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Structure
Synthesis and Secretions
Physiological Anatomy
Physiological Functions
Regulation
Feedback Effect of Thyroid Hormone
The thyroid gland is an endocrine organ found in
the neck, it is responsible for regulating the body’s
metabolic rate via hormones it produces. It is a
ductless alveolar gland found in the anterior neck,
just below the laryngeal prominence (Adam’s
apple). It is roughly butterfly-shaped, with two
lobes wrapping round the trachea and connected in
the middle by an isthmus.
 About 93 percent of the metabolically active hormones
secreted by the thyroid gland is thyroxine, and 7 percent
triiodothyronine.
 Thyroxine is eventually converted to triiodothyronine in
the tissues.
 The functions of these two hormones are qualitatively
the same, but they differ in rapidity and intensity of
action.
 Triiodothyronine is about four times as potent as
thyroxine, but it is present in the blood in much smaller
quantities and persists for a much shorter time than does
thyroxine.
 The thyroid gland is composed, of large numbers of
closed follicles (100 to 300 micrometers in diameter).
 It filled with a secretory substance called colloid and
lined with cuboidal epithelial cells that secrete into the
interior of the follicles.
 The major constituent of colloid is the large
glycoprotein thyroglobulin, which contains the thyroid
hormones.
 Once the secretion has entered the follicles, it must be
absorbed back through the follicular epithelium into the
blood before it can function in the body.
Fig: Anatomy and Microscopic appearance of Thyroid Gland
 To form normal quantities of thyroxine, about 50
milligrams of ingested iodine in the form of iodides are
required each year, or about 1 mg/week.
 Iodides ingested orally are absorbed from the
gastrointestinal tract into the blood.
 one fifth are selectively removed from the circulating
blood by the cells of the thyroid gland and used for
synthesis of the thyroid hormones.
 The first stage in the formation of thyroid hormones, is
transport of iodides from the blood into the thyroid
glandular cells and follicles.
 The basal membrane of the thyroid cell has the specific
ability to pump the iodide actively to the interior of the
cell.
 This is achieved by the action of a sodium-iodide
symporter (NIS), which co-transports one iodide ion
along with two sodium ions across the basolateral
(plasma) membrane into the cell.
 This process of concentrating the iodide in the cell is
called iodide trapping.
 Iodide is transported out of the thyroid cells across the
apical membrane into the follicle by a chloride-iodide
ion counter-transporter molecule called pendrin.
 The endoplasmic reticulum and Golgi apparatus
synthesize and secrete into the follicles a large
glycoprotein molecule called thyroglobulin.
 Each molecule of thyroglobulin contains about 70
tyrosine amino acids, and they are the major substrates
that combine with iodine to form the thyroid
hormones.
 conversion of the iodide ions to an oxidized form of
iodine, that is then capable of combining directly with
the amino acid tyrosine. This oxidation of iodine is
promoted by the enzyme peroxidase.
 The binding of iodine with the thyroglobulin
molecule is called organification of the thyroglobulin.
 Tyrosine is first iodized to monoiodotyrosine and then
to diiodotyrosine.
 The major hormonal product of the coupling reaction
is the molecule thyroxine (T4 ), which is formed
when two molecules of diiodotyrosine are joined
together; the thyroxine then remains part of the
thyroglobulin molecule.
 Or one molecule of monoiodotyrosine couples with
one molecule of diiodotyrosine to form
triiodothyronine (T3 ).
Fig: Chemistry of Thyroxine and Triiodothyronine formation
 Stimulation of Carbohydrate Metabolism:
It increase uptake of glucose by the cells, enhanced
glycolysis, enhanced gluconeogenesis, increased rate of
absorption from the gastrointestinal tract.
 Increased Basal Metabolic Rate:
Because thyroid hormone increases metabolism in
almost all cells of the body, excessive quantities of the
hormone can occasionally increase the basal metabolic rate
60 to 100 percent above normal. Conversely, when no
thyroid hormone is produced, the basal metabolic rate falls
to almost one-half normal.
 Increased Respiration:
The increased rate of metabolism increases the
utilization of oxygen and formation of carbon dioxide;
these effects activate all the mechanisms that increase the
rate and depth of respiration.
 Effect on the Function of the Muscles:
Slight increase in thyroid hormone usually makes the
muscles react with vigor, but when the quantity of
hormone becomes excessive, the muscles become
weakened because of excess protein catabolism.
 Effect on Other Endocrine Glands:
Increased thyroid hormone increases the rates of
secretion of several other endocrine glands, but it also
increases the need of the tissues for the hormones.
