Difference between revisions of "Stride 2012 Front Physiol"
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{{Publication | {{Publication | ||
|title=Stride N, Larsen S, Treebak JT, Hansen CN, Hey-Mogensen M, Speerschneider T, Jensen TE, Jeppesen J, Wojtaszewski JF, Richter EA, KĆøber L, Dela F (2012) 5'-AMP Activated Protein Kinase is Involved in the Regulation of Myocardial Ī²-Oxidative Capacity in Mice. Front Physiol Epub. Ā | |title=Stride N, Larsen S, Treebak JT, Hansen CN, Hey-Mogensen M, Speerschneider T, Jensen TE, Jeppesen J, Wojtaszewski JF, Richter EA, KĆøber L, Dela F (2012) 5'-AMP Activated Protein Kinase is Involved in the Regulation of Myocardial Ī²-Oxidative Capacity in Mice. Front Physiol Epub. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed?term=5%E2%80%B2-AMP%20Activated%20Protein%20Kinase%20is%20Involved%20in%20the%20Regulation%20of%20Myocardial%20%CE%B2-Oxidative%20Capacity%20in%20Mice PMID: 22371704 ] | |info=[http://www.ncbi.nlm.nih.gov/pubmed?term=5%E2%80%B2-AMP%20Activated%20Protein%20Kinase%20is%20Involved%20in%20the%20Regulation%20of%20Myocardial%20%CE%B2-Oxidative%20Capacity%20in%20Mice PMID: 22371704 ] | ||
|authors=Stride N, Larsen S, Treebak JT, Hansen CN, Hey-Mogensen M, Speerschneider T, Jensen TE, Jeppesen J, Wojtaszewski JF, Richter EA, KĆøber L, Dela F | |authors=Stride N, Larsen S, Treebak JT, Hansen CN, Hey-Mogensen M, Speerschneider T, Jensen TE, Jeppesen J, Wojtaszewski JF, Richter EA, KĆøber L, Dela F | ||
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|abstract=5'-adenosine monophosphate-activated protein kinase (AMPK) is considered central in regulation of energy status and substrate utilization within cells. In heart failure the energetic state is compromised and substrate metabolism is altered. We hypothesized that this could be linked to changes in AMPK activity and we therefore investigated mitochondrial oxidative phosphorylation capacity from the oxidation of long- and medium-chain fatty acids (LCFA and MCFA) in cardiomyocytes from young and old mice expressing a dominant negative AMPKĪ±2 (AMPKĪ±2-KD) construct and their wildtype (WT) littermates. We found a 35-45% (Pā<ā0.05) lower mitochondrial capacity for oxidizing MCFA in AMPKĪ±2-KD of both age-groups, compared to WT. This coincided with marked decreases in protein expression (19/29%, Pā<ā0.05) and activity (14/21%, Pā<ā0.05) of 3-hydroxyacyl-CoA-dehydrogenase (HAD), in young and old AMPKĪ±2-KD mice, respectively, compared to WT. Maximal LCFA oxidation capacity was similar in AMPKĪ±2-KD and WT mice independently of age implying that LCFA-transport into the mitochondria was unaffected by loss of AMPK activity or progressing age. Expression of regulatory proteins of glycolysis and glycogen breakdown showed equivocal effects of age and genotype. These results illustrate that AMPK is necessary for normal mitochondrial function in the heart and that decreased AMPK activity may lead to an altered energetic state as a consequence of reduced capacity to oxidize MCFA. We did not identify any clear aging effects on mitochondrial function. | |abstract=5'-adenosine monophosphate-activated protein kinase (AMPK) is considered central in regulation of energy status and substrate utilization within cells. In heart failure the energetic state is compromised and substrate metabolism is altered. We hypothesized that this could be linked to changes in AMPK activity and we therefore investigated mitochondrial oxidative phosphorylation capacity from the oxidation of long- and medium-chain fatty acids (LCFA and MCFA) in cardiomyocytes from young and old mice expressing a dominant negative AMPKĪ±2 (AMPKĪ±2-KD) construct and their wildtype (WT) littermates. We found a 35-45% (Pā<ā0.05) lower mitochondrial capacity for oxidizing MCFA in AMPKĪ±2-KD of both age-groups, compared to WT. This coincided with marked decreases in protein expression (19/29%, Pā<ā0.05) and activity (14/21%, Pā<ā0.05) of 3-hydroxyacyl-CoA-dehydrogenase (HAD), in young and old AMPKĪ±2-KD mice, respectively, compared to WT. Maximal LCFA oxidation capacity was similar in AMPKĪ±2-KD and WT mice independently of age implying that LCFA-transport into the mitochondria was unaffected by loss of AMPK activity or progressing age. Expression of regulatory proteins of glycolysis and glycogen breakdown showed equivocal effects of age and genotype. These results illustrate that AMPK is necessary for normal mitochondrial function in the heart and that decreased AMPK activity may lead to an altered energetic state as a consequence of reduced capacity to oxidize MCFA. We did not identify any clear aging effects on mitochondrial function. | ||
|keywords=dominant negative AMPKĪ±2 (AMPKĪ±2-KD), 5'-adenosine monophosphate-activated protein kinase (AMPK) | |keywords=dominant negative AMPKĪ±2 (AMPKĪ±2-KD), 5'-adenosine monophosphate-activated protein kinase (AMPK) | ||
|mipnetlab=DK Copenhagen Dela F | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
Revision as of 14:31, 12 March 2012
| Stride N, Larsen S, Treebak JT, Hansen CN, Hey-Mogensen M, Speerschneider T, Jensen TE, Jeppesen J, Wojtaszewski JF, Richter EA, KĆøber L, Dela F (2012) 5'-AMP Activated Protein Kinase is Involved in the Regulation of Myocardial Ī²-Oxidative Capacity in Mice. Front Physiol Epub. |
Stride N, Larsen S, Treebak JT, Hansen CN, Hey-Mogensen M, Speerschneider T, Jensen TE, Jeppesen J, Wojtaszewski JF, Richter EA, KĆøber L, Dela F (2012) Front Physiol
Abstract: 5'-adenosine monophosphate-activated protein kinase (AMPK) is considered central in regulation of energy status and substrate utilization within cells. In heart failure the energetic state is compromised and substrate metabolism is altered. We hypothesized that this could be linked to changes in AMPK activity and we therefore investigated mitochondrial oxidative phosphorylation capacity from the oxidation of long- and medium-chain fatty acids (LCFA and MCFA) in cardiomyocytes from young and old mice expressing a dominant negative AMPKĪ±2 (AMPKĪ±2-KD) construct and their wildtype (WT) littermates. We found a 35-45% (Pā<ā0.05) lower mitochondrial capacity for oxidizing MCFA in AMPKĪ±2-KD of both age-groups, compared to WT. This coincided with marked decreases in protein expression (19/29%, Pā<ā0.05) and activity (14/21%, Pā<ā0.05) of 3-hydroxyacyl-CoA-dehydrogenase (HAD), in young and old AMPKĪ±2-KD mice, respectively, compared to WT. Maximal LCFA oxidation capacity was similar in AMPKĪ±2-KD and WT mice independently of age implying that LCFA-transport into the mitochondria was unaffected by loss of AMPK activity or progressing age. Expression of regulatory proteins of glycolysis and glycogen breakdown showed equivocal effects of age and genotype. These results illustrate that AMPK is necessary for normal mitochondrial function in the heart and that decreased AMPK activity may lead to an altered energetic state as a consequence of reduced capacity to oxidize MCFA. We did not identify any clear aging effects on mitochondrial function. ā¢ Keywords: dominant negative AMPKĪ±2 (AMPKĪ±2-KD), 5'-adenosine monophosphate-activated protein kinase (AMPK)
ā¢ O2k-Network Lab: DK Copenhagen Dela F
Labels:
Stress:Genetic Defect; Knockdown; Overexpression"Genetic Defect; Knockdown; Overexpression" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Mouse Tissue;cell: Cardiac Muscle"Cardiac Muscle" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property. Preparation: z in prep"z in prep" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property. Enzyme: z in prep"z in prep" 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. Regulation: z in prep"z in prep" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property., Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property.
HRR: Oxygraph-2k
