Kits
FT4 ELISA
Kits
Description
The thyroid hormone, thyroxine (T4) is produced by
the thyroid gland. An important component in the
synthesis is iodine. The major form of thyroid
hormone in the blood is thyroxine (T4). Thyroxine is
converted to the active T3 (three to four times more
potent than T4) within cells by deiodinases (5'-
iodinase).
Thyroxine-binding globulin (TGB) is the major carrier
protein for circulating thyroid hormone. Only a very
small fraction of the circulating hormone is free
(unbound) - T4 0.03%. When thyroid hormone is
bound, it is not active, so the amount of FT3/FT4 is
what is important. For this reason, measuring total
thyroxine in the blood can be misleading.
The concentration of free thyroid hormones in the
blood is regulated by a negative feedback mechanism
involving TSH. The binding of T4 by TBG plays a key
role in this feedback mechanism and the most
significant changes that occur in T4 binding capacity
are the result of alterations in TBG. Changes in the
circulating levels of TBG will result in a proportional
increase or decrease in the concentration of total T4.
However, measurement of serum FT4 is unaffected
by changes in T4 protein binding levels and therefore
correlates well with the functional thyroid state in most
individuals. Factors responsible for discrepancies
between serum total T4 levels and true thyroid states
include TBG concentration, estrogenic hormones
(pregnancy, oral contraceptives and estrogen) and
drugs that bind to TBG preventing its binding to FT4
The thyronines act on the body to increase the basal
metabolic rate, affect protein synthesis 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 carbohydrate
metabolism, affecting how human cells use energetic
compounds. Numerous physiological and pathological
stimuli influence thyroid hormone synthesis.
Thyrotoxicosis or hyperthyroidism is the clinical
syndrome caused by an excess of circulating free
thyroxine, free triiodothyronine, or both. Both T3 and
T4 are used to treat thyroid hormone deficiency
(hypothyroidism).
the thyroid gland. An important component in the
synthesis is iodine. The major form of thyroid
hormone in the blood is thyroxine (T4). Thyroxine is
converted to the active T3 (three to four times more
potent than T4) within cells by deiodinases (5'-
iodinase).
Thyroxine-binding globulin (TGB) is the major carrier
protein for circulating thyroid hormone. Only a very
small fraction of the circulating hormone is free
(unbound) - T4 0.03%. When thyroid hormone is
bound, it is not active, so the amount of FT3/FT4 is
what is important. For this reason, measuring total
thyroxine in the blood can be misleading.
The concentration of free thyroid hormones in the
blood is regulated by a negative feedback mechanism
involving TSH. The binding of T4 by TBG plays a key
role in this feedback mechanism and the most
significant changes that occur in T4 binding capacity
are the result of alterations in TBG. Changes in the
circulating levels of TBG will result in a proportional
increase or decrease in the concentration of total T4.
However, measurement of serum FT4 is unaffected
by changes in T4 protein binding levels and therefore
correlates well with the functional thyroid state in most
individuals. Factors responsible for discrepancies
between serum total T4 levels and true thyroid states
include TBG concentration, estrogenic hormones
(pregnancy, oral contraceptives and estrogen) and
drugs that bind to TBG preventing its binding to FT4
The thyronines act on the body to increase the basal
metabolic rate, affect protein synthesis 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 carbohydrate
metabolism, affecting how human cells use energetic
compounds. Numerous physiological and pathological
stimuli influence thyroid hormone synthesis.
Thyrotoxicosis or hyperthyroidism is the clinical
syndrome caused by an excess of circulating free
thyroxine, free triiodothyronine, or both. Both T3 and
T4 are used to treat thyroid hormone deficiency
(hypothyroidism).