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183 Cards in this Set

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Generally, what are the five stages of synthesis Dr. Cool would like us to know for each hormone?
1. Synthesis
2. Packaging
3. Processing
4. Release
5. Degradation
The five classification criteria for hormones?
1. Chemical composition
2. Solubility
3. Location of receptors
4. Where they are produced
5. The second messenger
The eight general hormone types (excluding the gonadal protein and steroid hormones)
Peptide, Thyroid, Catecholamine/Seratonin/Melatonin, Acetylcholine, Histamine, Nitric Oxide, Eicosanoid, Steroids
The three types of steroid hormones (non-gonadal) and their common origin.
Androgens, Mineralcorticoids, Glucocorticoids. They are all from the adrenal gland.
Level of hormones in extracellular fluid?
10^-15 - 10^-9 M.
Two possible locations for the hormone receptor
Plasma membrane (proteins) and within the cytoplasm/nucleus (steroids)
Is the affinity of a receptor for the hormone high or low?
Very very high. The Kd value is usually .0000001-00000000001
Characteristics of hormone binding
effect increases with concentration, saturable, highly specific.
How is hormone binding coupled to signal transduction?
second messengers, phosphorylation, and gene transcription regulation.
Flow of hormone release from a sensory input
External/internal receptor (touch or temperature) -> CNS -> hypothalamus -> pituitary -> target cell. THERE ARE SOME MAJOR EXCEPTIONS TO THIS RULE. Consider the pineal gland.
The triad center of the neuroendocrine system
Hypothalamus-Pituitary-Adrenal, this is often called the HPA axis.
Hormone evolved from long protein precursors?
Proteins or peptide
Hormones that are amino acid derivatives?
Thyroid, Catecholamines, Serotonin, Melatonin, Histamine
Hormones that begin as phospholipids and become arachidonic acids?
Hormones derived from cholesterol?
Hormone made from the individual components of amino acids?
Nitric Oxide
Hormone that doubles as a small organic neurotransmitter?
3 regulatory mechanisms for hormone synthesis
Negative, positive, and feedback control. Dr. Ream and cool have differing opinions on the meaning of these terms. I'd go with Dr. Ream's (negative feedback control and positive feedback control)
2 hormone inactivation mechanisms
1. Inactivation via enzymes
2. Removal from receptor region.
Generally, the three pathologies associated with hormones are?
1. Overproduction, say, in cancer.
2. Underproduction, in auto-immune disorders
3. Target cell insensitivity--genetic receptor lack or downregulation
4 glands that produce peptide hormones and BE CAREFUL, because there are really only 3.
1. Adenohypophysis
2. Neurohypophysis
(Dr. Cool considers these separate, but they are both the pituitary)
3. hypothalamus
4. Pancreas
2 pituitary hormones of the neurohypophysis and their functions. Are these peptides?
1. AVP/ADH: water resorption in principal cells and arteriole constriction
2. Oxytocin: Milk ejection and uterine contractions
6 HUMAN pituitary hormones of the adenohypophysis and their functions. Are these peptides?
Don't worry about acidophil or basophil on this flashcard.
1. TSH: Synthesize/secrete thyroid hormones
2. FSH: Sperm maturation or follicular/estrogen development
3. LH: Testosterone synthesis or ovulation
4. GH: Growth
5. Prolactin: Make milk
6. ACTH: Synthesis/Secrete adrenal cortex hormones
6 peptide hormones of the hypothalamus and their functions on the pituitary
TRH: secrete TSH, prolactin
CRH: secrete ACTH
GnRH: secrete LH/FSH
SRIF: inhibit secretion GH
PIF: inhibit secretion of prolactin
GHRH: secretion of GH
If you see somatostatin, what should you assume it's doing?
Inhibiting the hell out of someone else. It's not an activator. From the latin SOMATO (Body) STASIS (Unchanging)
Thyroid peptide hormone
Calcitonin: decrease blood calcium
Parathyroid peptide hormone
PTH: increase blood calcium (remember osteoclasts and PTH)
2 placental peptide hormones
HCG: stimulates estr/progest in corpus luteum.
HPL: The l is for lactose. Makes milk in similar fashion to prolactin when pregnant.
2 main pancreatic hormones
alpha:(glucagon): increase blood glucose
beta: (insulin): decrease blood glucose.
If you don't know this by now, OfficeMax is hiring
Kidney peptide hormone
Renin: Cleaves angiotensinogen to angiotensin I
Is this flashcard just filler?
Preprohormone vs. prohormone vs. hormone
A preprohormone has three regions, from start to finish, that I'll call 0,1,2. 0 is a little weird cap of nucleotides, and 2 is a really long string of non-hormonal nucleotides. 1 is the hormone.
