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ZOO 225: Endocrinology
I. MECHANISM OF HORMONE ACTION
1. Follicle Stimulating Hormone (FSH)
In the male, FSH develops and maintains the male phenotype along with
other andronergic steroid hormones. An example of this is its action on Sertoli
cells to promote sperm formation.
Source:
Norman, A.W. & G. Litwack. 1997. Hormones (2nd ed.). Academic Press : USA.
2. Thyroid Stimulating Hormone (TSH)
TSH controls thyroid cell growth and hormone production by binding to
specific receptors located on the basolateral cell membrane of a thyroid cell. And
also stimulates the metabolism of iodine. Upon binding, it activates camp and
phosphoinositol pathway for signal transduction. Its actions are also mediated
through the GproteinadenylylcyclasecAMP system and possibly through the
phosphatidylinositol system (that then results in the increase of calcium).
Source:
Cooper, D.S., F.S. Greenspan & P.W. Ladenson. The Thyroid Gland. In Gardner, D.G. & D.
Shoback. 2007. Greenspan’s Basic & Clinical Endocrinology (8th ed.). McGrawHill : USA.
3. Testosterone
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Testosterone is the major male androgen hormone that induces activity of
the Sertoli cells found in the seminiferous tubules. Leydig cells secrete
testosterone.
The biological effects of testosterone are well documented. Some of these
are: (a) differentiation of the male reproductive system; (b) skeletal muscle
growth and larynx development and other secondary sexual characteristics.
Testosterone also accounts for male behavior.
Testosterone is free and unbound or may be bound to serum proteins if it
enters circulation. One of the major binding proteins is sex hormonebinding
globulin (SHBG). Once testosterone leaves circulation, it is converted into
dihydrotestosterone by an isoenzyme.
Source:
Jameson, E.W. 1988. Vertebrate Reproduction. John Wiley & Sons : USA.
4. Parathyroid Hormone
Parathyroid hormone or Parathormone is secreted by parathyroid glands. It
acts to increase the calcium levels in the blood through the promotion of kidney
retention of calcium.
This hormone act in two ways: (1) It induces tissues (such as kidney
tubules, bone, and intestine) to release calcium in the bloodstream; (2) it
facilitates excretion of phosphate into the urine even if PTH promotes calcium
reabsorption into the kidney tubule. These two actions primarily raise the amount
of plasma levels of calcium and concomitantly lower phosphate levels.
Source:
Fried, G.H. & G.J. Hademenos. 1999. Schaum’s Outline of Theory and Problems of Biology (2nd
ed.). McGrawHill : USA.
5. Insulin
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Insulin is a peptide hormone released by B cells found in the islets of
Langerhans of the pancreas in response to elevated blood glucose levels.
Glucagon acts on the liver cells to decrease glucose levels in the blood. Once
blood glucose is decreased, it feeds back on B cells to halt the secretion of
insulin. Somatostatin inhibits further secretion of insulin.
Source:
Van De Graaff, K.M. & R. W. Rhees. 1997. Schaum’s outline of Theory and Problems of Human
Anatomy and Physiology (2nd ed.). McGrawHill : USA.
Randall, D., W. Burggren & K. French. 2002. Eckert Animal Physiology (5th ed.). W.H. Freeman
and Company : NY, USA.
6. Kidney Hormones
Antidiuretic hormone (vasopressin) regulates water turnover and its primary
action is to increase water reabsorption. ADH achieves water reabsorption by
increasing the water (from urine) permeability of the kidney collecting ducts. ADH
originates from the posterior pituitary gland and is stimulated by the increase
plasma osmotic pressure or a decrease in blood volume.
Atrial natriuretic peptide originates from the atrium and acts on the kidneys
by reducing sodium and water absorption. Increased venous pressure stimulates
release of this hormone.
Mineralocorticoids, such as aldosterone, come from the adrenal cortex and
target the distal kidney tubules, with angiotensin II stimulating its release.
Mineralcorticoids are steroid hormones that function to promote sodium
reabsorption from the urinary filtrate.
Parathyroid hormones also act on the kidneys by decreasing renal calcium
excretion.
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Source:
Randall, D., W. Burggren & K. French. 2002. Eckert Animal Physiology (5th ed.). W.H. Freeman
and Company : NY, USA.
