SALUMBRE,RenzL. ZOO225:Endocrinology I.MECHANISMOFHORMONEACTION 1.FollicleStimulatingHormone(FSH) A peptide hormone released by the folliculotrophic cells in the anterior pituitary.Itsprimaryroleisthedevelopmentofmajorreproductiveprocessesin bothmaleandfemale. Inthemale,FSHdevelopsandmaintainsthemalephenotypealongwith other andronergic steroidhormones.Anexampleofthisisitsactionon Sertoli cellstopromotespermformation. Inthefemale,FSHactson thecalcellsand Ovarian granulosa topromote thematurationofovarianfollicleandalsotostimulateestrogenproduction.Source: Norman,A.W.&G.Litwack.1997.Hormones(2nded.).AcademicPress:USA.

2.ThyroidStimulatingHormone(TSH) TSH controls thyroid cell growth and hormone production by binding to specificreceptorslocatedonthebasolateralcellmembraneofathyroidcell.And alsostimulatesthemetabolismofiodine. Uponbinding,itactivatescampand phosphoinositol pathwayfor signal transduction. Itsactionsarealsomediated throughtheGproteinadenylylcyclasecAMP systemandpossiblythroughthe phosphatidylinositolsystem(thatthenresultsintheincreaseofcalcium).Source: Cooper, D.S., F.S. Greenspan & P.W. Ladenson. The Thyroid Gland. In Gardner, D.G. & D. Shoback.2007.GreenspansBasic&ClinicalEndocrinology(8thed.).McGrawHill:USA.

3.Testosterone 1

Testosterone isthemajormaleandrogenhormonethatinducesactivityof the Sertoli cells found in the seminiferous tubules. Leydig cells secrete testosterone. Thebiologicaleffectsoftestosteronearewelldocumented.Someofthese are: (a) differentiation of the male reproductive system; (b) skeletal muscle growth and larynx development and other secondary sexual characteristics. Testosteronealsoaccountsformalebehavior. Testosteroneisfreeandunboundormaybeboundtoserumproteins ifit enters circulation. One of the major binding proteins is sex hormonebinding globulin (SHBG). Once testosterone leaves circulation, it is converted into dihydrotestosteronebyanisoenzyme.Source: Braunstein,G.D. Testes. InGardner,D.G.&D. Shoback. 2007. GreenspansBasic&Clinical Endocrinology(8thed.).McGrawHill:USA. Jameson,E.W.1988.VertebrateReproduction.JohnWiley&Sons:USA.

4.ParathyroidHormone ParathyroidhormoneorParathormoneissecretedbyparathyroidglands.It actstoincreasethecalciumlevelsinthebloodthroughthepromotionofkidney retentionofcalcium. 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 facilitatesexcretionofphosphateintotheurineevenifPTHpromotescalcium reabsorptionintothekidneytubule.Thesetwoactionsprimarilyraisetheamount ofplasmalevelsofcalciumandconcomitantlylowerphosphatelevels.Source: Fried,G.H.&G.J.Hademenos.1999.SchaumsOutlineofTheoryandProblemsofBiology(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. Glucagonactsonthelivercellstodecreaseglucoselevelsintheblood.Once blood glucose is decreased, it feeds back on B cells to halt the secretion of insulin.Somatostatininhibitsfurthersecretionofinsulin.Source: VanDeGraaff,K.M.&R.W.Rhees.1997.SchaumsoutlineofTheoryandProblemsofHuman AnatomyandPhysiology(2nded.).McGrawHill:USA. Randall,D.,W.Burggren&K.French.2002.EckertAnimalPhysiology(5thed.).W.H.Freeman andCompany:NY,USA.

6.KidneyHormones

Avarietyofhormonesactonthe kidney,which isthemajororganforthe regulationofwaterandelectrolytebalanceinthebody.Thesehormonesare: Antidiuretichormone(vasopressin)regulateswaterturnoveranditsprimary actionistoincrease water reabsorption.ADHachieveswater reabsorption by increasingthewater(fromurine)permeabilityofthekidneycollectingducts.ADH originates from the posterior pituitary gland and is stimulated by the increase plasmaosmoticpressureoradecreaseinbloodvolume. Atrialnatriureticpeptideoriginatesfromtheatriumandactsonthekidneys byreducingsodiumandwaterabsorption.Increasedvenouspressurestimulates releaseofthishormone. The parafollicular cells of the thyroid secrete calcitonin. It acts on both kidneysandbonebydecreasingthereleaseofcalciumionsfromboneand,in thekidney,increasesrenalcalciumandphosphateexcretion.Increasedlevelsof plasmacalciumstimulatefurthersecretion. Mineralocorticoids,suchasaldosterone,comefromtheadrenalcortexand target the distal kidney tubules, with angiotensin II stimulating its release. Mineralcorticoids are steroid hormones that function to promote sodium reabsorptionfromtheurinaryfiltrate. Parathyroidhormonesalsoactonthekidneysbydecreasingrenalcalcium excretion. 3

Source: Randall,D.,W.Burggren&K.French.2002.EckertAnimalPhysiology(5thed.).W.H.Freeman andCompany:NY,USA.

