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TSH Thyroid Stimulating Hormone (Thyrotropin)

TSH Thyroid Stimulating Hormone (Thyrotropin). Function. Controls the synthesis of Triiodothronine (T3 ) and Thyroxin (T4), which regulates body’s metabolic activities

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TSH Thyroid Stimulating Hormone (Thyrotropin)

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  1. TSHThyroid Stimulating Hormone(Thyrotropin)

  2. Function • Controls the synthesis of Triiodothronine (T3) and Thyroxin (T4), which regulates body’s metabolic activities • T3 increases ability to consume Oxygen for production of energy, increases Metabolic Rate, and stimulates rate of protein synthesis in the Body • T4 increases heart rate, BMR, & improves brain development.

  3. Biochemical Traits • Protein Hormone that is Glycosylated • (long chains of amino acids with sugar residues) • glycoprotein hormone which consists of two, noncovalently linked subunits: • Alpha subunit is common in the Anterior Pituitary Hormones (like LH & FSH) • Beta subunit provides binding specificity to TSH Receptor

  4. Biochemical Traits • Globular and water-soluble. • Binds to G-Protein Coupled Receptors (GPCR) • Integral membrane proteins • Two principal signal transduction pathways involved in G Protein Coupled Receptors: Camp and Phosphotidylinolsitol pathways. • TSH has a half life of about an hour • TSH peak excretion is between midnight and 4am

  5. How is it Produced • It is produced when the hypothalamus releases the tripeptide TRH (thyrotropin-releasing hormone) • TRH binds to G protein-coupled receptors in the cells of Anterior Pituitary, called Thyrotrophs. • This activates enzyme, Phospholipase C (PLC), which forms Diacylglycerol (DAG) & Inositol Triphosphate (Ip3). • DAG activates Protein Kinase C (PKC) which phosphorylates proteins and enzymes that stimulate synthesis of TSH

  6. Ip3 ions stimulate release of Ca+ ions from internal storage which leads to release of TSH by exocytosis. • TSH is released into bloodsream by Anterior Pituitary and is like a messenger sent to knock on the door of the Thyroid. • Binds to G protein-coupled receptor of the follicular cells, activating the G-alpha protein on the receptor, • This activates Adenylate Cyclase, which produces cAMP from ATP.

  7. Importance of TSH • Causes thyroid follicles to become active once it is bound to membrane receptors in thyroid: • Stimulates Iodide transport into cells • Stimulates thyroglobulin production • Stimulates Release of T3 and T4 • Increases proliferation of follicular cells (hyperplasia) • TSH concentration in blood determines how much thyroid hormone is released

  8. T3 & T4 • Triiodothyronine (T3): • More biologically active • High binding affinity to TH receptor, compared to T4. • Thyroxine (T4): • Higher binding affinity to plasma proteins • Immediately converted to T3 as it enters target cells.

  9. Regulation of TSH • Synthesis and Release: • Positively regulated by TRH • Negatively Regulated by T3: • T3 & T4, released by thyroid, transported into thyrotroph of Ant. Pituitary, where T4 is converted into T3 by enzyme Type-2-deiodinase as soon as it enters the cell. • When intracellular T3 increases, T3 will bind to TRH receptor to interact with transcription of GATA-2 and Pit-1 factors to stop transcription of TSH Alpha and Beta chains. (You do not need to know this step.)

  10. NegativeFeedback Loop

  11. Disorders and Problems

  12. Disorders and Problems Hashimotos Thyroiditis (Chronic Lymphocytic Thyroiditis)- most common cause of hypothyroidism.. Auto-immune disease attacking thyroid gland.Graves Disease- hereditary, autoimmune dieasease that also attacked the thyroid glad which can affect regulation of metabolism. Most common cause of hyperthyroidism. Goiter- non-cancerous enlargement of the thyroid gland. Most common cause is iodine deficiency. Symptom of hyperthyroidism.Thyroid Nodules- growths that form on or in thyroid gland, which are solid or fluid filled. Common causes are iodine deficiency and Hashimotos Disease. During Embryogenesis/Post Natal Development: can cause intellectual disabilities, impaired motor function and short stature.

  13. THE END

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