SALUMBRE, Renz L. ZOO 225: Endocrinology I. MECHANISM OF HORMONE ACTION 1. Follicle Stimulating Hormone (FSH) A peptide hormone released by the folliculotrophic cells in the anterior pituitary. Its primary role is the development of major reproductive processes in both male and female. 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. In the female, FSH acts on thecal cells and Ovarian granulosa to promote the maturation of ovarian follicle and also to stimulate estrogen production. 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 1
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: Braunstein, G.D. Testes. In Gardner, D.G. & D. Shoback. 2007. Greenspan’s Basic & Clinical Endocrinology (8th ed.). McGrawHill : USA. 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 2
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
A variety of hormones act on the kidney, which is the major organ for the regulation of water and electrolyte balance in the body. These hormones are: 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. The parafollicular cells of the thyroid secrete calcitonin. It acts on both kidneys and bone by decreasing the release of calcium ions from bone and, in the kidney, increases renal calcium and phosphate excretion. Increased levels of plasma calcium stimulate further secretion. 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. 3
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:
4
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
Dwarfism is a common manifestation of a growth hormone secretion disorder. This is characterized by having a decreased growth hormone before the normal height has been reached. A person afflicted with this disorder exhibits a small body but normally proportioned; mild obesity with lack of appetite; tender and thin skin. This particular disorder can be treated using injection of 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 5
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. Diabetes insipidus is another condition associated with the deficiency of ADH in circulation. This condition may be considered heritable associated with diabetes mellitus, optic atrophy and sensorineural deafness. Secondary conditions also pose the possibility of acquiring diabetes insipidus such as head injury, pituitary surgery, tuberculosis and other granulomatous diseases, infection, tumors, etc. Often symptoms of this disease includes increase fluid intake, hypertonicity and increased urination (in children, it may cause bed wetting). Source: Diabetes Insipidus Foundation. 2006. Symptoms of Diabetes Insipidus. Retrieved at http://www.diabetesinsipidus.org/symptomsofdi.htm 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 Hyperaldosteronism is a condition caused by excessive production of aldosterone. Hypersecretion of aldosterone may also be influenced by high rennin levels. This condition is most common in females than in males and usually result in hypertension. Excessive levels of aldosterone act on the distal renal tubule promoting sodium retention, which then results in water retention and volume expansion with hypertension. Potassium is also secreted and may result in hypokalemia. Other symptoms may include polyuria, headache and lethargy. The condition wherein a decreased levels of aldosterone is called hypoaldosteronism, or hyporeninemic hypoaldosteronism. This occurs in geriatric patients who are already suffering from diabetes and mild renal insufficiency. 6
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/.
7