The thyroid hormones, thyroxine (T4) and triiodothyronine (T3), are tyrosine-based hormones produced by the thyroid gland primarily responsible for regulation of metabolism. An important component in the synthesis of thyroid hormones is iodine. The major form of thyroid hormone in the blood is thyroxine (T4), which has a longer half life than T3.
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Background
Triiodothyronine (T3) is a critical hormone produced by the thyroid gland, a small, butterfly-shaped organ located in the front of the neck. The synthesis of T3 occurs through the conversion of thyroxine (T4), the main hormone secreted by the thyroid gland. This conversion process is facilitated by enzymes called deiodinases. T4 is relatively inactive and serves as a precursor hormone, while T3 is the biologically active form responsible for exerting its effects on tissues and cells throughout the body.
Figure 1. TH biosynthesis and regulation. (Source: Somasundaram, N. P. et al., 2020)
T3 influences a wide range of bodily functions, including metabolism, growth and development, body temperature regulation, heart rate, and cognitive function. It acts as a molecular signal, binding to specific receptors within cells and modulating gene expression. This intricate mechanism of action allows T3 to regulate metabolic pathways, cellular growth, and differentiation. The transportation of T3 within the bloodstream occurs with the help of carrier proteins, ensuring its efficient distribution to target tissues and organs. Once inside the cells, T3 binds to nuclear receptors, initiating a cascade of events that regulate various metabolic processes and provide essential energy for cellular function.
Triiodothyronine (T3) [BSA] refers to a conjugate of the hormone T3 and BSA (bovine serum albumin). BSA is a protein commonly used as a carrier molecule. The conjugation of T3 with BSA creates a stable form of T3 that can be utilized as a molecular tool in various biochemical and immunological applications. This conjugate has been employed in research settings to study the effects and mechanisms of T3 on cellular processes. Additionally, T3 [BSA] has found utility in chemical assays, drug development, and other scientific investigations.
Alternative Names
T3 [BSA] Triiodothyronine (T3), BSA-Conjugated T3, BSA-Conjugated
References
1. Somasundaram N P, et al. Thyroid Disorders. Sri Lanka Journal of Diabetes Endocrinology and Metabolism. 2020, 10(1).
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References
Triiodothyronine and breast cancer
World Journal of Clinical Oncology
Authors: De Sibio, M. T., de Oliveira, M., Moretto, F. C. F., Olimpio, R. M. C., Conde, S. J., Luvizon, A. C., Nogueira, C. R.
The thyroid hormones (THs), triiodothyronine (T3) and thyroxine (T4), are essential for survival; they are involved in the processes of development, growth, and metabolism. In addition to hyperthyroidism or hypothyroidism, THs are involved in other diseases. The role of THs in the development and differentiation of mammary epithelium is well established; however, their specific role in the pathogenesis of breast cancer (BC) is controversial. Steroid hormones affect many human cancers and the abnormal responsiveness of the mammary epithelial cells to estradiol (E2) in particular is known to be an important cause for the development and progression of BC. The proliferative effect of T3 has been demonstrated in various types of cancer. In BC cell lines, T3 may foster the conditions for tumor proliferation and increase the effect of cell proliferation by E2; thus, T3 may play a role in the development and progression of BC. Studies show that T3 has effects similar to E2 in BC cell lines. Despite controversy regarding the relationship between thyroid disturbances and the incidence of BC, studies show that thyroid status may influence the development of tumor, proliferation and metastasis.
Triiodothyronine levels for risk stratification of patients with chronic heart failure
The American Journal of Medicine
Authors: Pingitore, A., Landi, P., Taddei, M. C., Ripoli, A., L’Abbate, A., Iervasi, G.
Purpose We sought to explore the use of triiodothyronine (T3) concentrations as an adjunct to clinical and functional parameters when estimating prognosis in patients with chronic heart failure. Methods We enrolled 281 patients with postischemic (n = 153) or nonischemic (n = 128) dilated cardiomyopathy. Total and free T3 concentrations, and traditional clinical and functional cardiac parameters, were measured 2 to 5 days after hospital admission. A multivariate model was utilized to predict all-cause and cardiac mortality. Results All-cause mortality was 23% (n = 64) after a mean (±SD) of 12 ± 7 months of follow-up; 47 (73%) of the patients died from cardiac causes. The mean ejection fraction was lower in those patients who died than in those who survived (26% ± 8% vs. 31% ± 8%, P < 0.001), as were levels of total T3 (1.0 ± 0.4 nmol/L vs. 1.3 ± 0.3 nmol/L, P < 0.001) and free T3 (3.2 ± 1.4 pmol/L vs. 3.7 ± 1.0 pmol/L, P < 0.001). In a multivariate model, ejection fraction (odds ratio [OR] = 2.0 per 10% decrease; 95% confidence interval [CI]: 1.4 to 2.8 per 10% decrease; P < 0.001) and total T3 level (OR = 0.3 per 1-nmol/L increase; 95% CI: 0.1 to 0.5 per 1-nmol/L increase; P < 0.001) were the only independent predictors of all-cause mortality. In an alternative model using free T3 levels, ejection fraction (OR = 1.9; 95% CI: 1.4 to 2.7; P < 0.001) and free T3 level (OR = 0.6 per 1 pmol/L; 95% CI: 0.5 to 0.8 per 1 pmol/L; P <0.02) were associated with all-cause mortality. When we considered cardiac mortality alone, male sex (OR = 3.5; 95% CI: 1.7 to 13; P < 0.04), ejection fraction (OR = 1.7; 95% CI: 1.2 to 2.5; P < 0.006), and total T3 level (OR = 0.3; 95% CI: 0.2 to 0.7; P < 0.002) were independent predictors with the multivariate model. Conclusion Low T3 levels are an independent predictor of mortality in patients with chronic heart failure, adding prognostic information to conventional clinical and functional cardiac parameters.
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Figure 1. TH biosynthesis and regulation.
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