7. Intestinal Hormones
There are two hormones active in the intestine. One is secretin, which is
released from the duodenal mucosa stimulated by acid digestion. Bayliss and
Starling demonstrated that this hormone’s release elicits the flow of digestive
enzymes from the pancreas.
The second digestive hormone is cholecytoskinin. This hormone is similar to
secretin in that it is released from the mucosal lining of the duodenum.
Cholecytoskinin maintains a steady flow of bile from the gallbladder.
Source:
Fried, G.H. & G.J. Hademenos. 1999. Schaum’s Outline of Theory and Problems of Biology (2nd
ed.). McGrawHill : USA.
8. Adrenaline
Adrenaline (epinephrine) is both hormone and amines and is responsible for
flightorfight situations. This hormone is commonly associated with the adrenal
medulla and exhibits a variety of effects that prepares the body when in stress.
Such actions on the body are: (a) elevation of blood pressure by increasing
cardiac output and peripheral vasoconstriction; (b) acceleration of the respiratory
rate and the subsequent dilation of respiratory passageways; (c) increased
muscular contraction; (d) increase rate of glycogen breakdown into glucose
resulting in high blood glucose level; (e) increase in the conversion of fats into
fatty acids resulting in high blood fatty acids; and lastly, (f) increase release of
adenocorticotrophic hormone and thyroid stimulating hormone from the anterior
pituitary.
Source:
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Van De Graaff, K.M. & R. W. Rhees. 1997. Schaum’s outline of Theory and Problems of Human
Anatomy and Physiology (2nd ed.). McGrawHill : USA.
II. SYMPTOMS OF DISORDERS/DISEASES OR HYPER/HYPOSECRETION
` 1. Growth Hormone
Gigantism is a condition wherein growth hormones are produced in excess
before closure of the epiphyseal growth plates in long bones. Symptoms
presented by an individual include a pathological acceleration of growth; also, if
tumors are found in the pituitary, it may cause impaired vision. Treatment is
through surgical removal of the tumor of the pituitary gland.
Acromegaly occurs when excess growth hormone are produced after the
closure of the epiphyseal plates. The symptoms presented by an individual
include enlarged jaw; thickened and puffy nose; increased basal metabolic rate;
and loss of visual fields. Treatment includes irradiation, radioisotope implantatio,
or surgical removal of the tumor in the pituitary gland (if present) or the surgical
removal of the pituitary gland itself.
Source:
Van De Graaff, K.M. & R. W. Rhees. 1997. Schaum’s outline of Theory and Problems of Human
Anatomy and Physiology (2nd ed.). McGrawHill : USA.
2. Antidiuretic Hormone
Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) occurs
when antidiuretic hormones are produced in excess. This causes the body to
retain water with certain levels of the electrolyts to fall. SIADH is common in
people with heart failure or those afflicted with a diseased hypothalamus. Also
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certain cancers may also trigger SIADH. The symptoms of this condition include
nausea, seizures and coma. It may also trigger behavioral changes such as
irritability, competitiveness, confusion, hallucination and stupor. Medication
includes ADHsuppressants and regulation of fluid intake.
Source:
Gardner, D.G. Endocrine Emerencies. In Gardner, D.G. & D. Shoback. 2007. Greenspan’s Basic
& Clinical Endocrinology (8th ed.). McGrawHill : USA.
Health System. 2004. Diabetes and other Endocrine and Metabolic Disorders. University of
Virginia. Retrieved at
http://www.healthsystem.virginia.edu/uvahealth/peds_diabetes/siadh.cfm
3. Mineralocorticoids
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However, patients appear asymptomatic but hyperkalemia and acidosis may be
detected during screenings. Hyperkalemia may pose a threat in that it can cause
a heart block upon administration of betaandrenergic blocking agent. If
hyperkalemia does not occur, fludcortisone or furosemide may be used to treat
hypoaldosteronism coupled with potassiumrestricted diet.
Source:
Greenspan, S.L. & N.M. Resnick. Geriatric Endocrinology. In Gardner, D.G. & D. Shoback. 2007.
Greenspan’s Basic & Clinical Endocrinology (8th ed.). McGrawHill : USA.
Patient UK. 2008. Hyperaldosteronism. Retrieved at http://www.patient.co.uk/showdoc/40000954/.