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SUBJECT: BIOCHEMISTRY
 
TOPIC: MOLECULAR ENDOCRINOLOGY 1
 
LECTURER: DRA. UY
 
DATE: JANUARY 2011
 
 
Hormone Receptors
Biomedical Importance of Hormones  Hormones are present at very low concentrations
 Survival of multicellular organism in the ECF (compared to other proteins in ECF)
*they have to be low since hormones causes
 Intercellular communication (for survival)
significant changes when not controlled or plenty;
 Nervous system and endocrine system (as a whole) in signalling pathway, one hormone can amplify
millions and millions of response

Hormones  High degree of discrimination is provided by cell-


associated recognition molecules -> RECEPTORS
 They coordinate metabolism in the body
*receptor – protein; recogniton molecule
 They are substances that carry information from
 Hormones initiate their biologic effects by binding
sensor cells, which senses changes in the
to the receptors
environment (electrolyte iimbalance, anoxia or
hypoxia or low blood sugar level) to target cells,  A target cell is defined by its ability to the
which respond to these changes selectively bind a given hormone to its cognate
o Biochemical and physiological way of receptors
defining a hormone *Hormone receptors are selective and specific. Each of the
cells will have its own receptors or binding sites of
hormones. Low amount of hormone in the ECF will bind
Hormones right away to the receptor and initiate the biologic effect.
 Can be categorized by the site of synthesis: There is an amplification of signals in the binding of
hormone and receptor.
1. Endocrine hormones – are synthesized by
endocrine glands and transported by the blood
to their target cells. Classification of hormones by mechanism of action
- Production of hormone is faraway 1. Hormones that bind to intracellular receptors
from the target
 Androgens
2. Paracrine hormones - are synthesized near
their targets of action (ex. intestine)  Cacitriol (1,25(OH)2-D3)
3. Autocrine hormones – affect the cells that  Estrogens
synthesize them  Glucocorticoids
 Mineralocorticoids
Hormones are also categorized by Chemical Structure:  Progestins
1. Proteins or peptides – ex: insulin, glucagon;
 Retinoic Acid
synthesized as larger precursors that undergo
processing and secretion.  Thyroid Hormones (T3 and T4)
2. Amino Acid derivatives – cathecolamines and *PETCAT – Progesterone, Estrogen, Testosterone, Cortisol,
thyroid hormones Aldosterol, Thyroid Hormones (mnemonic)
Ex: Triiodothyronine, T3, T4, Epinephrine, 2. Hormones that bind to cell surface receptors
Norepinephrine, Levothyroxine, Thyroxine
A. The second messenger is cAMP
*tyrosine – very important amino acids
 a2 -adrenergic catecholamines
*TSH is not a thyroid hormone but a pituitary
hormone!  B – Adrenergic catecholamines

3. Fatty acid derivatives – eicosanoids  Adrenocorticotropic hormone (ACTH)


(ex.prostaglandins)  Antidiuretic Hormne (ADH)
4. Cholesterol derivatives – steroids  Calcitonin
5. Gases – nitric oxide (not a hormone in the strict  Chorionic gonadotropin, Human (hCG)
sense of the word but it can act on target cells)
 Corticotropin-releasing Hormone
*In the endothelial Nitric oxide synthase (ENOS)
 FSH
 Glucagon

