Medical Advisor Journals

Tuesday, May 23, 2017

Thyroid hormone: Triiodothyronine stimulates glucose transport in bone cells

Kyle J. Norton(Scholar and Master of Nutrients, all right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published on line, including world wide health, ezine articles, article base, healthblogs, selfgrowth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
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Some articles have been used as references in medical research, such as international journal Pharma and Bio science, ISSN 0975-6299.

Thyroid hormone

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 T3and T4, deficiency of Iodine can lead to enlarge thyroid grand and goitre.

Thyroid hormone: Triiodothyronine stimulates glucose transport in bone cells

In the study to evaluate whether 3,3',5-triiodo-l-thyronine (T₃) stimulates the uptake of glucose in osteoblastic cells, PyMS (a cell line derived from rat bone) cells were kept in serum-free culture medium and treated with T₃, found that T₃ did not influence the cell number but slightly (1.3-fold) increased the protein content of the cell cultures. 2DG ([1-¹⁴C]-2-deoxy-D: -glucose)uptake was low in serum-deprived cell cultures and was increased by T₃ (up to 2.5-fold at 1 nmol l⁻¹ after 4 days) in a dose- and time-dependent manner. Triiodothyronine at 1 nmol l⁻¹ increased GLUT1 and GLUT3 abundance in membranes. Therefore, increased glucose uptake induced by T₃ in osteoblasts may be mediated by the known high-affinity glucose transporters GLUT1 and GLUT3(13).

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Sources
(13) http://www.ncbi.nlm.nih.gov/pubmed/22258767

Monday, May 22, 2017

Thyroid hormone and skeletal growth

Thyroid hormone and skeletal growth

Understanding how bone growth is regulated by hormonal and mechanical factors during early growth periods is important for optimizing the attainment of peak bonemass to prevent or postpone the occurrence of fragility fractures later in life. According to the study by Musculoskeletal Disease Center, Loma Linda VA HealthCare System , there is an important period prior to puberty when the effects of GH are surprisingly small and TH plays a critical role in the regulation of skeletal growth. Daily administration of T3/T4 during days 5 to 14, the time when serum levels of T3 increase rapidly in mice, rescued the skeletal deficit in TH-deficient mice but not in mice lacking both TH and GH. However, treatment of double-mutant mice with both GH and T3/T4 rescued the bone density deficit. Increased body fat in the TH-deficient as well as TH/GH double-mutant mice was rescued by T3/T4 treatment during days 5 to 14(12).

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Sources
(12) http://www.ncbi.nlm.nih.gov/pubmed/22513648

Sunday, May 21, 2017

Thyroid hormone stimulates protein synthesis

Thyroid hormone stimulates protein synthesis

According to the study by North Shore-Long Island Jewish Health System, Thyroid hormones affect cardiac growth and phenotype; however, the mechanisms by which the hormones induce cardiomyocyte hypertrophy remain uncharacterized. Tri-iodo-L-thyronine (T3) treatment of cultured cardiomyocytes for 24 h resulted in a 41 +/- 5% (p < 0.001) increase in [(3)H]leucine incorporation into total cellular protein. This response was abrogated by the phosphatidylinositol 3-kinase (PI3K) inhibitor, wortmannin. Co-immunoprecipitation studies showed a direct interaction of cytosol-localized thyroid hormone receptor TRalpha1 and the p85alpha subunit of PI3K. T3 treatment rapidly increased PI3K activity by 52 +/- 3% (p < 0.005)(11).

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Sources
(11) http://www.ncbi.nlm.nih.gov/pubmed/16717100

Saturday, May 20, 2017

Thyroid hormone; Thyroid disease in pregnancy and childhood

Thyroid hormone Thyroid disease in pregnancy and childhood

Thyroid function in pregnancy is characterised by a T4 surge at 12 weeks declining thereafter. Serum thyroid hormone concentrations fall in the second half of pregnancy. According to the study by Cardiff University School of Medicine, Fetal brain development depends on T4 transport into the fetus which in turn depends on sufficient maternal iodine supply. There is current concern that adequate iodisation is not present in large parts of Europe. There is increasing evidence that thyroid autoimmunity is associated with fetal loss but the mechanism is unclear and therapy requires carefully conducted studies. While hyperthyroidism in pregnancy is uncommon, effects on both mother and child are critical if untreated. Screening for thyroid function in early pregnancy and levothyroxine intervention therapy for maternal subclinical hypothyroidism should be considered but evidence is awaited. Screening for both thyroid dysfunction and thyroid antibodies ideally at a preconception clinic but certainly in early gestation is recommended(10)

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(10) http://www.ncbi.nlm.nih.gov/pubmed/15988403

Friday, May 19, 2017

Thyroid hormone: Thyroid disease in pregnancy

Thyroid hormone: Thyroid disease in pregnancy

Thyroid diseases are common in women of childbearing age and it is well known that untreated thyroid disturbances result in an increased rate of adverse events, particularly miscarriage, preterm birth and gestational hypertension. According to the study by Division of Endocrinology, "V. Fazzi" Hospital, Lecce, overt dysfunctions (hyper- or hypothyroidism) have deleterious effects on pregnancy, subclinical disease, namely subclinical hypothyroidism, has still to be conclusively defined as a risk factor for adverse outcomes. Additionally, other conditions, such as isolated hypothyroxinemia and thyroid autoimmunity in euthyroidism, are still clouded with uncertainty regarding the need for substitutive treatment(9).

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Sources
(9) http://www.ncbi.nlm.nih.gov/pubmed/22115167

Thursday, May 18, 2017

Thyroid hormone and Delayed development

Thyroid hormone and Delayed development

In the study to investigate the phenotype of TTR(Transthyretin (TTR) is a TH distributor protein in the circulatory system and is the only TH distributor protein synthesised in the central nervous system) null mice during development by The University of Melbourne, showed that TTR null mice also displayed a delayed suckling-to-weaning transition, decreased muscle mass, delayed growth and retarded longitudinal bone growth. In addition, ileums from postnatal day 0 (P0) TTR null mice displayed disordered architecture and contained fewer goblet cells than wild type. Protein concentrations in cerebrospinal fluid from P0 and P14 TTR null mice were higher than in age-matched wild type mice(8).

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Sources
(8) http://www.ncbi.nlm.nih.gov/pubmed/23092911

Wednesday, May 17, 2017

Thyroid hormone and the cardiovascular system

Thyroid hormone and the cardiovascular system

Increased or reduced action of thyroid hormone on certain molecular pathways in the heart and vasculature causes relevant cardiovascular derangements. It is well established that overt hyperthyroidism induces a hyperdynamic cardiovascularstate (high cardiac output with low systemic vascular resistance), which is associated with a faster heart rate, enhanced left ventricular (LV) systolic and diastolic function, and increased prevalence of supraventricular tachyarrhythmias - namely, atrial fibrillation - whereas overt hypothyroidism is characterized by the opposite changes.In the study of Effects of thyroid hormone on the cardiovascular system, researchers suggested that administration of thyroid hormone or its analogue 3,5-diiodothyropropionic acid greatly benefits these patients, highlighting the potential role of thyroid hormone treatment in patients with acute and chronic cardiovascular disease(7).

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Sources
(7) http://www.ncbi.nlm.nih.gov/pubmed/14749496