 Effect of Thyroid Hormone on Growth:
Thyroid hormone is essential for the metamorphic
change of the tadpole into the frog. In humans, the effect
of thyroid hormone on growth is manifest mainly in
growing children. In those who are hypothyroid, the rate
of growth is greatly retarded. In those who are
hyperthyroid, excessive skeletal growth often occurs,
causing the child to become considerably taller at an
earlier age. However, the bones also mature more rapidly
and the epiphyses close at an early age, so the duration of
growth and the eventual height of the adult may actually
be shortened.
To maintain normal levels of metabolic activity in the body,
precisely the right amount of thyroid hormone must be
secreted at all times; to achieve this, specific feedback
mechanisms operate through the hypothalamus and
anterior pituitary gland to control the rate of thyroid
secretion.
 Increased activity of the iodide pump, which
increases the rate of “iodide trapping” in the
glandular cells.
 Increased iodination of tyrosine to form the thyroid
hormones
 Increased size and increased secretory activity of the
thyroid cells
 Anterior pituitary secretion of TSH is controlled by
a hypothalamic hormone, thyrotropin-releasing
hormone
 1-Binaco, AC. 2011. Cracking the metabolic code for thyroid
hormone signaling. Med. Clin. North America. p. 96-257.
 2-Cooper, DS. and B. Biondi. 2012. Subclinical thyroid disease.
p.379.
 3-Danzi, S. and I. Klein. 2012. Thyroid hormone and the
cardiovascular system. Endocrinology., p.152.
 4-De la Vieja, A., O.Dohan and N. Carrasco. 2000. Molecular
analysis of the sodium/iodine symporter: impact on thyroid
and extrathyroid pathophysiology. Physiol. Rev., 80: p.1083-1105.
 5-Kharlip, J. and DS. Cooper. 2009. Recent developments in
hyperthyroidism.
 Lacent. p.373.
 6-Levy, O. and N. Carrasco. 1997. Structure and function of the
thyroid iodide Transporter and its implications for thyroid disease.
Curr. Opin. Endocrinol Diabetes., 4: p.364-370.
 7-Mazzaferri, EL. and RT. Kloos. 2001. Current approaches to
primary therapy for
 Papillary and follicular thyroid cancer. Clin. Endocrinol
Metab., 86: p.1447-1463.
Functios of thyroid hormones

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Functios of thyroid hormones

  • 1.
  • 2. Structure Synthesis and Secretions Physiological Anatomy Physiological Functions Regulation Feedback Effect of Thyroid Hormone
  • 3. The thyroid gland is an endocrine organ found in the neck, it is responsible for regulating the body’s metabolic rate via hormones it produces. It is a ductless alveolar gland found in the anterior neck, just below the laryngeal prominence (Adam’s apple). It is roughly butterfly-shaped, with two lobes wrapping round the trachea and connected in the middle by an isthmus.
  • 4.
  • 5.  About 93 percent of the metabolically active hormones secreted by the thyroid gland is thyroxine, and 7 percent triiodothyronine.  Thyroxine is eventually converted to triiodothyronine in the tissues.  The functions of these two hormones are qualitatively the same, but they differ in rapidity and intensity of action.  Triiodothyronine is about four times as potent as thyroxine, but it is present in the blood in much smaller quantities and persists for a much shorter time than does thyroxine.
  • 6.  The thyroid gland is composed, of large numbers of closed follicles (100 to 300 micrometers in diameter).  It filled with a secretory substance called colloid and lined with cuboidal epithelial cells that secrete into the interior of the follicles.  The major constituent of colloid is the large glycoprotein thyroglobulin, which contains the thyroid hormones.  Once the secretion has entered the follicles, it must be absorbed back through the follicular epithelium into the blood before it can function in the body.
  • 7. Fig: Anatomy and Microscopic appearance of Thyroid Gland
  • 8.  To form normal quantities of thyroxine, about 50 milligrams of ingested iodine in the form of iodides are required each year, or about 1 mg/week.  Iodides ingested orally are absorbed from the gastrointestinal tract into the blood.  one fifth are selectively removed from the circulating blood by the cells of the thyroid gland and used for synthesis of the thyroid hormones.
  • 9.  The first stage in the formation of thyroid hormones, is transport of iodides from the blood into the thyroid glandular cells and follicles.  The basal membrane of the thyroid cell has the specific ability to pump the iodide actively to the interior of the cell.  This is achieved by the action of a sodium-iodide symporter (NIS), which co-transports one iodide ion along with two sodium ions across the basolateral (plasma) membrane into the cell.  This process of concentrating the iodide in the cell is called iodide trapping.  Iodide is transported out of the thyroid cells across the apical membrane into the follicle by a chloride-iodide ion counter-transporter molecule called pendrin.
