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Departments of Medicine and Surgery, North Shore University Hospital, Manhasset 10030; and Cornell University Medical College, New York, New York 10021
The
low-T3 syndrome is a metabolic
response resulting in a decreased serum triiodothyronine
(T3) concentration that has
uncertain effects on thyroid hormone-responsive gene expression and
function. We measured cardiac myocyte gene expression and cardiac
contractility in young adult female rats using chronic calorie
deprivation as a model of the
low-T3 syndrome. Sarcoplasmic
reticulum calcium adenosinetriphosphatase (SERCA2) and myosin heavy
chain (MHC) isoform mRNA content were measured after 28 days on a 50%
calorie-restricted diet (low T3)
with or without T3 treatment (6 µg · kg body
wt
1 · day1).
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 but 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 pathophysiological response to calorie restriction.
triiodothyronine; energy expenditure; sarcoplasmic reticulum calcium-binding protein; myosin heavy chain; euthyroid sick syndrome; left ventricular function
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