Alterations in cardiac contractility and gene expression during the
low t3 syndrome: prevention with t3.
Katzeff, Harvey L., Saul R. Powell & Kaie Ojamaa.
Departments of Medicine and Surgery, North Shore University
Hospital-Cornell University Medical College
APStracts 4:0151E, 1997.
The Low T3 Syndrome is a metabolic response resulting in a decreased
serum triiodothyronine (T3) concentration which has uncertain effects
on thyroid hormone responsive gene expression and function. We
measured cardiac myocyte gene expression and cardiac contractility in
young female rats using chronic calorie deprivation as a model of the
Low T3 Syndrome. Sarcoplasmic reticulum calcium ATPase (SERCA2) and
myosin heavy chain (MHC) isoform mRNA content were measured following
28 days on a 50% calorie-restricted diet (Low T3) with and without T3
treatment (6 (g/kg//BW/day). The Low T3 animals had decreased maximal
rates of contraction (-13%; P<0.05) and relaxation (-18%; P<0.05)
compared with the Control and the T3 treated groups. There was a 21%
(P<0.05) increase in left ventricular (LV) relaxation time in the
Low T3 animals vs both Control and T3 treated groups. The LV content
of the SERCA2 mRNA was decreased significantly (37%) in the Low T3
rats and was increased (p<0.05) with T3 treatment vs Controls. The
(-MHC mRNA isoform decreased in the Low T3 animals was unchanged in
the T3 treated animals. T3 supplementation normalized both cardiac
function and phenotype of calorie-restricted animals suggesting a
role for the Low T3 syndrome in the pathophysiologic response to
calorie restriction.
Received 13 December 1996; accepted in final form 7 July 1997.
APS Manuscript Number E613-6.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 24 July 1997