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 Lipotropin (LPH) Hormone Ca2+,
Complex metabolites of
 LH complex
 Melanocyte-stimulating hormone (MSH) phosphoinositols,
kinase cascades
 Parathyroid Hormone (PTH)
 Somatostatin
 Thyroid-stimulating hormone (TSH)
Diversity of Endocrine System
B. The second messenger is cGMP
 Hormones are synthesized in a variety of cellular
 Atrial Natriuretic Factor arrangements
 Nitric Oxide  Discrete Organs – Thyroid, Pituitary and Adrenals
C. The second messenger is calcium or *what they are is what they secrete
phosphatidylinositol (or both)
Organs perform 2 distinct but closely related funtions:
 Acetylcholine (muscarinic)
 Ovaries – mature oocytes and estradiol and
 a1 – Adrenergic catecholamines progesterone
 Angiotensin II  Testes – mature spermatozoa and testosterone
 Antidiuretic Hormone (vasopressin) *this testosterone is weak compared to DHT
 Cholecystokinin (dihydrotestosterone
Specialicez cell within other organs:
 Gastrin
 Small intestine – glucagon like peptide (targets for
 Gonadotropin Releasing Hormone
new medication in diabetes)
 Oxytocin
 Thyroid – calcitonin (action is in bones and
 Platelet-derived growth factor (PDGF) parathyroid)
 Substance P  Kidney – Angiotensin II (control of blood pressure;
target for all Angiotensin II blockers)
 Thyrotropin-releasing hormone (TRH)
*kidneys also produces eryhtopoietin
D. The second messenger is a kinase or
phosphatase cascade
 Adiponectin Parenchymal Cells of more than one organ:
 Chrionic somatomammotropin  Skin, liver, kidney – calcitriol (vitamin B3)
 Epidermal growth factor
 Erythropoietin Hormones are chemically diverse

 Fibroblast growth factor (FGF)  They are synthesizied from a wide variety of
chemical building blocks:
 Growth Hormone (GH)
o Cholesterol Derivatives (all ssteroid hormones
 Insulin came here)
 Insulin-like growth factors I and II  17B – estradiol
 Leptin  Testosterone
 Nerve growth factor (NGF)  Cortisol
 Platelet-derived growth factor  Progesterone
 Prolactin  1,25 (OH)2 – D3
*common to them is the cyclopentanoperhydropenantrene
ring
General Feature of Hormone Classes
o Tyrosine
GROUP 1 GROUP 2
 T3 and T4
Types Steroid, Polypeptides,
iodothyronines, proteins,  Norepinephrine
calcitriol, glycoproteins,  Epinephrine
retinoids catecholamines
o Iodine – very important building bloackof
Solubility Lipophilic/ Hydrophilic/ Thyroxine or the thyroid hormone
Hydrophobic Liphophobic
o Polypeptides
Transport Yes No  TRH
Proteins
 ACTH
Plasma Half-Life Long (hrs- days) Short (min.)
o Glycoproteins (TSH, FSH, LH)
Receptor Intracellular Plasma
Membrane  Common a subunits
Mediator Receptor- cAMP,cGMP,  Unique b subunits

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*all of glycoproteins have a common a
subunits but differ in be subunites
*very low cholesterol can lead to brain tumors
Hormones are synthesized and modified for full activity in
variety of ways:
 Hormones synthesized in final form and secreted
immediately: those derived from cholesterol; ACTH
 Hormones synthesized in final form and stored:
catecholamines; fight and flight response
 Those synthesized from precursor molecules, then
processed and secreted upon cue: insulin (cue for
insulin is hyperglycemia or high blood glucose)
*blood sugar level is important in release of
pancreatic hormones
 Those converted to active forms from precursor
molecules in the periphery: thyroid hormones and
DHT
*thyroid hormones is more secreted as T4 and
peripherally converted to T3 which is more active
of the two.

Adrenal Steroid Hormones


 Adrenal steroid hormones are synthesized
from cholesterol.
*this image is very important!
*17  - Hydroxylase – if this enzyme act first (along with
An ACTH – dependent 17,20 lyase), you will produce dehydroepiandosterone (for
 steroidogenic acute regulatory (STaR) protein is masculinity)
essential for the transport of cholesterol to p450 *3B – hydroxysteroid dehydrogenase isomerase – regulator
scc (side chain cleavage) in the inner and should act first than 17a- hydroxylase so that
mitochondrial membrane. hormones can be regulated; progesterone will be produced
*cholesterol in P450 scc will be cleaved to produce from pregnenolone
pregnenolone and isocaproaldehyde *There is cellular specificity in adrenal steroidogenesis*
 All mammalian steroid hormones are formed from *there are three zones in the adrenal cortex: zona
cholesterol via pregnenolone through series of glomerulosa, zona fasciculate and zona reticularis
reactions (shuttling) occurring either in the
mitochondria or ER of the adrenal cell. *Aldosterone synthesis will occur only in the zona
glomerulosa cells because the enzymes 18 – hydroxylase
*adrenecorticotrophin and ACTH is the same (aldosterone synthase) & 18 – hydroxysteroid
dehydrogenase are found only in that region.
*aldosterone acts on the renin-angiotensin-aldosterone-
system for blood pressure
*most common problem of mutation or deficiency in the
adrenal gland is the 21 hydroxylase enzyme (deficiency is
also called the masculinization syndrome since deficiency
in this enzyme, you will have abundant masculine
hormones since the formation of aldosterone and cortisol is
blocked)
*17  - Hydroxylase and 21- hydroxylase are smooth ER
enzymes while 11  - hydroxylase is a mitochondrial
enzyme.
*Steroidogenesis - involves the repeated shuttling of
substrates into and out of the mitochondria. (along the way
they will be caught by other proteins during shuttling -
problem)
*adrenal medulla produces cathecolamines
adrenal cortex produces the thyroid hormones
*basic steroid hormones – differ only in attachment
Testicular Steroidogenesis
 Immediate precursor is cholesterol

