Difference between revisions of "Boyle 2011 Int J Obes"
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{{Publication | {{Publication | ||
|title=Boyle KE, Zheng D, Anderson EJ, Neufer PD, Houmard JA (2011) Mitochondrial lipid oxidation is impaired in cultured myotubes from obese humans. Int J Obes | |title=Boyle KE, Zheng D, Anderson EJ, Neufer PD, Houmard JA (2011) Mitochondrial lipid oxidation is impaired in cultured myotubes from obese humans. Int J Obes 36: 1025-1031 | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/22024640 PMID: 22024640] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/22024640 PMID: 22024640] | ||
|authors=Boyle KE, Zheng D, Anderson EJ, Neufer PD, Houmard JA | |authors=Boyle KE, Zheng D, Anderson EJ, Neufer PD, Houmard JA | ||
|year=2011 | |year=2011 | ||
|journal=Int J Obes | |journal=Int J Obes | ||
|abstract=Objective: The skeletal muscle of obese humans is characterized by an inability to appropriately respond to alterations in substrate availability. The purpose of this study was to determine if this metabolic inflexibility with obesity is retained in mitochondria of human skeletal muscle cells raised in culture (HSkMC) and to identify potential mechanisms involved. | |abstract=''Objective'': The skeletal muscle of obese humans is characterized by an inability to appropriately respond to alterations in substrate availability. The purpose of this study was to determine if this metabolic inflexibility with obesity is retained in mitochondria of human skeletal muscle cells raised in culture (HSkMC) and to identify potential mechanisms involved. | ||
Design: Mitochondrial respiration was measured in permeabilized myotubes cultured from lean and obese individuals before and after a 24-h lipid incubation. | ''Design'': Mitochondrial respiration was measured in permeabilized myotubes cultured from lean and obese individuals before and after a 24-h lipid incubation. | ||
Results: Mitochondrial respiration ([[State 3]]) in the presence of lipid substrate (palmitoyl carnitine) increased by almost twofold after lipid incubation in HSkMC from lean, but not obese subjects, indicative of metabolic inflexibility with obesity. The 24-h lipid incubation increased mitochondrial DNA (mtDNA) copy number in HSkMC from lean subjects by +16% (''P''<0.05); conversely, mtDNA copy number decreased in myotubes cultured from obese individuals (-13%, ''P''=0.06). When respiration data were normalized to mtDNA copy number and other indices of mitochondrial content (COX-IV protein content and CS activity), the significant treatment effects of lipid incubation persisted in the lean subjects, suggesting concomitant alterations in mitochondrial function; no similar adjustment was evident in HSkMC from obese individuals. | ''Results'': Mitochondrial respiration ([[State 3]]) in the presence of lipid substrate (palmitoyl carnitine) increased by almost twofold after lipid incubation in HSkMC from lean, but not obese subjects, indicative of metabolic inflexibility with obesity. The 24-h lipid incubation increased mitochondrial DNA (mtDNA) copy number in HSkMC from lean subjects by +16% (''P''<0.05); conversely, mtDNA copy number decreased in myotubes cultured from obese individuals (-13%, ''P''=0.06). When respiration data were normalized to mtDNA copy number and other indices of mitochondrial content (COX-IV protein content and CS activity), the significant treatment effects of lipid incubation persisted in the lean subjects, suggesting concomitant alterations in mitochondrial function; no similar adjustment was evident in HSkMC from obese individuals. | ||
Conclusion: These data indicate that the skeletal muscle of obese individuals inherently lacks metabolic flexibility in response to lipid exposure, which consists of an inability to increase mitochondrial respiration in the presence of lipid substrate and perhaps by an inability to induce mitochondrial proliferation. | ''Conclusion'': These data indicate that the skeletal muscle of obese individuals inherently lacks metabolic flexibility in response to lipid exposure, which consists of an inability to increase mitochondrial respiration in the presence of lipid substrate and perhaps by an inability to induce mitochondrial proliferation. | ||
|keywords=Obesity | |||
|mipnetlab=US NC Greenville Anderson EJ, US NC Greenville Neufer PD, US NC Greenville Houmard JA, US NC Greenville East Carolina Univ | |mipnetlab=US NC Greenville Anderson EJ, US NC Greenville Neufer PD, US NC Greenville Houmard JA, US NC Greenville East Carolina Univ | ||
}} | }} | ||
Revision as of 16:31, 8 March 2013
| Boyle KE, Zheng D, Anderson EJ, Neufer PD, Houmard JA (2011) Mitochondrial lipid oxidation is impaired in cultured myotubes from obese humans. Int J Obes 36: 1025-1031 |
Boyle KE, Zheng D, Anderson EJ, Neufer PD, Houmard JA (2011) Int J Obes
Abstract: Objective: The skeletal muscle of obese humans is characterized by an inability to appropriately respond to alterations in substrate availability. The purpose of this study was to determine if this metabolic inflexibility with obesity is retained in mitochondria of human skeletal muscle cells raised in culture (HSkMC) and to identify potential mechanisms involved.
Design: Mitochondrial respiration was measured in permeabilized myotubes cultured from lean and obese individuals before and after a 24-h lipid incubation.
Results: Mitochondrial respiration (State 3) in the presence of lipid substrate (palmitoyl carnitine) increased by almost twofold after lipid incubation in HSkMC from lean, but not obese subjects, indicative of metabolic inflexibility with obesity. The 24-h lipid incubation increased mitochondrial DNA (mtDNA) copy number in HSkMC from lean subjects by +16% (P<0.05); conversely, mtDNA copy number decreased in myotubes cultured from obese individuals (-13%, P=0.06). When respiration data were normalized to mtDNA copy number and other indices of mitochondrial content (COX-IV protein content and CS activity), the significant treatment effects of lipid incubation persisted in the lean subjects, suggesting concomitant alterations in mitochondrial function; no similar adjustment was evident in HSkMC from obese individuals.
Conclusion: These data indicate that the skeletal muscle of obese individuals inherently lacks metabolic flexibility in response to lipid exposure, which consists of an inability to increase mitochondrial respiration in the presence of lipid substrate and perhaps by an inability to induce mitochondrial proliferation. • Keywords: Obesity
• O2k-Network Lab: US NC Greenville Anderson EJ, US NC Greenville Neufer PD, US NC Greenville Houmard JA, US NC Greenville East Carolina Univ
Labels:
Stress:Mitochondrial Disease; Degenerative Disease and Defect"Mitochondrial Disease; Degenerative Disease and Defect" 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: Human Tissue;cell: Skeletal muscle Preparation: Permeabilized cells Enzyme: Marker Enzyme"Marker Enzyme" 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: Mitochondrial Biogenesis; Mitochondrial Density"Mitochondrial Biogenesis; Mitochondrial Density" 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., Fatty Acid"Fatty Acid" 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
