The Effects of Thyroid hormone (3)

 Thyroid hormone (triiodothyronine (T3) and thyroxine (T4)), produced by the thyroid gland, plays an important role in regulation of metabolism, including directly boosts energy metabolism and triggers rapid protein synthesis and regulates mitochondrial gene transcription, etc. Iodine is necessary for the production of T₃ and T₄, deficiency of Iodine can lead to enlarge thyroid grand and goitre.
21. Analysis of serum adiponectin, resistin and leptin levels in children and adolescents with autoimmune thyroid diseases
Leptin, adiponectin and resistin, mainly produced by adipocytes, play a major role in body weight regulation. In the study  to analyze the levels of leptin, adiponectin and resistin in children with untreated Graves' disease, subclinical hypothyroidism in Hashimoto's thyroiditis and in children with simple goiter, researchers at the Medical University of Białystok, showed that disturbances in thyroid hormones in thyroid diseases have an essential effect on the levels of adiponectin and resistin released by adipose tissue(21).

22. Serum antibodies against three eye muscle antigens and the connective tissue antigen collagen XIII in patients with Graves' disease
In the study cohort consisted of patients with Graves' hyperthyroidism with and without ophthalmopathy, controls patients with other thyroid or other autoimmune disorders and healthy subjects, by The University of Sydney, Nepean Hospital, found that prevalences of positive antibody tests to calsequestrin (75.0%) and collagen XIII (43.8%) were significantly greater in Graves' disease (GD) patients with ophthalmopathy than in healthy subjects, whereas modest significance was demonstrated with antibodies against Fp, but not G2s. Significantly greater serum levels of antibodies against calsequestrin, G2s, and collagen XIII, but not Fp, were found in GD patients with ophthalmopathy compared to control patients without eye disease and healthy subjects(22).

23. Serum levels of thyroid hormones in liver diseases
In the study to measure the concentrations of thyroid hormones and thyrotropin (TSH) in sera of clinically euthyroid patients with various liver diseases and compared with normal controls, found that the marked alterations of peripheral conversion of thyroxine (T4) to rT3 or T3 may be found only in a state of decompensated liver cirrhosis among the various liver diseases(23).

24. Thyroid hormones and TSH in chronic active hepatitis
The study of a  total and free circulating thyroid hormones, rT3, TBG and TSH behaviour on chronic liver disease in 11 subjects with cirrhosis of the liver with ascites(C.E.) and in 6 subjects with chronic active hepatitis (E.C.A.) in comparison with 15 healthy and euthyroid controls, indicated that serum T3,FT3,T4 and FT4 levels were decreased significantly and serum rT3 values increased significantly both in the subjects with C.E. and in patients with E.C.A. Moreover no significantly changes of TSH and TBG levels has been found in 3 groups studied. These data suggest that the alteration of circulating thyroid hormones in chronic liver disease, may represent a compensatory way of reducing the patient's metabolic requirements(24).

25. Transient Willis-Ekbom's disease (restless legs syndrome) during pregnancy
Willis-Ekbom's disease (WED), formerly called restless legs syndrome, is more common in pregnant than in non-pregnant women, implying that the physiological and biochemical changes during pregnancy influence its development. Researchers at the Faculdade de Medicina de Jundiaí, Rua Francisco Telles, found that during pregnancy, the activity of the thyroid axis is enhanced to meet the increased demand for thyroid hormones during this state. Dopamine is a neuroendocrine hormone that diminishes the levels of thyrotropin and consequently of thyroxine, and one of the roles of the dopaminergic system is to counteract the activity of thyroid hormones. When the activity of dopamine is not sufficient to modulate thyroid hormones, WED may occur(25).

26. Maternal hyperthyroidism and the pattern of expression of cardiac renin-angiotensin system components
Changes in perinatal environment can lead to physiological, morphological, or metabolic alterations in adult life. In the study to evaluate the effect of maternal hyperthyroidism on cardiac RAS components in pups during development, showed that Maternal hyperthyroidism is associated with alterations in fetal development and altered pattern of expression in RAS components, which in addition to cardiac hypertrophy observed on GD20 may represent an important predisposing factor to cardiovascular diseases in adult life(26).

27. Vitamin E management of oxidative damage-linked dysfunctions of hyperthyroid tissues
Thyroid hormones affect growth, development, and metabolism of vertebrates, and are considered the major regulators of their homeostasis and elevated circulating levels of thyroid hormones are associated with modifications in the whole organism (weight loss and increased metabolism and temperature) and in several body regions. Indeed, tachycardia, atrial arrhythmias, heart failure, muscle weakness and wasting, bone mass loss, and hepatobiliary complications are commonly found in hyperthyroid animals and humans. In the study of vitamin E and oxdative linked dysfunctions of huperthroid tissues, showed that vitamin E has a primary function to destroy peroxyl radicals, thus protecting polyunsaturated fatty acids biological membranes from oxidative damage. However, results are also available indicating that protective vitamin E effects against oxidative damage can be obtained even through different mechanisms(27).

28. Progesterone Therapy increases Free Thyroxine Levels
Thyroid hormones and progesterone both influence core temperature, metabolism and are crucial during pregnancy. In the study to discover whether progesterone therapy caused changes in thyroid physiology compared with placebo, researchers at the University of British Columbia and Vancouver Coastal Health Research Institute, found that progesterone caused a significant FreeT4 increase that was discovered during this randomized controlled VMS trial. The clinical importance of this increased FreeT4 level remains to be documented(28).

29.  Resistance to Thyroid Hormone and Episodes of Thyrotoxicosis
In the study of a 44-year-old Japanese woman with resistance to thyroid hormone, which was confirmed by the P453A mutation in the thyroid hormone receptor ß (TRß) gene, showed a slight elevation of the basal levels of thyroid hormones, which indicated that her pituitary resistance to thyroid hormone was mild. She experienced a slight exacerbation of hyperthyroxinemia concomitant with TSH suppression, showed that Mild pituitary resistance to thyroid hormone can be overcome by slight exacerbation of hyperthyroxinemia during mild thyrotoxicosis. When pituitary resistance is severe and TSH is not suppressed, thyrotoxicosis may be overlooked(29).

30. Thyroid hormone receptors in health and disease
Thyroid hormones (TH) play a key role in energy homeostasis throughout life. In the study conducted by Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands, found that thyroid hormone has to be transported into the cell, where it can bind to the thyroid hormone receptor (TR) in the nucleus to exert its effect on cellular gene-transcription. Mutations in both the THRA and THRB gene have been described, each inducing a characteristic phenotype clearly showing the selective effect of an excess or shortage of thyroid hormone in specific TRα and TRβ regulated organs. Profound changes in thyroid hormone metabolism occur during a variety of non-thyroidal illnesses, each associated with reduced TR expression in a tissue-specific manner(30).
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Sources
(21) http://www.ncbi.nlm.nih.gov/pubmed/20583542
(22) http://www.ncbi.nlm.nih.gov/pubmed/17042681
(23) http://www.ncbi.nlm.nih.gov/pubmed/7357737
(24) http://www.ncbi.nlm.nih.gov/pubmed/6518098
(25) http://www.ncbi.nlm.nih.gov/pubmed/23257652
(26) http://www.ncbi.nlm.nih.gov/pubmed/23257210
(27) http://www.ncbi.nlm.nih.gov/pubmed/23255045
(28) http://www.ncbi.nlm.nih.gov/pubmed/23252963
(29) http://www.ncbi.nlm.nih.gov/pubmed/23240983
(30) http://www.ncbi.nlm.nih.gov/pubmed/23235186