To get a prohormone, you have to cleave off 0, leaving 1 and 2. To get the functional hormone, you need to cleave off 2, leaving 1. 1 is the hormone encoding string. pg. 919
What does Dr. Cool call a hormone that releases secretory product in the regulatory pathway?
A secretagogue. Please don't ask me why.
REVIEW: Cellular peptide synthesis, step 1
Synthesis begins, the signal peptide is recognized, synthesis continues in the ER: signal peptide cleavage/disulfides formed/folding/glycosylation, etc. The peptide is moved to Golgi.
REVIEW: Cellular peptide packaging, step 2
Prohormone is packaged in immature granules in TGN, with processing enzymes.
REVIEW: Cellular peptide processing, step 3
The processing enzyme cleaves the paired-basic residues at C-terminus, in an acidic ISG made so by proton pumps.
After removal, the prohormone is amidated and made active
REVIEW: Cellular peptide secretion, step 4
Now mature, the SG's move to cell membrane to await the signal to release their contents in the extracellular environment
REVIEW: Cellular peptide degradation
Live for a few minutes, eaten by serum and cell-surface proteases, swallowed via endocytosis and degraded in lysosomes. The receptor may be recycled.
What enzyme removes paired-base residues?
Carboxypeptidase E
What enzyme amidates residues?
What cleaves (trims) the prohormone in the ISG?
Prohormone convertases 1 and 2
The RSP in endocrine and neuroendocrine cells?
Specialized for secretion of peptide hormones
What is a sorting signal?
A string in the propeptide that causes it to be "sorted" away from constitutive proteins
What are the four inhibitors of ACTH release and how do they work?
1. Cortisol: feedback inhibition at the pituitary--NO ACTH
2. Cortisol: feedback inhibition at the hypothalamus--NO CRH
3. Dopamine: inhibits RELEASE of ACTH from adenohypophysis
4. ACTH: self-inhibition at hypothalamus--NO CRH
What do ACTH and cortisol have in common?
A nearly-simultaneous circadian rhythm and episodic releases.
What is Cushing's syndrome?
Hypercortisolism as a result of an adenoma in adrenal cortex.
What is Cushing's disease?
Hypercortisolism as a result of pituitary tumor. ACTH never shuts off.
Two drugs used to treat Cushing's syndrome
Ketoconazole and Metyrapone
How do you treat Cushing's disease?
Remove the pituitary tumor.
How can you tell if someone has either Cushing's disease or syndrome, since they both result in excess cortisol?
1. If it is the syndrome, the adrenal gland is malfunctioning. Therefore, there won't be a lot of ACTH around because the pituitary is working normally.
2. If it is the disease, there will be a boatload of ACTH and relatively less (suppressed) cortisol, because the cortex is fine while the pituitary is out of control.
Common symptoms of Diabetes Insipidus
Weakness, polydipsia, polyuria and occasionally in youth mental retardation due to prolonged dehydration
What are the four causes of diabetes insipidus and how do you treat them?
Nephrogenic: ADH receptors in kidneys are dimished or mutated. Give ibuprofen.
Gestational: a side effect of pregnancy, use desmopressin or wait it out.
Dipsogenic: excessive fluid intake. STOP DRINKING SO MUCH WATER.
Neurogenic: defect in ADH secretion, x-linked or dominant. Use desmopressin
3 characteristics of catecholamines, seratonin, and melatonin?
1. Made from AA
2. Small
3. Neurotransmitters
What's the main function of catecholamine derived hormones?
Severe stress response.
Function of epi
Fight or flight. short-term distal artery expansion, proximal constriction, dilated pupils, elevates blood-sugar, breakdown lipids and glycogen, **suppression of immune system
Function of norepi
Fight or flight, attention, muscle readiness, increase energy
Function of dopamine
Focus, inhibit release of prolactin
What is the locus ceruleus?
A part of the brainstem where stress response, particularly the norepi pathways, initiates.
Epi is made where?
adrenal medulla.
Norepi is made where?
CNS, adrenal medulla, sympathetic nerves
Dopamine is made where?
CNS, but it cannot cross the BBB
Catecholamine production, flow from tyrosine entering the cell...
Tyrosine hydroxylase makes DOPA from tyrosine -> DOPA decarboxylase makes dopamine from DOPA -> dopamine enters a secretory vesicle
Catecholamine production, flow from dopamine entering the secretory vesicle.
Dopamine-b-hydroxylase makes norepi from dopamine
phenylethanolamine-N-methyltransferase makes epi from norepi
Catecholamine packaging
Dopamine uses ATP to get into a secretory vesicle
Catecholamine processing
Other than making epi/norepi from dopamine, that's it
Catecholamine secretion
Typical depolarization, Ca influx yadda yadda yadda
Catecholamine degradation
MAO/COMT degrade, the catecholamines can be reuptaken as well.
