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Human Physiology, Fox chapter 11
Undergraduate 3

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the chemical classifications of the hormones:

and are they lipid soluable




amines =              from tyrosine and tryptophen = water soluble

                            amines are from adrenal medulla,  pineal

                           thyroid (but is fat soluble)


polypeptide = ADH  < 100 in chain   insulin 


protein =   GH  > 100    these are polar/ H2O soluable


Glycoprotein =  FSH  and LH


Steroids = from cholesterol = testosterone, estradiol,   

                progesteron and     cortisol

      steroids can be given po as can thyroid


         polypeptide   like insulin cannot be po


Meletonin from the pineal glad is polar but still can go through the membrane


Polar are H2O soluable = polypeptide, glycoprotein, catechomine and are too polar to go through the plasma membrane.

say something about prohormones or prehormones or parent or precursor hormones

Insulin is made from a proinsulin

Testosterone and D3 are made active in target cells


Where are steroids made?



steroids are made in only 2 glands

the gonad and the adrenal cortex 


the adrenal cortex makes the steroid hormones cortison and aldosterone and a little sex hormone


sterolds can be given op

what does the action of the hormone depend on?

the electrical properties


movement of ions down electrochemical gradients accompany actions of some hormones


Target cells much have what

and do what and

what else is required of the hormones?


specific receptor protein to combine with regulatory molecule   hormone or neurotransmitter


combinations must cause specific changes in the target cell


Must be something there to turn off the action of regulator.....aremoval or chemical inactivation


Hormone   to   hormone

Discuss target and response

as well as hormones interacting


Target organs are responsive to a bunch of hormones


hormones may work against or with each other


synergistic = additive or complimentary + epi and norepi


permissive =  1st hormone enhances 2nd hormones responsr  such as estradiol makes receptors for progesterone

D3 prehormone modified by kidney and liver to raises Ca++

parathyroid PTH permission in action of D causes it to stimulate making of enzymes in liver andkidney

increased PTS permissive effect on D3 to stimulat gut to absob Ca++


Antagonistic  =  Lactation in pregnacy vs estrogen and estrogen inhibits prolactin

Insulin (increases fat)   and glucagon (fat breaking) 


concentration in blood of hormones

tissue response


rate of secretion and rate removed by target and liver


half life   from minutes to hours...thyroid for days

on what does the hormones effect depend

concentration...must be normal level


binding site   too high a does may cause weird effects


steroids may cause making of derivatives with unexpected effects  it can inhibit FSH  or LH shrink testes  and increase LDL cholesterol and triglycerides

Say something about priming

concentration can affect responsiveness of target cells


polypeptide and glycoproteins can change the number of receptors   ....priming can cause more receptor proteins to form  ( and I guess less too)


example of more receptors forming

GnRH secreted by hypothalamum ...upregulation of receptors  =  increase in umber of receptor protein for hormone  hen GnRh causes a greater respons from anterior pituitary



example of desensitization    downregulation    prolonged high concentration of polypeptide causes less target tissue response and fewer receptor = insulin and adipos

hormones pulsate secretions..what hormones and why
testicular cells and LH and glycoprotein pulsatile secretions  =  reproductive system

Water soluable hormones

what they are

how they work


Polar molecules     o0o

cannot pass through membrane

polypeptides and glycoprotein

require activation of a 2nd messenger within the cell



Lipid soluable hormones

what they are

how they work


nonpolar molecules   0-0

do not disolve in water in plasma

have carriers attached

they unattach from carriers and go through membrane

pass through membrane

nuclear hormone receptor proteins

activate genetic transcription (make mRNA)


First have to be activated by binding to their hormone ligands


Ligand= a small molecule that binds to a larger molecule (protein)


a new RNA formed by activated genes directs synthesis of specific proteins including enzyme proteins that change the metabolism of the target cell


Each nuclear hormone receptor has 2 regions or domains = a ligand (hormone) binding domain

and a DNA binding domain


1st the receptro must be activated by binding to its hormone ligand  before it can bind to a specific region of DNA (hormone response element)


hormone ligand binds first to the hormone and the ligand then grabs onto DNA   the ligand binds it to DNA


Nuclear receptors have 2 superfamilies + steroid family and thyroid hormone


The thyroid hormone receptor also has receptors for active D3 and retinoic acid


Steroid hormone action  enters target cells;  binds to nuclear receptor protein

Influence target tissue by stimulating genetic transcription (genomic action)  of steroids too fast an action to be the result of binding and genetic expresion.



genomic mechanism of steroid hormone action...