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 Rate limiting step: delivery of cholesterol into the
inner membrane of the mitochondria by the STaR Ovarian Steroidogenesis
protein
Estrogen are of 3 types:
 The conversion of cholesterol to pregnenolone in
the ovary & testes is promoted by LH rather than  17  - Estradiol is the primary estrogen of ovarian
ACTH. origin; most potent of the three; responsible for
femininity;
*ACTH is responsible for children, but as you grow up it
 Estriol is abundant estrogen during pregnancy;
is the LH
this comes from the placenta;
 Estrone – abundant when post-menopausal since
there are no more production of 17B-estradiol;
*female cannot live without men since you cannot have
estradiol comes from testosterone.
*Aromatase – very important enzyme; responsible for
female odor (in dogs: pheromones); Aromatase is
responsible for synthesizing estradiol from testosterone
and also converts androstenodione to estrone.
*16a-hydroxylase- converts estrone to estriol; abundant in
placenta during preganancy

*progesterone also comes from pregnenolone;


Progesterone is also more fluid-retaining than other
estradiol thus when at the end of the term there is edema
formation because of increase in progesterone

Biosynthesis of Estrogen

*At the adrenals, the final form is the androstenedione and


dehydroepiandrosterone, but in the testicular level meaning
males, they will be converted to Testosterone through the
enzyme 17B-hydroxysteroid dehydrogenase (in
Dehydroepiandrosterone, it first become androstenodione
before testosterone.)
*This happens when the child is in puberty (testicular
steroidogenesis). Adrenal steroidogenesis happens even
before puberty.
*Dihydrotestosterone is formed from Testosterone in
Peripheral Tissues (prostate and testis). DHT is most
potent even than testosterone. DHT is the cause of the
benign prostatic hypertrophy too much production of DHT)
*The most significant Metabolic product of
testosterone is DHT, the active form of this
hormone. DHT is an active metabolite since it got another
H+.
* 5a-reductase +NADPH – another important enzyme and
another important cofactor; for reduction process from
Testosterone to DHT.
*5a-reductase inhibitor is used for treating benign prostatic
hypertrophy. Ex: Xatral, Finasteral, Dutasteride

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*1, 25 (OH)2 – D3 (Calcitriol) is synthesized from a
Cholesterol Derivative; needs 3 organs to be formed;
*7-Dehydrocholesterol comes from the adrenal. With the
action of the sunlight on the skin, you will form previtamin
D3 and then the liver you have 3 different enzymes:
 25 Hydroxylase – Forms 25-
Hydroxycholecalciferol (25[OH]-D3) and
activated by the following 2 hydroxylases
 24-hydroxylase – forms 24,25 (OH)2-D3
 1a- hydroxylase – forms 1,25 (OH)2-D3
(calcitriol)
*Both 24-hydroxylase and 1a-hydroxylase are needed for
the formation of the 1,24,25 (OH)3-D3

Catecholamines & Thyroid Hormones - made from Tyrosine


 Catecholamines are synthesized in final form and *Tyrosine is the immediate precursor of catecholamines.
stored in secretion granules.
 Epinephrine – major product of adrenal medulla *Tyrosine hydroxylase is the rate-limiting enzyme in the
(80%) catecholamine synthesis that forms Dopa from Tyrosine