Catecholamine reuptake inhibitors? (cures for depression, anyone?)
Cocaine, tricyclic antidepressants (MAOI inhibitors)
What does Dr. Cool call the catecholamine post-synaptic receptors?
What is COMT? Why do we care?
Catechol-O-methyltransferase. It is a membrane-bound uptake transporter for released catecholamines. If you inhibit it, for example, L-DOPA will remain near active receptors longer and can reduce symptoms of Parkinsons
Where is COMT?
Postsynaptic neurons, glia
What is MAO? Why do we care?
Monoamine oxidase. Catabolizes monoamines in food. Serotonin, Norepi, and epi are broken down by MAO-A, and phenylethylamine is broken down by MAO-B. Both eat dopamine.
Where is MAO?
Membrane of mitochondria, neurons, astroglia. B is is CNS, while A hangs out all over the gut.
What is the final product of catecholamine degradation?
Homovanillic acid
The most common diseases of catecholamines?
Parkinson's, tumors in adrenal medulla or sym ganglia
Causes of Parkinson's?
Viral encephalitis, toxins, drugs, neurodegeneration, idiopathic, multiple infarct, trauma, etc etc.
Treatments for Parkinsons
L-DOPA, Levodopa/Carbidopa, any agonist for dopamine.
Symptoms of tumors of adrenal medulla or sym ganglia? Treatments?
Hypertension, tachycardia. Standard cancer triad.
Serotonin affects what?
mood, sleep, appetite, sexuality, emesis, **liver regeneration
4 psychiatric disorders associated with serotonin malfunction?
Bipolar, depression, anxiety, migraines.
Function of melatonin?
Turned on by darkness, induces and regulates sleep, prevent jet lag, prevent aging and depression. Works best if ingested by day.
Where are seratonin and melatonin made? Where is seratonin secreted?
Pineal gland. Small intestine.
How does the circadian rhythm relate to cortisol?
The cycles of cortisol release often mirror the sleep-wake cycle, and so may be regulated by serotonin.
What does serotonin do in the small intestine?
Vasoconstrict, stimulate smooth muscle.
Flow of serotonin/melatonin production
1. Tryptophan enters cell
2. Tryptophan hydroxylase + others make Serotonin
3. 5HT N-acetyltransferase makes melatonin from serotonin.
4. Packaged in vesicles
5. No processing other than steps above
6. Depolarization, Ca influx, release
7. MAO eats both down to 5HT, which enters the cell with Na and is recycled.
Common treatments for depression
MAO inhibitors, SSRIs, Prozac, Paxil, eetc.
What's the take-home message on depression?
Anything that keeps dopamine and serotonin from being degraded after being secreted will, in theory, cure depression. That includes anything that keeps it from being reuptaken, too.
What is Hartnup's disease? How do you treat it?
A genetic defect in the absorption of tryptophan. Administer a form of tryptophan that can be successfully absorbed via di-peptide transporter.
What are MIT and DIT?
Monoiodotyrosine and Diiodotyrosine. They are produced from iodination of TYROSINE residues in thyroglobulin. They are the building blocks of thyroid proteins T3 and T4.
Who makes MIT and DIT?
The membrane-bound enzyme thyroidal peroxidase (TPO). In the colloid, TPO oxidizes iodine and attaches it to thyroglobulin.
What do MIT and DIT do?
Undergo coupling reactions to form either DIT+DIT=T4 or MIT+DIT=T3
How many tyrosine residues in Tgb can be iodinated?
Up to 4.
Where are T3 and T4 and Tgb all stored?
In the colloid.
Synthesis of T3 T4?
Tgb is made by follicular cell and pumped into colloid
Packaging of T3 T4?
Tgb is iodinated and waits in colloid.
What happens when TSH (from the pituitary) binds to basal receptors on the follicular cells?
cAMP increases. The "immature" iodinated Tgb is endocytosed and fuses with lysosomes. Lysosomal enzymes cleave some bonds resulting in T3 or T4, and the mature hormones are secreted through the basal membrane.
Major degradation method of T3 and T4? Where?
1. Sequential deiodination, i.e., T4 becomes T3 becomes T2. The liver is the major site, but they can undergo conjugation with gluconorides and sulfates and enter the bile. They are then recycled.
What aren't recycled are peed out. 20% of T4 is excreted by stool. We pee out less as we get older.
Can the follicular cells break down T3 T4 themselves?
Yes, they contain a deiodinase that will eventually yield tyrosine again.
Why does the thyroid make almost 4 times as much T4 as it does T3?
Because a simple deiodination of T4 yield T3 anyway.
Regulation pathway of thyroid hormones? Any feedback?
Hypothalamus: TRH -> Adenohypophysis: TSH -> Thyroid:T3, T4. T3 and T4 will shut off the hypothalamus.
