Alterations in cardiac contractility and gene expression during low-T3 syndrome: prevention with T3

Area of Science:

• Endocrinology
• Cardiovascular Physiology
• Molecular Biology

Background:

• Low-triiodothyronine (T3) syndrome, characterized by decreased serum T3, has unclear impacts on thyroid hormone-responsive genes and function.
• Chronic calorie deprivation serves as a model to investigate the low-T3 syndrome's effects on cardiac myocytes.

Purpose of the Study:

• To assess the impact of low-T3 syndrome on cardiac myocyte gene expression and contractility in rats.
• To determine if T3 supplementation can mitigate the cardiac effects of calorie restriction.

Main Methods:

• Young adult female rats were subjected to 50% calorie restriction for 28 days to induce low-T3 syndrome.
• Cardiac contractility was measured, alongside sarcoplasmic reticulum calcium ATPase 2 (SERCA2) and myosin heavy chain (MHC) isoform mRNA levels.
• Groups included control, calorie-restricted (low T3), and calorie-restricted with T3 treatment.

Main Results:

• Calorie-restricted rats exhibited significantly impaired cardiac contraction and relaxation rates.
• Left ventricular relaxation time increased, and SERCA2 mRNA levels decreased in low-T3 rats.
• T3 supplementation normalized cardiac function and SERCA2 mRNA levels, while also affecting MHC isoform expression.

Conclusions:

• The low-T3 syndrome significantly impairs cardiac contractility and alters cardiac gene expression, as demonstrated in calorie-restricted rats.
• T3 supplementation effectively reverses the detrimental cardiac effects of calorie restriction, highlighting the role of T3 in adaptation.
• These findings suggest the low-T3 syndrome is a key factor in the pathophysiology of calorie restriction's impact on the heart.