Difference between revisions of "Holmstroem 2012 Am J Physiol Endocrinol Metab"
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|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-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. | |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, | |mipnetlab=ES Barcelona Garcia-Roves PM, SE Stockholm Morein T | ||
}} | }} | ||
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Latest revision as of 13:11, 13 March 2015
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:E731-9. |
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: MiParea: Respiration, mt-Biogenesis;mt-density, Genetic knockout;overexpression, Comparative MiP;environmental MiP, Exercise physiology;nutrition;life style, mt-Medicine
Pathology: Diabetes, Obesity
Organism: Mouse Tissue;cell: Skeletal muscle, Liver
HRR: Oxygraph-2k