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Healthy Effective Raw Steroids Powder L - Triiodothyronine T3 For Weight Loss

Categories Fat Burners Supplements
Brand Name: HongKong Blue Universal Co., Limited.
Model Number: 55-06-1
Certification: ISO 9001, USP, BP, GMP, HSE
Place of Origin: China
MOQ: 1 gram
Price: Negotiated
Payment Terms: Money Gram, Western Union, Bitcoin, Bank Transfer
Supply Ability: 1000 kg / Month
Delivery Time: Send out within 5h after payment confirmed, arrival in 5-7 work days
Packaging Details: Discreet and Safe Packages for Safe Shipping
T3 Name: L - Triiodothyronine
T3 Aliases: T3
T3 Key Words: L - Triiodothyronine T3 For Weight Loss
T3 Molecular formula: C15H12I3NO4
T3 Molecular Weight: 650.97
T3 Content: 99%
T3 CAS NO: 55-06-1
T3 Chemical name: 3,3',5-Triiodo-L-thyronine, sodium salt
T3 Boiling point: 205℃
T3 water-solubility: 4 M NH4OH in methanol: 125 g/5mL, clear, yellow-brown
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    Healthy Effective Raw Steroids Powder L - Triiodothyronine T3 For Weight Loss

    Healthy Effective Raw Steroids Powder L - Triiodothyronine T3 For Weight Loss


    1. Quick Details


    Skype: lily_3566

    My Email: lily@sinosteroids.com

    Name

    L - Triiodothyronine

    Aliases

    T3

    CAS No.

    55-06-1

    Purity

    99%

    Packaging

    Discreet and Safe Packages for Safe Shipping

    Certification

    ISO 9001, USP, BP, GMP, HSE

    MOQ

    1 gram

    Usage

    Fat Burners Supplements

    Markets

    Global


    2. L-Triiodothyronine(T3)



    As a thyroid hormone, L-Triiodothyronine, T3, affects almost every physiological process in the body, including growth and development,metabolism, body temperature, and heart rate.



    L-triiodothyronine, T3, regulates cellular growth rate, growth hormone production, the levels of nuclear T3 receptors via distinct dose response ranges in cultured GC cells.



    Evidence for mediation by the nuclear T3 receptor, L-Triiodothyronine (T3) stimulates growth of cultured GC cells by action early in the G1 period.



    Evidence for Cellular Binding Proteins and Conversion of T4 to T3, metabolism of L-Thyroxine (T4) and L-Triiodothyronine (T3) by Human Fibroblasts in Tissue Culture.




    3. L-Triiodothyronine(T3) Works



    As a true hormone, T3 effects on target tissues are roughly four times more potent than those of T4. Of the thyroid hormone that is produced, just about 20% is T3, whereas 80% is produced as T4. Roughly 85% of the circulating T3 is later formed in the liver and pituitary by removal of the iodine atom from the carbon atom number five of the outer ring of T4.



    In any case, the concentration of T3 in the human blood plasma is about one-fortieth that of T4. This is observed in fact because of the short half-life of T3, which is only 2.5 days. This compares with the half-life of T4, which is about 6.5 days.



    L-Triiodothyronine(T3) and L-Thyroxine(T4) is activated by thyroid-stimulating hormone (TSH), which is released from the pituitary gland. The pathway is part of a closed loop feedback process, elevated concentrations of T3, and T4 in the blood plasma inhibit the production of TSH in the pituitary gland. As concentrations of these hormones decrease, the pituitary gland increases production of TSH, and by these processes, a feedback control system stabilizes the amount of thyroid hormones that are in the bloodstream.



    4. T3 and T4



    T4 is deiodinated by three deiodinase enzymes to produce the more-active triiodothyronine.T3 is the more metabolically active hormone produced from T4.



    Deiodinase enzyme one accounts for 80% of the deiodination of T4, present in liver, kidney, thyroid, and (to a lesser extent) pituitary.



    Deiodinase enzyme two presents in CNS, pituitary, mediates negative feedback on thyroid-stimulating hormone, also presents in brown adipose tissue, and heart vessel, which is predominantly intracellular.



