Myocardial mitochondrial and contractile function are preserved in mice lacking adiponectin

PloS One
Martin BraunHeiko Bugger

Abstract

Adiponectin deficiency leads to increased myocardial infarct size following ischemia reperfusion and to exaggerated cardiac hypertrophy following pressure overload, entities that are causally linked to mitochondrial dysfunction. In skeletal muscle, lack of adiponectin results in impaired mitochondrial function. Thus, it was our objective to investigate whether adiponectin deficiency impairs mitochondrial energetics in the heart. At 8 weeks of age, heart weight-to-body weight ratios were not different between adiponectin knockout (ADQ-/-) mice and wildtypes (WT). In isolated working hearts, cardiac output, aortic developed pressure and cardiac power were preserved in ADQ-/- mice. Rates of fatty acid oxidation, glucose oxidation and glycolysis were unchanged between groups. While myocardial oxygen consumption was slightly reduced (-24%) in ADQ-/- mice in isolated working hearts, rates of maximal ADP-stimulated mitochondrial oxygen consumption and ATP synthesis in saponin-permeabilized cardiac fibers were preserved in ADQ-/- mice with glutamate, pyruvate or palmitoyl-carnitine as a substrate. In addition, enzymatic activity of respiratory complexes I and II was unchanged between groups. Phosphorylation of AMP-activated protein kin...Continue Reading

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Citations

Nov 3, 2015·Canadian Journal of Physiology and Pharmacology·Christoph KoentgesHeiko Bugger
Oct 12, 2017·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·David N HuynhSylvie Marleau
Sep 3, 2020·Einstein·Mariela Carolina Santos CarballoMarcus Vinicius Henriques Brito
Oct 22, 2020·International Journal of Molecular Sciences·Sandra Feijóo-BandínFrancisca Lago

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Methods Mentioned

BETA
PCR
electron microscopy
acetylation

Software Mentioned

GraphPad Prism
GraphPad

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