The thyroid hormones, triiodothyronine (T3) and its prohormone, thyroxine (T4), are tyrosine-basedhormones produced
by the thyroid
gland that are primarily
responsible for regulation of metabolism.Iodine is
necessary for the production of T3 and
T4. A
deficiency of iodine leads to decreased production of T3 and T4, enlarges the thyroid tissueand will cause the disease known as simple goitre. The major form of thyroid hormone in the blood
is thyroxine (T4), which has a longer half-life than T3. In humans, the ratio of T4 to T3 released
into the blood is roughly 20 to 1. T4 is
converted to the active T3 (three
to four times more potent than T4) within cells by deiodinases (5'-iodinase).
These are further processed bydecarboxylation and
deiodination to produceiodothyronamine (T1a) and thyronamine (T0a). All three isoforms of the deiodinases are selenium-containing enzymes, thus dietary selenium is
essential for T3 production.
The thyronines act on nearly every cell in the body. They
act to increase the basal metabolic rate,
affect protein synthesis, help regulate long bone growth (synergy
with growth hormone) and neural maturation, and increase the body's
sensitivity to catecholamines (such
as adrenaline) by permissiveness. The
thyroid hormones are essential to proper development and differentiation of all
cells of the human body. These hormones also regulate protein, fat,
and carbohydratemetabolism, affecting how human cells use
energetic compounds. They also stimulate vitamin metabolism. Numerous
physiological and pathological stimuli influence thyroid hormone synthesis.
Thyroid
hormone leads to heat generation in humans. However, thethyronamines function
via some unknown mechanism to inhibitneuronal activity;
this plays an important role in the hibernation cycles
of mammals and the moulting behaviour
of birds.
One effect of administering the thyronamines is a severe drop in body temperature.
Selenium
supplementation in treating autoimmune thyroid conditions. Selenium
supplementation had a significant impact on inflammatory activity in
thyroid-specific autoimmune disease, and reducing inflammation may limit damage
to thyroid tissue. This may be due to the increase in glutathione peroxidase
and thioredoxin reductase activity, as well as the decrease in toxic
concentrations of hydrogen peroxide and lipid hydroperoxides which result from
thyroid hormone synthesis. Selenium supplementation reduced thyroid peroxidase
antibody levels in the blood, even
in selenium sufficient patients. While these studies show
promise for the use of selenium supplementation in preventing thyroid tissue
damage, further research is needed to determine the long-term clinical effects
of selenium treatment on inflammatory autoimmune thyroiditis.
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