Abstract
Objective The main purpose of this study was to explore the relationships between serca2a, Ryr2, adipokines, and the left ventricular function in the subclinical hypothyroidism with different TSH levels and to determine the impact of L-T4 treatment on these indexes. Methods Sixty-five male Wistar rats were randomly divided into five groups: control group; sHT A, B, and C group; and sHT + T4 group. The sHT rats were induced by methimazole (MMI), and the sHT + T4 rats were administered with L-T4 treatment after 8 weeks of MMI administration. Serum TT4, TSH, APN, chemerin, and TNF-α were detected by radioimmunoassay kits and ELISA kits; left ventricular function was measured by PowerLab system via subclavian artery catheter. The expression of Serca2a, Ryr2, APN, chemerin, and TNF-α were detected by RT-PCR, Western blot, and immunohistochemistry. Results The sHT groups had significantly higher TSH, chemerin, and TNF-α and lower Serca2a, Ryr2, and APN. The left ventricular pressure and heart rate in sHT groups were significantly lower in control and sHT + T4 group. Histopathological examination revealed the pathological changes in the sHT rats' heart. L-T4 administration reduced TSH level and improved left ventricular function. Conclusions TSH can impair left ventricular function by regulating several factors, and L-T4 treatment ameliorates it in sHT rats.
Highlights
Subclinical hypothyroidism is a common thyroid dysfunction, which has a milder thyroid-stimulating hormone (TSH) and a normal range of serum thyroid hormone level [1]
We found that the Subclinical hypothyroidism (sHT) rats experienced a stunted growth pattern compared with the control rats, and L-T4 treatment improved the body weights of sHT rats (Figure 1)
Alterations in increased serum levels of chemerin and TNF-α in sHT A, B, and C coincided with the trend of TSH, and LT4 treatment could decrease these changes in the sHT + T4
Summary
Subclinical hypothyroidism (sHT) is a common thyroid dysfunction, which has a milder thyroid-stimulating hormone (TSH) and a normal range of serum thyroid hormone level [1]. It is generally known that TSH is one of the important factors of cardiovascular disease in sHT, and increasing studies show that dysfunction of cardiac systolic and diastolic is the common abnormality in sHT [2, 3], especially left ventricular diastolic function impaired. Previous studies demonstrate that sarcoplasmic/endoplasmic reticulum Ca2 + ATPase 2a (Serca2a) and ryanodine receptor (Ryr2) have significant roles for abnormalities of cardiac systolic and diastolic functions [4], but these changes in sHT with different TSH levels are still unclear. Our previous study found that the Serca2a activity can be inhibited by prolonged exposure to elevated TSH levels by binding to TSHR [5] and the changes independent of thyroid hormone, but which hardly represent physiological status in vivo. Serca2a and Ryr2’s activity and expression are worth studying in sHT
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