    Deiodinase enzyme three, converts T4 into reverse T3, which, unlike T3, is inactive, it present in placenta, CNS, and hemangioma.



    5. T4 is synthesised in the thyroid gland follicular cells as follows



    As a secondary active transporter, utilises the concentration gradient of Na+ to move I− against its concentration gradient.The sodium-iodide symporter transports two sodium ions across the basement membrane of the follicular cells along with an iodine ion.



    I− is moved across the apical membrane into the colloid of the follicle.



    Iodide is non-reactive, and only the more reactive iodine is required for the next step.Thyroperoxidase oxidises two I− to form I2.



    The thyroglobulin was synthesised in the ER of the follicular cell and secreted into the colloid. The thyroperoxidase iodinates the tyrosyl residues of the thyroglobulin within the colloid.



    Thyroid-stimulating hormone (TSH) released from the pituitary gland binds the TSH receptor (a Gs protein-coupled receptor) on the basolateral membrane of the cell, stimulates the endocytosis of the colloid.



    The lysosomal enzymes cleave the T4 from the iodinated thyroglobulin. The endocytosed vesicles fuse with the lysosomes of the follicular cell.



    Then vesicles are exocytosed, releasing the thyroid hormones.



    6. Thyroid gland produces small amounts of T3 directly



    The thyroid gland also produces small amounts of T3 directly. In the follicular lumen, tyrosine residues become iodinated. This reaction requires hydrogen peroxide. Iodine bonds carbon 3 or carbon 5 of tyrosine residues of thyroglobulin in a process called organification of iodine.



    The iodination of specific tyrosines yields monoiodotyrosine (MIT) and diiodotyrosine (DIT). One MIT and one DIT are enzymatically coupled to form T3. The enzyme is thyroid peroxidase.



    Different tissues have different sensitivities to T4 due to differences in deiodinase ubiquitination in different tissues link, the small amount of T3 could be important.



    7. T3 and T4 Mechanism of action



    T3 and T4 bind to nuclear receptors (thyroid hormone receptors), although being lipophilic, are not able to passively diffuse through the phospholipid bilayers of target cells, instead relying on transmembrane iodothyronine transporters.



    The lipophilicity of T3 and T4 requires their binding to the protein carrier thyroid-binding protein (TBG) such as thyroxine-binding globulins, thyroxine binding prealbumins, and albumins for transport in the blood.



    The sensitivity of a tissue to T3 is modulated through the thyroid receptors. The thyroid receptors bind to response elements in gene promoters, thus enabling them to activate or inhibit transcription.



    8. L-Triiodothyronine(T3) Effects



    T3 may increase serotonin in the brain, in particular in the cerebral cortex, and down-regulate 5HT-2 receptors.



    T3 stimulates the breakdown of cholesterol and increases the number of LDL receptors, increases the rate of lipolysis.



    T3 potentiates the effects of the β-adrenergic receptors on the metabolism of glucose, increases the rate of glycogen breakdown and glucose synthesis ingluconeogenesis.



    T3 affects the lungs and influences the postnatal growth of the central nervous system, stimulates the production of myelin, the production of neurotransmitters, and the growth of axons, also important in the linear growth of bones, has profound effect upon the developing embryo and infants.



    T3 stimulates the production of RNA Polymerase, increases the rate of protein synthesis and protein degradation, and the rate of protein degradation exceeds the rate of protein synthesis in excess, then the body may go into negative ion balance.



    The basal metabolic rate is the minimal caloric requirement needed to sustain life in a resting individual. T3 increases the basal metabolic rate and, thus, increases the body's oxygen and energy consumption.


    With a few exceptions including the spleen and testis, T3 acts on the majority of tissues within the body. It increases the production of the Na+/K+ -ATPase without disrupting transmembrane ion balance, and increases the turnover of different endogenous macromolecules by increasing their synthesis and degradation generally.



    T3 increases the heart rate and force of contraction, then increases cardiac output by increasing β-adrenergic receptor levels in myocardium, and results in increased systolic blood pressure and decreased diastolic blood pressure. The latter two effects act to produce the typical bounding pulse seen in hyperthyroidism, also upregulates the thick filament protein myosin, which helps to increase contractility.



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