7.IntestinalHormones Therearetwohormonesactiveintheintestine.Oneissecretin,whichis releasedfromtheduodenalmucosastimulatedbyaciddigestion.Baylissand Starlingdemonstratedthatthishormonesreleaseelicitstheflowofdigestive enzymesfromthepancreas. Theseconddigestivehormoneischolecytoskinin.Thishormoneissimilarto secretininthatitisreleasedfromthemucosalliningoftheduodenum. Cholecytoskininmaintainsasteadyflowofbilefromthegallbladder.Source: Fried,G.H.&G.J.Hademenos.1999.SchaumsOutlineofTheoryandProblemsofBiology(2nd ed.).McGrawHill:USA.

8.Adrenaline Adrenaline(epinephrine)isbothhormoneandaminesandisresponsiblefor flightorfightsituations. Thishormoneiscommonlyassociatedwiththeadrenal medullaandexhibitsavarietyofeffectsthatpreparesthebodywheninstress. Suchactionsonthebodyare:(a)elevationofbloodpressurebyincreasing cardiacoutputandperipheralvasoconstriction;(b)accelerationoftherespiratory rate and the subsequent dilation of respiratory passageways; (c) increased muscular contraction; (d) increase rate of glycogen breakdown into glucose resultinginhighbloodglucoselevel;(e)increaseintheconversionoffatsinto fattyacidsresultinginhighbloodfattyacids;andlastly,(f)increasereleaseof adenocorticotrophic hormoneandthyroidstimulatinghormonefromtheanterior pituitary.Source:

4

VanDeGraaff,K.M.&R.W.Rhees.1997.SchaumsoutlineofTheoryandProblemsofHuman AnatomyandPhysiology(2nded.).McGrawHill:USA.

II.SYMPTOMSOFDISORDERS/DISEASESORHYPER/HYPOSECRETION ` 1.GrowthHormone

Dwarfism is a common manifestation of a growth hormone secretion disorder.Thisischaracterizedbyhavingadecreasedgrowthhormonebeforethe normalheighthasbeenreached.Apersonafflictedwiththisdisorderexhibitsa smallbodybutnormallyproportioned;mildobesitywithlackofappetite;tender andthinskin.Thisparticulardisordercanbetreatedusinginjectionofgrowth hormone. Gigantismisaconditionwhereingrowthhormonesareproducedinexcess before closure of the epiphyseal growth plates in long bones. Symptoms presentedbyanindividualincludeapathologicalaccelerationofgrowth;also,if tumors are found in the pituitary, it may cause impaired vision. Treatment is throughsurgicalremovalofthetumorofthepituitarygland. Acromegaly occurswhenexcessgrowthhormoneareproducedafterthe closure of the epiphyseal plates. The symptoms presented by an individual includeenlargedjaw;thickenedandpuffynose;increasedbasalmetabolicrate; andlossofvisualfields.Treatmentincludesirradiation,radioisotopeimplantatio, orsurgicalremovalofthetumorinthepituitarygland(ifpresent)orthesurgical removalofthepituitaryglanditself.Source: VanDeGraaff,K.M.&R.W.Rhees.1997.SchaumsoutlineofTheoryandProblemsofHuman AnatomyandPhysiology(2nded.).McGrawHill:USA.

2.AntidiureticHormone SyndromeofInappropriateAntidiureticHormoneSecretion(SIADH)occurs when antidiuretic hormonesareproduced in excess. Thiscauses the bodyto retain water with certain levels of the electrolyts to fall. SIADH is common in peoplewithheartfailureorthoseafflictedwithadiseasedhypothalamus.Also 5

certaincancersmayalsotriggerSIADH.Thesymptomsofthisconditioninclude nausea, seizures and coma. It may also trigger behavioral changes such as irritability, competitiveness, confusion, hallucination and stupor. Medication includesADHsuppressantsandregulationoffluidintake. Diabetes insipidus is another condition associated with the deficiency of ADHincirculation.Thisconditionmaybeconsideredheritableassociatedwith diabetes mellitus, optic atrophy and sensorineural deafness. Secondary conditionsalsoposethepossibilityofacquiringdiabetesinsipidussuchashead 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.EndocrineEmerencies.InGardner,D.G.&D.Shoback.2007.GreenspansBasic &ClinicalEndocrinology(8thed.).McGrawHill:USA. HealthSystem.2004.DiabetesandotherEndocrineandMetabolicDisorders.Universityof Virginia.Retrievedat 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 usuallyresultinhypertension.Excessivelevelsof aldosterone actonthedistal renaltubulepromotingsodiumretention,whichthenresultsinwaterretentionand volumeexpansionwithhypertension.Potassiumisalsosecretedandmayresult inhypokalemia.Othersymptomsmayincludepolyuria,headacheandlethargy. The condition wherein a decreased levels of aldosterone is called hypoaldosteronism,orhyporeninemichypoaldosteronism.Thisoccursingeriatric patients who are already suffering from diabetes and mild renal insufficiency. 6

However,patientsappearasymptomaticbut hyperkalemia andacidosismaybe detectedduringscreenings.Hyperkalemiamayposeathreatinthatitcancause a heart block upon administration of betaandrenergic blocking agent. If hyperkalemia doesnotoccur, fludcortisone or furosemide maybeusedtotreat hypoaldosteronismcoupledwithpotassiumrestricteddiet.Source: Greenspan,S.L.&N.M.Resnick.GeriatricEndocrinology.InGardner,D.G.&D.Shoback.2007. GreenspansBasic&ClinicalEndocrinology(8thed.).McGrawHill:USA. PatientUK.2008.Hyperaldosteronism.Retrievedathttp://www.patient.co.uk/showdoc/40000954/.

7