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Difference between revisions of "Kristensen 2013 PLoS One"

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|title=Kristensen JM, Larsen S, Helge JW, Dela F, Wojtaszewski JFP (2013) Two weeks of metformin treatment enhances mitochondrial respiration in skeletal muscle of AMPK kinase dead but not wild type mice. PLoS One PLoS ONE 8: e53533.  
|title=Kristensen JM, Larsen S, Helge JW, Dela F, Wojtaszewski JFP (2013) Two weeks of metformin treatment enhances mitochondrial respiration in skeletal muscle of AMPK kinase dead but not wild type mice. PLoS One PLoS ONE 8: e53533.
|info=[http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0053533 doi:10.1371/journal.pone.0053533 Open Access]
|info=[http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0053533 doi:10.1371/journal.pone.0053533 Open Access]
|authors=Kristensen JM, Larsen S, Helge JW, Dela F, Wojtaszewski JFP
|authors=Kristensen JM, Larsen S, Helge JW, Dela F, Wojtaszewski JFP
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We conclude that two weeks of in vivo metformin treatment enhances mitochondrial respiration in the mitochondrial deficient AMPK KD but not WT mice. The improvement seems to be unrelated to AMPK, and does not involve changes in key mitochondrial proteins.
We conclude that two weeks of in vivo metformin treatment enhances mitochondrial respiration in the mitochondrial deficient AMPK KD but not WT mice. The improvement seems to be unrelated to AMPK, and does not involve changes in key mitochondrial proteins.
|keywords=5′AMP activated protein kinase (AMPK), Type 2 diabetes,  
|keywords=Metformin, 5′AMP activated protein kinase (AMPK), Type 2 diabetes,
|mipnetlab=DK Copenhagen Dela F,  
|mipnetlab=DK Copenhagen Dela F,
}}
}}
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Revision as of 15:59, 27 January 2013

Publications in the MiPMap
Kristensen JM, Larsen S, Helge JW, Dela F, Wojtaszewski JFP (2013) Two weeks of metformin treatment enhances mitochondrial respiration in skeletal muscle of AMPK kinase dead but not wild type mice. PLoS One PLoS ONE 8: e53533.

» doi:10.1371/journal.pone.0053533 Open Access

Kristensen JM, Larsen S, Helge JW, Dela F, Wojtaszewski JFP (2013) PLoS One

Abstract: Metformin is used as an anti-diabetic drug. Metformin ameliorates insulin resistance by improving insulin sensitivity in liver and skeletal muscle. Reduced mitochondrial content has been reported in type 2 diabetic muscles and it may contribute to decreased insulin sensitivity characteristic for diabetic muscles. The molecular mechanism behind the effect of metformin is not fully clarified but inhibition of complex I in the mitochondria and also activation of the 5′AMP activated protein kinase (AMPK) has been reported in muscle. Furthermore, both AMPK activation and metformin treatment have been associated with stimulation of mitochondrial function and biogenesis. However, a causal relationship in skeletal muscle has not been investigated. We hypothesized that potential effects of in vivo metformin treatment on mitochondrial function and protein expressions in skeletal muscle are dependent upon AMPK signaling. We investigated this by two weeks of oral metformin treatment of muscle specific kinase dead α2 (KD) AMPK mice and wild type (WT) littermates. We measured mitochondrial respiration and protein activity and expressions of key enzymes involved in mitochondrial carbohydrate and fat metabolism and oxidative phosphorylation. Mitochondrial respiration, HAD and CS activity, PDH and complex I-V and cytochrome c protein expression were all reduced in AMPK KD compared to WT tibialis anterior muscles. Surprisingly, metformin treatment only enhanced respiration in AMPK KD mice and thereby rescued the respiration defect compared to the WT mice. Metformin did not influence protein activities or expressions in either WT or AMPK KD mice.

We conclude that two weeks of in vivo metformin treatment enhances mitochondrial respiration in the mitochondrial deficient AMPK KD but not WT mice. The improvement seems to be unrelated to AMPK, and does not involve changes in key mitochondrial proteins. Keywords: Metformin, 5′AMP activated protein kinase (AMPK), Type 2 diabetes

O2k-Network Lab: DK Copenhagen Dela F


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Organism: Mouse  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue  Enzyme: Complex I, Complex II; Succinate Dehydrogenase"Complex II; Succinate Dehydrogenase" is not in the list (Adenine nucleotide translocase, Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase, Inner mt-membrane transporter, Marker enzyme, Supercomplex, TCA cycle and matrix dehydrogenases, ...) of allowed values for the "Enzyme" property., Complex IV; Cytochrome c Oxidase"Complex IV; Cytochrome c Oxidase" is not in the list (Adenine nucleotide translocase, Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase, Inner mt-membrane transporter, Marker enzyme, Supercomplex, TCA cycle and matrix dehydrogenases, ...) of allowed values for the "Enzyme" property. 

Coupling state: LEAK, OXPHOS 

HRR: Oxygraph-2k