- not made in extramedullary tissue *Dopa carboxylase – forms dopamine from Dopa
*Dopamine b-hydroxylase – forms Norepinephrine from
dopamine.
*PNMT (phenylethanolamine-N-methytransferase – forms
epinephrine from norepinephrine.
*Catecholamines cannot cross the blood, brain barrier;
hence in the brain they must be synthesized locally.
*Parkinson’s disease - a CNS disorder where there is local
deficiency of dopamine synthesis; symptom: shuffling gait
* L- Dopa (levodopa or sinemet) - important agent in
treatment of Parkinson’s disease since it readily crosses
the BBB (blood brain barrier; you will produce Dopamine

*aromatase – responsible in patient with cirrhosis or


hepatic enceopathy in which they have a problem where
the androstenedione will be converted to estrediol so you
will have estrogenezation of the males. Males with this wil
have big breasts and some are even milking. Aromatase
are abundant in liver and in adipose tissues (thus fat =
boobs)
Thyroid Hormone Synthesis:
1. These hormones require Iodine, a rare element, for
bioactivity
2. They are synthesized as part of a very large
precursor molecule (thyroglobulin)
3. They are stored in an intracellular reservoir
(colloid).
4. There is peripheral conversion of T4 to T3

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*if all T4 are converted to T3 immediately, you wll have *to test for the diabetes, you need to test for C peptide
hyperthyroidism or very fast metabolism (connecting) since they will be cleaved in the liver and are
*NADPH, oxygen, tyrosine and iodine is needed in this the active ones. This mean it will not be destroyed since it
processes will not be stored for so long and recycled.

*Thyroglobulic iodination – iodination of thyroglubulin after


Iodine was oxidized by peroxidase coming from the Parathyroid Hormone (PTH)
capturing of NADPH of oxygen and H+
• Secreted as 84 – amino acid peptide
*Coupling of the MIT and DIT will result to T3. Coupling of • its biosynthesis & secretion are regulated by the plasma
the DIT with DT results to T4. This stored intracellularly as a
ionized Ca+ concentratio
colloid that is part of large precursor molecule called the
thyroglobulin. As the demand increases for T3 and T4, the • a decrease in Ca+  marked increase in PTH synthesis
more T3 and T4 is released extracellularly. & secretion
*Na+-K+ ATPase trasporter is also needed in this pathway. • Also has a C-fragment sequence
*All are from the anterior pituitary except PTH.

Insulin:
 synthesized as a prohormone & modified within
the  - cell.
 one of the hormones made from larger peptide
precursors made up of: *Angiotensin II is also synthesized from a large precursor;
o Connecting peptide – produced from liver; is also involved in aldosterione regulation
connects a-chains and B-chains *The RAS is involved in the regulation, of BP and
o a-chains – has a intra-sulfide bond (Cys11 electrolyte metabolism (thru aldosterone production)
– Cys6)
o B-chains – *In the diagram below, Angiotensinogen is converted by
Renin to Angiotensin I. Angiotensin - converting Enzyme
*a-chains & B-chains - has 2 separate inter-sulfide bonds converts Angiotensin I to II which is acted upon by
(bet. Cys20 of alpha and Cys19 of Beta and bet. 2 Cys7) Aminopeptidase to for Angiotensin III. Degradation products
*insulin in the market is modified in the B-chains. are formed by angiontensinases from angiotensin III. The
active form is the angiotensin II.

