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Baekkerud 2019 Cardiovasc Toxicol
Additional label Labels  + , 2019-04  +
Coupling states LEAK  + , OXPHOS  +
Diseases Diabetes  +
Has abstract Both human and animal studies have shown m
Both human and animal studies have shown mitochondrial and contractile dysfunction in hearts of type 2 diabetes mellitus (T2DM). Exercise training has shown positive effects on cardiac function, but its effect on the mitochondria have been insufficiently explored. The aim of this study was to assess the effect of exercise training on mitochondrial function in T2DM hearts. We divided T2DM mice (db/db) into a sedentary and an interval training group at 8 weeks of age and used heterozygote db/+ as controls. After 8 weeks of training, we evaluated mitochondrial structure and function, as well as the levels of mRNA and proteins involved in key metabolic processes from the left ventricle. db/db animals showed decreased oxidative phosphorylation capacity and fragmented mitochondria. Mitochondrial respiration showed a blunted response to Ca<sup>2+</sup> along with reduced protein levels of the mitochondrial calcium uniporter. Exercise training ameliorated the reduced oxidative phosphorylation in complex (C) I + II, CII and CIV, but not CI or Ca<sup>2+</sup> response. Mitochondrial fragmentation was partially restored. mRNA levels of isocitrate, succinate and oxoglutarate dehydrogenase were increased in db/db mice and normalized by exercise training. Exercise training induced an upregulation of two transcripts of peroxisome proliferator activated receptor gamma coactivator 1 alpha (PGC1α1 and PGC1α4) previously linked to endurance training adaptations and strength training adaptations, respectively. The T2DM heart showed mitochondrial dysfunction at multiple levels and exercise training ameliorated some, but not all mitochondrial dysfunctions.
e, but not all mitochondrial dysfunctions.  +
Has editor [[Plangger M]]  +
Has info [https://www.ncbi.nlm.nih.gov/pubmed/30927207 PMID: 30927207]  +
Has publicationkeywords Diabetes  + , Diabetic cardiomyopathy  + , Exercise training  + , Mitochondria  +
Has title Bækkerud FH, Salerno S, Ceriotti P, Morlan
Bækkerud FH, Salerno S, Ceriotti P, Morland C, Storm-Mathisen J, Bergersen LH, Høydal MA, Catalucci D, Stølen TO (2019) High intensity interval training ameliorates mitochondrial dysfunction in the left ventricle of mice with type 2 diabetes. Cardiovasc Toxicol 19:422-31.
2 diabetes. Cardiovasc Toxicol 19:422-31.  +
Instrument and method Oxygraph-2k  +
Mammal and model Mouse  +
MiP area Respiration  + , Exercise physiology;nutrition;life style  +
Pathways N  + , S  + , CIV  + , NS  + , ROX  +
Preparation Permeabilized tissue  +
Tissue and cell Heart  +
Was published by MiPNetLab NO Trondheim Rognmo O +
Was published in journal Cardiovasc Toxicol +
Was published in year 2019  +
Was written by Baekkerud FH + , Salerno S + , Ceriotti P + , Morland C + , Storm-Mathisen J + , Bergersen LH + , Hoeydal MA + , Catalucci D + , Stoelen TO +
Categories Publications
Modification date
"Modification date" is a predefined property that corresponds to the date of the last modification of a subject and is provided by Semantic MediaWiki.
13:21:53, 15 October 2019  +
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