  • 10.  The endoplasmic reticulum and Golgi apparatus synthesize and secrete into the follicles a large glycoprotein molecule called thyroglobulin.  Each molecule of thyroglobulin contains about 70 tyrosine amino acids, and they are the major substrates that combine with iodine to form the thyroid hormones.  conversion of the iodide ions to an oxidized form of iodine, that is then capable of combining directly with the amino acid tyrosine. This oxidation of iodine is promoted by the enzyme peroxidase.
  • 11.
  • 12.  The binding of iodine with the thyroglobulin molecule is called organification of the thyroglobulin.  Tyrosine is first iodized to monoiodotyrosine and then to diiodotyrosine.  The major hormonal product of the coupling reaction is the molecule thyroxine (T4 ), which is formed when two molecules of diiodotyrosine are joined together; the thyroxine then remains part of the thyroglobulin molecule.  Or one molecule of monoiodotyrosine couples with one molecule of diiodotyrosine to form triiodothyronine (T3 ).
  • 13. Fig: Chemistry of Thyroxine and Triiodothyronine formation
  • 14.  Stimulation of Carbohydrate Metabolism: It increase uptake of glucose by the cells, enhanced glycolysis, enhanced gluconeogenesis, increased rate of absorption from the gastrointestinal tract.  Increased Basal Metabolic Rate: Because thyroid hormone increases metabolism in almost all cells of the body, excessive quantities of the hormone can occasionally increase the basal metabolic rate 60 to 100 percent above normal. Conversely, when no thyroid hormone is produced, the basal metabolic rate falls to almost one-half normal.
  • 15.  Increased Respiration: The increased rate of metabolism increases the utilization of oxygen and formation of carbon dioxide; these effects activate all the mechanisms that increase the rate and depth of respiration.  Effect on the Function of the Muscles: Slight increase in thyroid hormone usually makes the muscles react with vigor, but when the quantity of hormone becomes excessive, the muscles become weakened because of excess protein catabolism.  Effect on Other Endocrine Glands: Increased thyroid hormone increases the rates of secretion of several other endocrine glands, but it also increases the need of the tissues for the hormones.
  • 16.  Effect of Thyroid Hormone on Growth: Thyroid hormone is essential for the metamorphic change of the tadpole into the frog. In humans, the effect of thyroid hormone on growth is manifest mainly in growing children. In those who are hypothyroid, the rate of growth is greatly retarded. In those who are hyperthyroid, excessive skeletal growth often occurs, causing the child to become considerably taller at an earlier age. However, the bones also mature more rapidly and the epiphyses close at an early age, so the duration of growth and the eventual height of the adult may actually be shortened.
  • 17. To maintain normal levels of metabolic activity in the body, precisely the right amount of thyroid hormone must be secreted at all times; to achieve this, specific feedback mechanisms operate through the hypothalamus and anterior pituitary gland to control the rate of thyroid secretion.
  • 18.  Increased activity of the iodide pump, which increases the rate of “iodide trapping” in the glandular cells.  Increased iodination of tyrosine to form the thyroid hormones  Increased size and increased secretory activity of the thyroid cells  Anterior pituitary secretion of TSH is controlled by a hypothalamic hormone, thyrotropin-releasing hormone
  • 19.
  • 20.  1-Binaco, AC. 2011. Cracking the metabolic code for thyroid hormone signaling. Med. Clin. North America. p. 96-257.  2-Cooper, DS. and B. Biondi. 2012. Subclinical thyroid disease. p.379.  3-Danzi, S. and I. Klein. 2012. Thyroid hormone and the cardiovascular system. Endocrinology., p.152.  4-De la Vieja, A., O.Dohan and N. Carrasco. 2000. Molecular analysis of the sodium/iodine symporter: impact on thyroid and extrathyroid pathophysiology. Physiol. Rev., 80: p.1083-1105.  5-Kharlip, J. and DS. Cooper. 2009. Recent developments in hyperthyroidism.  Lacent. p.373.  6-Levy, O. and N. Carrasco. 1997. Structure and function of the thyroid iodide Transporter and its implications for thyroid disease. Curr. Opin. Endocrinol Diabetes., 4: p.364-370.  7-Mazzaferri, EL. and RT. Kloos. 2001. Current approaches to primary therapy for  Papillary and follicular thyroid cancer. Clin. Endocrinol Metab., 86: p.1447-1463.