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Binding Very High Low
Specificity
Saturability Yes No
Reversibility Yes Yes
Signal Yes No
Transduction

Actions of Specific Hormones

HYPOTHALAMIC HORMONES
•VASOPRESSIN and OXYTOCIN
•OTHER HORMONES that regulate the synthesis and
release of hormones from the anterior pituitary

HORMONES OF THE ANTERIOR PITUITARY


•PROLACTINOMA
- the most common tumor of the pituitary
- double vision, amenorrhea, and galactorrhea
•Hyperprolactinona

Pro-opiomelanocortin (POMC) Peptide Family - can result from drugs that inhibit dopamine
action: antipsychotic drugs (Thorazine)
 consists of peptides that act as hormones (ACTH,
LPH, MSH) & others that may serve as *Galactorrhea – letting down of milk; spontaneous flow of
neurotransmitters or neuromodulators (endorphins) mlik
 Products of POMC cleavage:
o ACTH •GROWTH HORMONE (GH):
 a-MSH
 CLIP (corticotropin-like - Stimulates release of insulin-like growth factors
intermediate lobe peptide) (somatomedin)
o B-LPH (lipotropin) - Antagonizes the effects of insulin on
 y-LPH carbohydrates and fat metabolism
 B-endorphin
 B-MSH - its release is inhibited by somatostatin
 y-Endorphin
 a-Endorphin
•THYROID - STIMULATING HORMONE
- Stimulates the release of T3 and T4 from the
thyroid gland.
Diversity in the Storage of Hormones - released from anterior pituitary through the signal
Hormone Supply Store Cell of the TSHRH from hypothalamus

Steroid and 1,25 (OH)2-D3 None - used to screen patients for thyroid disease.
- elevated levels suggest hypothyroidism (negative
Catecholamines and PTH Hours
feedback)
Insulin Days
- low levels suggest hyperthyroidism (negative
T3 and T4 Weeks feedback)
*no patient will suffer from hypo or hyperthyroidism *If patient has hyperthyroidism, the feedback mechanism
immediately. Hyperthyroidism is a suttle disease. It can signals the anterior pituitary to decrease the release TSH.
occur years after you have thyroidectomy. The same can be said to those hypothyroidism.
*Type I diabetic patients can survive without insulin for 4-5
days and until day become coma. •LH and FSH:
*Catecholamines and PTH stores for hours that’s why you - stimulates the GONADS to release hormones that are
can have an adrenaline rush for hours and feel week after. involved in reproduction
Comparison of Receptors with Transport Proteins - their release is stimulated by GnRH and inhibited
Feature Receptors Transport Protein by GnIH from the hypothalamus
Concentration Very Low Very High
(thousands/cell) (billions/uL) •Protein product of the PRO-OPIOMELANOCORTIN gene
Binding affinity High (pmol – Low (umol/L - produced in response to CRH from the
nmol/L range) range) hypothalamus

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- cleaved to generate a number of peptides: - Cortisol and Epinephrine act in concert to supply
1. ACTH – cortisol ; has permissive effect on production of fuels to the blood so that energy can be produced to
aldosterone combat stressful situations
- Anti-inflammatory effects: induce synthesis of
2. Lipotropin (LPH)- cleaved to form MSH and endorphins
lipocortin which inhibits phospholipase A2, rate limiting
*If you have a pituitary problem that involves this, there will enzyme of protaglandin synthesis .
be a darkening of the skin.
- Suppress the immuned response by causing lysis
THYROID HORMONE of lymphocytes
•T3 is more active than T4 - Influence metabolism by causing movement of
•Most T3 is produced by deiodination of T4 fuels from peripheral tissues to the liver
•During starvation,T4 is converted to reversed T3 (RT3), - Promotes gluconeogenesis by inducing synthesis
which is not active of PEPCK
•Binds to nuclear receptors and regulates the expression
of many genes. HYPERCORTISOLEMIA
•Needed for growth, development, and maintenance of •likelihood of infection
almost all tissues
•Glucose CNS effects: hyperirritability or depression
•Stimulates oxidative metabolism and causes basal
•BONES : osteoporosis
metabolic rate to increase
•Muscle : loss of protein leading to weakness

•HYPOTHYROIDISM •Thinning of dermal and epidermal structures: striae

- Generation of ATP id reduced, causing a sense of •Increased vascular fragility : easy bruising
weakness, fatigue, and hypokinesis •Increased intolerance or overt diabetes
-the reduced BMR is assoc with decreased heat •Central obesity: buffalo hump and moon facies
production, causing cold intolerance and decreased
sweating.
•CUSHING SYNDROME
- Less demand for delivery of fuels and oxygen to
peripheral tissues hence circulation is slowed, decreased - If caused by excessive production of cortisol by an
heart rate and BP adrenal tumor or by intake of exogenous glucocorticoids

