Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Difference between revisions of "Holmstroem 2012 Am J Physiol Endocrinol Metab"

From Bioblast
Line 12: Line 12:
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|injuries=Mitochondrial Disease; Degenerative Disease and Defect, Genetic Defect; Knockdown; Overexpression
|injuries=Mitochondrial Disease; Degenerative Disease and Defect, Genetic Defect; Knockdown; Overexpression
|diseases=Diabetes
|organism=Mouse
|organism=Mouse
|tissues=Skeletal muscle, Liver
|tissues=Skeletal muscle, Liver
|topics=Mitochondrial Biogenesis; Mitochondrial Density
|topics=Mitochondrial Biogenesis; Mitochondrial Density
}}
}}

Revision as of 16:21, 14 March 2013

Publications in the MiPMap
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.

» PMID:22252943

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, ES Barcelona IDIBAPS Hospital Clinic


Labels: Pathology: Diabetes  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, Liver 


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