receptor waiting in cytoplasm or also in nucleus 

so in the cytoplasm when it binds,

it translocates to the nucleus and goes in and then its DNA binding domain binds to the specific hormone response element of DNA

so cytoplasmic receptor binds to ligand and translocates to inside the nucleus

its DNA binding domain binds to hormone response element of DNA




The hormonal response element of DNA  and steroid hormones

the hormone response element of DNA is

2 half - sites

One steroid receptor (bound to one molecule of steroid hormone.

it attached on one of the half sites on the DNA   and anotehr to the other half site

2 receptor units at the 2ne half site = dimerization


Both receptor units of the pair are the  same  = homodimes


dimerization then the activated nuclear hormone receptor stimulates transcription of 2 particular genes


When a steroid hormone ligand binds to its nuclear receptor portein it changes the receptor protein shape..theis causes

1.  removal of a group of proteine (heat shock proteins) tha tprevent the receptor from binding to DNA

2.  recruitment of coactivator proteins--while corepressor proteins are prevented from finding to receptor


coactivator proteins form a complex  that modifies the structure of chromatin and eases DNA transcription (RNA synthesis)

at the hormone response element of DNA and then cell produces the proteins stimulated by the steroid hormone

Mechanisms of Thyroid Hormone Actions

T4 in blood attached to carrier =TBG

(but there is lots of free T3 in the blood)


Only the free T3  can enter the target cells 

Protein bound are reserves


Once free the T$ goes into the target cell and is converted to T3


Thyroid hormone receptor proteins are located on nucleus bound to DNA   (even with out their thyroid hormone ligand T3 binds only to 1 of half sites...the otehr binds to receptor for retinoid acid


Thyroid hormone receptors (TR) and retinoid receptor (RXR) bind to each half site of the hormone receptor element  =  heterodimr


In the aabsence of their thyroid hormone ligand (T3) the thyroid receptors recruit corepressor proteins that inhibit transcription


But with T3 then T3 is bound to thyroid receptor and the corepressors are removed and coactivator is recurited


The production of specific on RNA codes for synthesis of specific enzymes that change the metabolism of the target cell  


if the D is the same + heterodimer  


The RXR receptor and its retinoic acid ligand form a link between mechanisms of thyroid hormone, vitamin A, vitamin D and other important regulators of genetic expresion.

hormones that use 2nd messengers

catecholamines, polypeptides, and glycoproteins cannot pass through lipid of target cell's membrane.


they bind to receptor proteins on outer surface of target cell membranes.  

the hormones are messengers from endocrine gland

and the mediator is the 2nd messenger that is within the cytoplasm

2nd messengers are part of   a  signal mechanism

extracellular hormones are transducted into intracellular by 2nd messengers


Must be specific proteins in the membrane for those hormones to bind to to get a second messenger. 


Based on enzyme in membrane that is activate one of the 3 second messengers is activated.

1.  adenylate cyclase

2.  phospholipase C

3.  tyrosine kinase


adenylate Cyclase Cyclic AMP 

cAMP second messenger


cAMP activates proein kinase in cytoplasm

the hormone increases cAMP productin   increased protein kinase withthe target cell

Active protein kinase catalyzes    

phosphorylation of different proteins in the target cells

modulates some ationd of enzymes

like all biologically active molecules, cAMP must be rapidly inactivated to functin as a second messenger in hormone action

Phosophidiestrace in target hydrolyzes cAMP into inactive form

the  hormone that uses cAMP for a second messenger depends on continuous making of new cAMP and depends on level of secretion of the hormone

Theophyline and caffine raises cAMP

smooth muscle stimulation by cGMP


Viagra inhibits phosphodiesterace enzyme

that breaks down cGMP

Phospholipase C Ca++  second messenger

For hormones that are polar and water soluagle and can't get through membrane


The concentration of Ca++ is kept low in the cytoplasm by the action of active transport carriers-calcium pumps-in the membrane

and endoplasmic reticulum have calcium pumpsthat pump Ca++ from the cytoplasm into the cisternae of the endoplasmic reticulum--then prn give Ca== to cytoplasm that signals other control systems.  And Ca++ itself is part of a second messenger system in some hormones


2 types of andrenergenic receptor in membrane= alpha and beta

stimulation of beta adrenergic receptor by epinephrine causes activation of cAMP

Stimulation of alpha adrenergic receptor by epinephrine in contract, activates the target cells via Ca++ second messenger system

the binding of epinephrine to its alpha adrenergic receptor activates G-protein called phospholipase C in membrane


Tyrosine Kinase second messenger

Insulin promotes glucose and amino acid transport and stimulates glycogen, fat and protein synthesis in the target organs, liver, muscle and adipose tissue.


