title: Hyperthyroidism causes cardiac dysfunction by mitochondrial impairment and energy depletion.
abstract: This study elucidates the role of metabolic remodeling in cardiac dysfunction induced by hyperthyroidism. Cardiac hypertrophy, structural remodeling, and expression of the genes associated with fatty acid metabolism were examined in rats treated with triiodothyronine (T3) alone (8 μg/100 g body weight (BW), i.p.) for 15 days or along with a peroxisome proliferator-activated receptor alpha agonist bezafibrate (Bzf; 30 μg/100 g BW, oral) and were found to improve in the Bzf co-treated condition. Ultrastructure of mitochondria was damaged in T3-treated rat heart, which was prevented by Bzf co-administration. Hyperthyroidism-induced oxidative stress, reduction in cytochrome c oxidase activity, and myocardial ATP concentration were also significantly checked by Bzf. Heart function studied at different time points during the course of T3 treatment shows an initial improvement and then a gradual but progressive decline with time, which is prevented by Bzf co-treatment. In summary, the results demonstrate that hyperthyroidism inflicts structural and functional damage to mitochondria, leading to energy depletion and cardiac dysfunction.
authors: Cell Biology and Physiology Division, CSIR-Indian Institute of Chemical Biology, 4, Raja S. C. Mullick Road, Kolkata 700032, India.
authors: Sangeeta
authors: S
authors: Maity
authors: Dipak
authors: D
authors: Kar
authors: Kakali
authors: K
authors: De
authors: Vivek
authors: V
authors: Chander
authors: Arun
authors: A
authors: Bandyopadhyay
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001629:Bezafibrate / Q000494:pharmacology; D006332:Cardiomegaly / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology*; D004195:Disease Models, Animal; D015536:Down-Regulation; D003576:Electron Transport Complex IV / Q000378:metabolism; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology*; D005227:Fatty Acids / Q000378:metabolism; D005260:Female; D006980:Hyperthyroidism / Q000139:chemically induced / Q000150:complications* / Q000503:physiopathology*; D008929:Mitochondria, Heart / Q000187:drug effects / Q000502:physiology*; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D047493:PPAR alpha / Q000819:agonists / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D014284:Triiodothyronine / Q000009:adverse effects / Q000494:pharmacology
chemical_list: D005227:Fatty Acids; D047493:PPAR alpha; D017382:Reactive Oxygen Species; D014284:Triiodothyronine; D000255:Adenosine Triphosphate; D003576:Electron Transport Complex IV; D001629:Bezafibrate