•HYPERTHYROIDISM •CUSHING DISEASE


-BMR is increased because the rate of oxidation of - hypercortisolemia caused by excessive secretion
fuels by muscles and other tissues is increased. of ACTH by a pituitary tumor
- increased heat production: heat intolerance and
increased sweating •EPINEPHRINE
-elevated tone of sympathetics: inc HR and BP - Increases blood glucose by stimulating liver
- Weight loss is severe because of excessive rate of glycogenolysis
fuel oxidation - Stimulates lipolysis in adipose tissue and
glycogen degredation in muscle
HORMONES that STIMULATE GROWTH - Makes fuels available for “fight or flight”
•INSULIN and GH
•GH antagonizes many of the metabolic actions of INSULIN, HORMONES that REGULATE SALT and WATER BALANCE
stimulating gluconeogenesis and promoting lipolysis. •ALDOSTERONE
•Alternative fuels are therefore made available so that -causes the production of proteins in cells of the
muscle protein can be preserved distal tubule and the collecting ducts of the kidney:
1. Permease is produced that allows
•GIGANTISM sodium to enter cells from the lumen
- Caused by excessive secretion of GH as a result 2. Citrate synthase is induced ( inc TCA
of a benign tumor of the ant pituitary gland and the hence ATP production)
hypersecretion begins before closures of the growth 3. Na-K ATPase pump is induced
centers in the long bones
- K and H ions are lost; Na is retained; water is
•ACROMEGALY resorbed; blood volume and pressure are increased
- if hypersecretion begins after the growth centers
have closed
•PRIMARY HYPERALDOSTERONISM
- Conn Syndrome
HORMONES THAT MEDIATE THE RESPONSE TO STRESS
- aldosterone-secreting tumor of adrenal gland
•GLUCOCORTICOIDS
- sodium retention and potassium secretion with
resultant hypertension and hypokalemia

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•LH stimulates Leydig cells to produce and secrete
•ADDISON DISEASE testosterone.
•FSH acts on Sertoli cells to promote the synthesis of
- loss of adrenocortical steroids
androgen-binding protein (ABP).
- the mineralocorticoid deficiency leads to:
•ABP binds testosterone and transports it to site of
loss of sodium ions and water in the spermatogenesis, where testosterone is converted to DHT
urine and reciprocal potassium retention by 5-α-reductase.
(hyperkalemia), and hydrogen ions (mild met.acidosis)
•Testosterone is responsible for masculinization during
- reduction in BP early devpt, and at puberty,sexual maturation of the male.

HORMONES THAT CONTROL PRODUCTION •5-α-reductase:


- required for normal male development.
The Action of FSH and LH on the OVARY - genetic deficiency results in a phenotype similar
•The Menstrual Cycle to androgen insensitivity syndrome.
1.FSH acts on the follicles to promote maturation - drugs that inhibit this enzyme (ex: finasteride) are
of ovum and to stimulate estradiol production used to inhibit the effects of DHT in males,like male pattern
and secretion. baldness and BPH.
2. Estradiol causes thickening and
vascularization of uterine endometrium.
3. LH surge at midcycle stimulates HORMONES THAT PROMOTE LACTATION
ovulation, formation of corpus luteum and
secretion of progesterone and estradiol.
4.Progesterone causes the endometrium to PREPARATION OF THE MAMMARY GLAND FOR LACTATION
continue to thicken and increase its secretory capacity. •Prolactin, glucocorticoids, and insulin are the major
hormones responsible for the differentiation of mammary
alveolar cells into secretory cells.
•Events in the Absence of Fertilization
•Prolactin stimulates the synthesis of milk proteins, casein
1. Corpus luteum regresses due to and α-lactalbumin.
declining LH levels. Progesterone and estradiol
•Progesterone inhibits milk protein production and
levels decrease.
secretion during pregnancy.
2. Low steroid hormone levels cause the cells to
•At term,when proesterone levels fall, the inhibition of milk
die and the endometrium is sloughed off (menstruation).
protein synthesis is relieved.
•Oral contraceptive pills – have low levels of estrogen and
progestin derivatives. *Dopamine – inhibit release of prolactin
REGULATION OF MILK SECRETION DURING LACTATION
- reduce both LH and FSH levels.
- destroy the normal cyclicity of hormones and •Prolactin causes milk proteins to be produced and
secreted into the alveolar lumen.
result in a failure to ovulate prevent conception.
•Oxytocin causes contraction of the myoepithelial cells
surrounding the alveolar cells and the lumen, and milk is
•Events following Fertilization ejected through the nipple.
1. Corpus luteum is maintained initially by hCG. •The secretion of both PRL and OT by the pituitary is
2.Subsequently, the placenta produces hCG and stimulated by the suckling of the infant and by other factors.
progesterone.
3.After the corpus luteum dies,placenta HORMONES INVOLVED IN GROWTH AND DIFFERENTIATION
continues to produce large amts.of
•Retinoids are produced in the body from dietary Vit. A.The
progesterone.
major source,β-carotene, is cleaved into 2 molecules of
4. Near term, progesterone levels fall. retinal.
5. PGF2α and oxytocin stimulate uterine •Retinal (an aldehyde) and retinol (an alcohol) are
contractions, and the infant is delivered. interconverted by oxidation and reduction reactions.
•Retinoic acid is produced by oxidation of retinal and
•Pregnancy Tests cannot be reduced.