Insulin's way of action is similar to regulatory molecules -growth factors

Growth Factors = autocrine regulators


Receptor protein in membranes and itself is an enzyme = Tyrosine Kinase


A kinase is = an enzyme that adds P groups to proteins


receptors are alpha and beta subunits.


Beta spans the membrane

alpha is on extracellular side andhas ligand (insulin) binding sites


Insulin binds to alpha then beta phosphorylaes each other = aotophosphorylation

This activates tyrosind kinase activity of insulin receptor


cause insertion of transport carrier protein for glucose into the plasma membrane--  therby promots lowering of plasma glucose concentration

Signal molecules activate second messenger systems in target cells  and lets insulin  and GF to regulate some of metabolism of target cells


Insulin uses tyrosine kinase second messenger system to stimulate glucose uptake in the liver  and its synthesis into glycogen   

glucogon from from pancreatic islets act on same cells for opposite effect    hydrolysis of glycogen and secretion of glucose   via cAMP


Glucagon is a hormone secreted by the pancrease that acts in opposition to insulin in the regulation of blood glucose levels.


glycogen is a storage for glucose occurring chiefly in the liver, in muscle


glucose is secreted into the blood only by the liver










Glucagon is a hormone secreted by the pancrease that acts in opposition to insulin in the regulation of blood glucose levels.


glycogen is a storage for glucose occurring chiefly in the liver, in muscle


glucose is secreted into the blood only by the liver


anterior pituitary

redish color



secretion of its hormones are controlled by hypothalmus releasing and inhibiting hormones


secretes tropic hormones



ATCH=can cause dark skin in Addison's disease


FSH =growth of ovarian follicles and production of sperm


LH= ovulation and conversion of of ovulated ovarian follicle into endocrine structure corpus luteum


LH stimulates secretin of testosterone from testes


PRL prolactin=milk productin and relates FSH and LH   acts on kidney to regulate water and lytes





Posterior pituitary

white, neuro

stores and releases 2 hormones

It make nothing, only stores


Oxytocin =stimulates uterin contractions and mamary glands and ducts for milk ejection


secretions are controlled by  target glands

negative feed back


hypothalmus has a hypophyseal portal system


target gland can act on hypothalmus to inhibit secretions of releasing hormone


the hormones from the hypothalmus end in RH for releasing hormone


target land an act on anterior pituitary to inhibit its response to releasing hormone


increased estradiol stimulates anterior pituitary to surge LH for ovulation  this is a positive feedback effct  but later increased estradiol is a negative feed back that inhibits LH


hypothalmus gets neural from amygdal and emotional stress

the anterior pituitary and target and perhaps hypothalmus

the actions are

referred to   as axis

like pituitary-gonad axis


hypothalmus gets neural input and can be affected by stress

Adrenal Cortex

outter area


Corticoids :


1 mineralcorticoids = aldosterone ALD is the stongest mineralcorticoid  stimulate kidney to keep Na+ and waer and excrete K+   this increases blood volume and blood pressure and regulates electrolyte baland


2 glucocorticoids = regulate organic molecules and glucose

cortisol mostly    stimulated by ATCH   effects on metabolism

stimulate gluconeogenesis (glucose from amino acids and lactic acid)

and inhibits glucose use which raises blood glucose level and promoes lipolysis and release of fatty acids

as medication, suppress immune response

side effects hyperglycemia and decreased glucose tolerance.....decreases synthesis of collegen and extracellular matrix proteins

increased bone resorption = osteoporosis

Cushing's syndrome from high ATCH or tumor of adrenal cortex

carb and protein metabolism changes, hyperglycemia, hypertension, muscular weakness, puffy look, buffalo hump and moon face



3 sex steroids DHEA for supplement ot gonads


All three are derived from cholesterol


Addison's disease

decreased glucocorticoids and mineralcorticoids


hypoglycemiea, Na= and K+ imbalance

hypotension, rapid weight loss, weakness

can die of electrolyte imbalance and dehydration

smoky color of skin from increased ATCH that can stimulate melanocytes

increased ATCH is from negative feedback form low glucocorticoid secretion

Medulla cortex

catecholamines  4:1 epinephrine

similar to sympthetic nervous system except hormonal effect lasts for 10 times longer


increased cardiac output, rate   dilates cornary blood vessels

increased alertness, increased respirations, increased metabolic rate, sweating


melulla innervated by preganglionic sympathetic axons and secretes hormones when sympthetic NS activated



tumor of medulla =  pheochromocytoma

  becomes totally fatigued and disease prone


pituitary-adrenal axis   

increased ATCH  so increased glucocorticoids from adrenal cortes


general adaption syndrome (GAS)


