Difference between revisions of "Holmstroem 2012 Am J Physiol Endocrinol Metab"
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|area=Respiration, mt-Biogenesis; mt-density, Genetic knockout; overexpression, Comparative MiP; environmental MiP, Exercise physiology; nutrition; life style, | |area=Respiration, mt-Biogenesis;mt-density, Genetic knockout;overexpression, Comparative MiP;environmental MiP, Exercise physiology;nutrition;life style, mt-Medicine | ||
|organism=Mouse | |organism=Mouse | ||
|tissues=Skeletal muscle, Liver | |tissues=Skeletal muscle, Liver |
Revision as of 17:25, 11 August 2013
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 ฮณ coactivator-1 ฮฑ (PGC-1ฮฑ), 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-1ฮฑ 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. โข Keywords: Type 2 diabetes, insulin resistance, mitochondrial dysfunction, mitochondrial biogenesis, oxidative capacity
โข O2k-Network Lab: ES Barcelona Garcia-Roves PM, SE_Stockholm_Morein T, ES Barcelona IDIBAPS Hospital Clinic
Labels: MiParea: Respiration, mt-Biogenesis;mt-density, Genetic knockout;overexpression, Comparative MiP;environmental MiP, Exercise physiology;nutrition;life style, mt-Medicine
Pathology: Diabetes 2"Diabetes 2" is not in the list (Aging;senescence, Alzheimer's, Autism, Cancer, Cardiovascular, COPD, Diabetes, Inherited, Infectious, Myopathy, ...) of allowed values for the "Diseases" property., Obesity
Organism: Mouse Tissue;cell: Skeletal muscle, Liver
HRR: Oxygraph-2k