- detect the presence of hCG in the urine. •Retinol,the transport form,is stored as retinyl esters.
- serum quantitation of hCG levels can be used to •Retinal is a funtional component of the visual cycle
differentiate a normal intrauterine pregnancy from an reactions.
ectopic pregnancy. •Retinoic acid is involved in growth and also in
•Pitocin – synthetic form of OT that can be administered differentiation and maintenance of epithelial tissue
during labor to initiate or augment labor.
HORMONES THAT REGULATE CALCIUM METABOLISM
The Action of FSH and LH on the Testis •Parathyroid hormone (PTH), 1,25-DHC,and Calcitonin are
the major regulators of Ca metab.
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•PTH, produced in response to low Ca levels,acts to •GASTRINOMAS
increase Ca levels in the ECF. - gastrin-secreting endocrine tumors associated
•1,25-DHC stimulates the synthesis of a protein involved in with Zollinger-Ellison syndrome.
Ca absorption by intestinal epithelial cells. - increased hydrochloric acid production with
Calcitonin lowers Ca levels by inhibiting its release from resultant recurrent peptic ulcers.
bone and stimulating its excretion
•VIPomas
- rare tumors that secrete VIP
•HYPERPARATHYROIDISM- patients can present with
- watery diarrhea, hypokalemia, and achlorhydria
fractures of long bones,renal stones, GI
disturbance,lethargy and weakness.
1. Primary – the result of tumor of the INSULIN AND GLUCAGON
parathyroid gland. •INSULIN
2. Secondary – as a result of renal failure. - elevated in the fed state
•HYPOPARATHYROIDISM –most often due to trauma to the - promotes storage of fuels: glycogen and
parathyroids during surgery of the thyroids triacylglycerol.
- stimulates glucose transport into muscle and
HORMONES THAT REGULATE UTILIZATION OF NUTRIENTS adipose cells.
- stimulates protein synthesis and growth
GUT HORMONES
•Gastrin from gastric antrum and the duodenum •GLUCAGON
stimulates gastric acid and pepsin secretion. - elevated during fasting
•Cholecystokinin (CCK) from the duodenum and jejunum - increases the availability of fuels (glucose
stimulates contraction of the GB and secretion of and fatty acids) in the blood.
pancreatic enzymes.
- stimulates glycogen degradation in the liver but
•Secretin from duodenum and jejunum stimulates the NOT in muscle.
secretion of bicarbonate by the pancreas.
- stimulates gluconeogenesis and lipolysis in
•Gastric inhibitory polypeptide (GIP) from the small bowel adipose tissue.
enhances insulin release and inhibit gastric acid secretion
Vasoactive intestinal polypeptide (VIP) from the pancreas
relaxes smooth muscles and stimulates bicarbonate <end of transcription>
secretion by the pancreas

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