1.  alarm =medulla activated

2. resistance =readjustment

3.  if 2 fails exhaustion and sickness or death


stress = from severe infection, trauma, burns surgery

maybe immune system depressed too


The larges purely endocrine gland


T3T4 for growth and development and BMR

thyroid follicles secrete T4


activation of genes   stimulates proteinsynthesis, promote maturations of NS, increases cell respiration

increases BMR


parathyroid is to regulate Calcium


secretes PTH which increases Ca++


parafollluclar cells of thyroid

C cells of thyroid


secretes calcitonin   works in concert with parathyroid hormone (PTH) to regulate Ca++ in blood.  


calcitonin decreases Ca++ in blood


blood calcium high causes secretion of calcitone


blood calcium low causes decrease calcitone secretion


Blood calcium low causes increase of PTH



The most important hormone for Ca++ control in the blood.

It is the only hormone secreted by the parathyroid gland.


if blood Ca+ is low=PTH increases blood levels

It acts on bones, kidneys and intestines


secretes 2 hormones


Insulin to decrease BS and increases glycogen and fat


Glucagon to increase BS


(Mostly it secretes pancreatic juice)


The pancreas is both an endocrine gland

and an exocrine gland


alpha secrete glucagon


beta cells secrete insulin (2 X more beta cells)


increased BS stimulates beta cells to secrete insulin.  Insulin binds to receptor in membrane of targets cells and intracellular visicles containing GLUT 4 carrier proteins translocate to plasma membrane,

carrier proteins promote facilitated diffusion of glucose into cells and insulin target organs (muscles, liver, adipose)


and indirectly stimulates ativity of the enzyme glycogen synthesis in muscles and liver that promote conversion of intracellular glucose into glycogen for storage.

in muscle cells and liver and fat


Insulin causes glucose to leave plasma and enter target cells.


By these effects it lowers BS as it promotes anabolism.


Test of beta cells ability to secrete insulin and action of insulin to decreas BS + glucose tolerance test for DM




Glucagon from alpha cells of islets act against insulin

it increases BS

secreted - stimulated- by fall in BS when fasting

Glucagon stimulates liver to hydrolyze glycogen

together with the glucocortcoid hormones


Glucagon promotes catabolic effects

includinglypolysis andketogenesis

free fatty acids and ketone bodies serve as energy sources in fasting






placenta is also an endocrine gland


secretes big amoujnt of estrogens and progesterones and polypeptid and protein hormones similar to some from anterior pituitary


hCG  human chorionic gonatropin   


Autocrine and paracrine regulation



these hormones act in the organs that produce them


Autocrine = signaling in which a cell secretes a hormone or chemical messenger  that binds to autocrine receptors on the same cell

hormones and neurotransmitter

cytocrines and growth factors


Paracrine = produced in one tissue and regulate different tissue of same organ


The most diverse group of autocrine regulatiors

Prostaglandins are members of the family = eicosanoids

derived from precursor arachinoic acid


ADH                               classification and if lipophilic

calcitonin                          are they fat soluable?







FSH and LH




Sex steroid







ADH                  Peptides     Not lipid soluable            






Insulin           amino     not lipid soluable


FSH and LH    glycoprotein   not lipid soluable


aldosterone         Steroids    ARE FAT  SOLUABLE

cortisol                               are polar

Sex steroid



Thyroid       amine     is FAT soluable   



which hormones use homodimers?

aldosterone,  cortisol,   sex steroids

they are lipophilic


It binds to mRNA in Steroid-RNA-Steroid



which hormones use heterodimer mechanism of action?



Thyroid hormone




uses retinoic acid-RNA-T3

dimerization pattern on mRNA


name proteins that use the second messenger


and it is fat soluable or water soluble?





which is not fat soluble

it is lipophobic and so requires a 2nd messenger

because it cannot pass through the plasma membrane

what hormones use phospholipase C second messenger?
ADH and  oxytocin
what hormones use tyrosine kinase mechanism?
what hormones use cAMP mechanism
LH , FHS,  calcitonin,  PTH,  glucagon
what hormones use the steroid mechanism and are the fat soluble and cross membrane?

they are fat soluble and cross the membrane


glucocorticoids,  estrogen, progesterone, testosterone, alsosterone, D3, T3

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