP-activated protein kinase (AMPK) is considered "a metabolic master-switch" in skeletal muscle reducing ATP- consuming processes whilst stimulating ATP regeneration. Within recent years, AMPK has also been proposed as a potential target to attenuate insulin resistance, although the exact role of AMPK is not well understood. Here we hypothesized that mice lacking a2AMPK activity in muscle would be more susceptible to develop insulin resistance associated with ageing alone or in combination with high fat diet. Young (~4 month) or old (~18 month) wild type and muscle specific a2AMPK kinase-dead mice on chow diet as well as old mice on 17 weeks of high fat diet were studied for whole body glucose homeostasis (OGTT, ITT and HOMA-IR), insulin signaling and insulin-stimulated glucose uptake in muscle. We demonstrate that high fat diet in old mice results in impaired glucose homeostasis and insulin stimulated glucose uptake in both the soleus and extensor digitorum longus muscle, coinciding with reduced insulin signaling at the level of Akt (pSer473 and pThr308), TBC1D1 (pThr590) and TBC1D4 (pThr642). In contrast to our hypothesis, the impact of ageing and high fat diet on insulin action was not worsened in mice lacking functional a2AMPK in muscle. It is concluded that a2AMPK deficiency in mouse skeletal muscle does not cause muscle insulin resistance in young and old mice and does not exacerbate obesity-induced insulin resistance in old mice suggesting that decreased a2AMPK activity does not increase susceptibility for insulin resistance in skeletal muscle.

U2 - 10.1371/journal.pone.0062338

DO - 10.1371/journal.pone.0062338

M3 - Journal article

VL - 8

SP - e62338

JO - P L o S One

JF - P L o S One

SN - 1932-6203

IS - 5

ER -

ID: 45692898