Adenosine monophosphate-activated protein kinase activation, substrate transporter translocation, and metabolism in the contracting hyperthyroid rat heart.

Endocrinology
Lisa C HeatherKieran Clarke

Abstract

Thyroid hormones can modify cardiac metabolism via multiple molecular mechanisms, yet their integrated effect on overall substrate metabolism is poorly understood. Here we determined the effect of hyperthyroidism on substrate metabolism in the isolated, perfused, contracting rat heart. Male Wistar rats were injected for 7 d with T(3) (0.2 mg/kg x d ip). Plasma free fatty acids increased by 97%, heart weights increased by 33%, and cardiac rate pressure product, an indicator of contractile function, increased by 33% in hyperthyroid rats. Insulin-stimulated glycolytic rates and lactate efflux rates were increased by 33% in hyperthyroid rat hearts, mediated by an increased insulin-stimulated translocation of the glucose transporter GLUT4 to the sarcolemma. This was accompanied by a 70% increase in phosphorylated AMP-activated protein kinase (AMPK) and a 100% increase in phosphorylated acetyl CoA carboxylase, confirming downstream signaling from AMPK. Fatty acid oxidation rates increased in direct proportion to the increased heart weight and rate pressure product in the hyperthyroid heart, mediated by synchronized changes in mitochondrial enzymes and respiration. Protein levels of the fatty acid transporter, fatty acid translocase (...Continue Reading

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Citations

May 10, 2012·Molecular Endocrinology·E Sandra ChocronJames D Lechleiter
Sep 5, 2013·Thyroid : Official Journal of the American Thyroid Association·Antonio C BiancoUNKNOWN American Thyroid Association Task Force on Approaches and Strategies to Investigate Thyroid Hormone Economy and Action
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Jun 4, 2010·Endocrine Reviews·Panayota MitrouGeorge Dimitriadis
Jan 15, 2015·American Journal of Physiology. Renal Physiology·David TaylorAnne-Marie L Seymour

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