Difference between revisions of "Holmstroem 2012 Am J Physiol Endocrinol Metab"
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{{Publication | {{Publication | ||
|title= | |title=Holmstroem MH, Iglesias-Gutierrez E, Zierath JR, Garcia-Roves PM (2012) Tissue-specific control of mitochondrial respiration in obesity-related insulin resistance and diabetes Am J Physiol Endocrinol Metab 302: E731-E739. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed?term=Tissue-Specific%20Control%20of%20Mitochondrial%20Respiration%20in%20Obesity-Related%20Insulin%20Resistance%20and%20Diabetes PMID:22252943] | |info=[http://www.ncbi.nlm.nih.gov/pubmed?term=Tissue-Specific%20Control%20of%20Mitochondrial%20Respiration%20in%20Obesity-Related%20Insulin%20Resistance%20and%20Diabetes PMID:22252943] | ||
|authors=Holmstroem MH, Iglesias-Gutierrez E, Zierath JR, Garcia-Roves PM | |authors=Holmstroem MH, Iglesias-Gutierrez E, Zierath JR, Garcia-Roves PM | ||
|year=2012 | |year=2012 | ||
|journal=Am J Physiol Endocrinol Metab | |journal=Am J Physiol Endocrinol Metab | ||
|abstract=The tissue-specific role of mitochondrial respiratory capacity in the development of insulin resistance and type 2 diabetes is unclear. We determined mitochondrial function in glycolytic and oxidative skeletal muscle and liver from lean (+/?) and obese diabetic (db/db) mice. In lean mice, the mitochondrial respiration pattern differed between tissues. Tissue-specific mitochondrial profiles were then compared between lean and db/db mice. In liver, mitochondrial respiratory capacity and protein expression, including peroxisome proliferator-activated receptor γ coactivator-1 α (PGC-1α), was decreased in db/db mice, consistent with increased mitochondrial fission. In glycolytic muscle, mitochondrial respiration, as well as protein and mRNA expression of mitochondrial markers, was increased in db/db mice, suggesting increased mitochondrial content and fatty acid oxidation capacity. In oxidative muscle, mitochondrial Complex I function and PGC-1α and mitochondrial transcription factor A (TFAM) protein level were decreased in db/db mice, along with increased level of proteins related to mitochondrial dynamics. In conclusion, mitochondrial respiratory performance is under the control of tissue-specific mechanisms and is not uniformly altered in response to obesity. Furthermore, insulin resistance in glycolytic skeletal muscle can develop by a mechanism independent of mitochondrial dysfunction. Conversely, insulin resistance in liver and oxidative skeletal muscle from db/db mice is coincident with mitochondrial dysfunction. | |abstract=The tissue-specific role of mitochondrial respiratory capacity in the development of insulin resistance and type 2 diabetes is unclear. We determined mitochondrial function in glycolytic and oxidative skeletal muscle and liver from lean (+/?) and obese diabetic (db/db) mice. In lean mice, the mitochondrial respiration pattern differed between tissues. Tissue-specific mitochondrial profiles were then compared between lean and db/db mice. In liver, mitochondrial respiratory capacity and protein expression, including peroxisome proliferator-activated receptor γ coactivator-1 α [[PGC-1alpha|(PGC-1α)]], was decreased in db/db mice, consistent with increased mitochondrial fission. In glycolytic muscle, mitochondrial respiration, as well as protein and mRNA expression of mitochondrial markers, was increased in db/db mice, suggesting increased mitochondrial content and fatty acid oxidation capacity. In oxidative muscle, mitochondrial Complex I function and [[PGC-1α]] and mitochondrial transcription factor A (TFAM) protein level were decreased in db/db mice, along with increased level of proteins related to mitochondrial dynamics. In conclusion, mitochondrial respiratory performance is under the control of tissue-specific mechanisms and is not uniformly altered in response to obesity. Furthermore, insulin resistance in glycolytic skeletal muscle can develop by a mechanism independent of mitochondrial dysfunction. Conversely, insulin resistance in liver and oxidative skeletal muscle from db/db mice is coincident with mitochondrial dysfunction. | ||
|keywords=Type 2 diabetes | |keywords=Type 2 diabetes, insulin resistance, mitochondrial dysfunction, mitochondrial biogenesis, oxidative capacity | ||
|mipnetlab=ES Barcelona Garcia-Roves PM, SE_Stockholm_Morein T | |mipnetlab=ES Barcelona Garcia-Roves PM, SE_Stockholm_Morein T | ||
}} | }} |
Revision as of 13:10, 12 June 2012
Holmstroem MH, Iglesias-Gutierrez E, Zierath JR, Garcia-Roves PM (2012) Tissue-specific control of mitochondrial respiration in obesity-related insulin resistance and diabetes Am J Physiol Endocrinol Metab 302: E731-E739. |
Holmstroem MH, Iglesias-Gutierrez E, Zierath JR, Garcia-Roves PM (2012) Am J Physiol Endocrinol Metab
Abstract: The tissue-specific role of mitochondrial respiratory capacity in the development of insulin resistance and type 2 diabetes is unclear. We determined mitochondrial function in glycolytic and oxidative skeletal muscle and liver from lean (+/?) and obese diabetic (db/db) mice. In lean mice, the mitochondrial respiration pattern differed between tissues. Tissue-specific mitochondrial profiles were then compared between lean and db/db mice. In liver, mitochondrial respiratory capacity and protein expression, including peroxisome proliferator-activated receptor γ coactivator-1 α (PGC-1α), was decreased in db/db mice, consistent with increased mitochondrial fission. In glycolytic muscle, mitochondrial respiration, as well as protein and mRNA expression of mitochondrial markers, was increased in db/db mice, suggesting increased mitochondrial content and fatty acid oxidation capacity. In oxidative muscle, mitochondrial Complex I function and PGC-1α and mitochondrial transcription factor A (TFAM) protein level were decreased in db/db mice, along with increased level of proteins related to mitochondrial dynamics. In conclusion, mitochondrial respiratory performance is under the control of tissue-specific mechanisms and is not uniformly altered in response to obesity. Furthermore, insulin resistance in glycolytic skeletal muscle can develop by a mechanism independent of mitochondrial dysfunction. Conversely, insulin resistance in liver and oxidative skeletal muscle from db/db mice is coincident with mitochondrial dysfunction. • Keywords: Type 2 diabetes, insulin resistance, mitochondrial dysfunction, mitochondrial biogenesis, oxidative capacity
• O2k-Network Lab: ES Barcelona Garcia-Roves PM, SE_Stockholm_Morein T
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., 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: Skeletal muscle, Hepatocyte; Liver"Hepatocyte; Liver" 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.
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.
HRR: Oxygraph-2k