What do thyroid hormones do in the fetus?
Skeleton and CNS growth.
What do thyroid hormones do in the adult?
Increase basal metabolic rate (BMR), increase protein synthesis, increase cardiac output.
What symptom do hyper and hypo thyroidism share in common?
Goiter. Gross.
Hypothyroidism? Treatment?
Not enough T3/T4, so pituitary keeps releasing TSH, the thyroid expands to try and keep up. Low BMR, hypertension on diastole. Synthetic thyroid hormones.
Hyperthyroidism? Treatment?
AKA Grave's Disease. Autoimmune disorder, antibodies to TSH receptor keep receptor on. Continuous production despite lack of signal from pituitary.
Enzyme responsible for synthesizing ACh?
choline acetyltransferase
How many molecules in one quanta of ACh?
Enzyme responsible for degrading ACh?
Two common diseases resulting from acetylcholine defects?
Myasthenia Gravis. CE Organophosphates.
Describe Myasthenia Gravis. Treatment?
Autoimmune response to ACh receptors. Pyridostigmine to inhibit acetylcholinesterase.
What are organophosphates and why are they lethal?
Irreversible binders to AChE active site, so ACh is not broken down. Result is hypercholinergic effect -> paralysis and death. I.E. Nerve gases and insectisides.
Treatment for organophosphate exposure?
Atropine, diazepam, 2-PAM
Sites and function of histamine
Trauma, inflammation, allergic reaction. VASODILATES and lowers blood pressure -> shock.
4 histamine receptors and their functions
H1: Smooth muscle activation, vasodilation, itching, motion sickness, secretion of gastric acid.
H2: Parietal gastric acid secretion
H3: Decreased neurotransmitter release
H4: Dunno.
Flow of histamine lifespan
Histidine is converted to histamine via aromatic decarboxylase -> Histamine is stored -> no processing -> secreted by mast/basophils -> methyltransferase/diamine oxidase eat histamine -> recycle.
Which receptor is responsible for allergic reactions?
H1, via creation of IP3 and DAG.
Competitive antagonist of histamine on H1 receptor
Diphenhydramine AKA Benadryl
and Allegra and Claritin. ALL CALLED ANTIHISTAMINES
What is NO?
A paracrine/autocrine vasodilator that increases cGMP synthesis -> smooth muscle relaxation.
Enzyme responsible for making NO?
Nitrogen Oxide synthase (L-arginine to L-citrulline)
Is NO secreted?
It is not packaged nor processed. It diffuses directly into blood.
2 enzymes responsible for the breakdown of NO?
Superoxide dismutase, hydrogen peroxide
What else can stimulate NO production (other than ACh)?
Calcium influx, bradykinin, immune cytokines
What inhibits NO synthesis?
Synthetic NO analogs?
What else can cGMP production do?
inhibit platelet clotting
What are the four eicosanoids and what is their primary function?
Prostaglandins, prostacyclins, leukotrienes, thromboxanes. THE INFLAMMATORY RESPONSE.
Who makes eicosanoids?
Everybody except RBCs
What do eicosanoids do, in general?
Bind locally to G-protein coupled receptors affecting the levels of cAMP (Engisch)
Characteristics of thromboxanes
1. Vasoconstriction
2. Clotting
3. Antagonist of prostacyclin
Where are thromboxanes made?
Platelets via COX enzyme on arachidonic acid.
How does thromboxane mediate clots?
Express glycoprotein GP on cell membrane of platelets, binding fibrinogen
Characteristics of prostacyclin
1. Vasodilator
2. Inhibits clotting
3. Antagonist of thromboxane
2 uses for synthetic of prostacyclin
1. Vasodilation in ischemia of a limb
2. pulmonary hypertension
Indirect inhibitor of prostacyclin?
NSAIDS, which inhibit COX1/COX2, inhibiting arachidonic acid conversion.
What happens in an aspirin allergy response and why?
Inhibition of COX1/COX2 by NSAIDS does stop production of prostacyclins and thromboxanes, but then the high concentration of arachidonic acid as a precursor will be shuttled towards producing leukotrienes, inducing inflammation.
Characteristics of leukotrienes?
Chemotaxis, inflammation, allergies, SRS-A (anaphylaxis), vasoconstrictors, bronchoconstriction, increase vascular permeability.
Who is more potent, a leukotriene or histamine?
Leukotrienes by a 1000-fold
Treatment for asthma, psoriasis, rheumatoid arthritis
Leukotriene receptor antagonists (montelukast)
Characteristics of prostaglandins?
Muscle constriction, inflammatory mediators, Ca movement, hormone regulation.
Where does eicosanoid synthesis occur?
In the granules of mast cells
Primary enzymatic destroyer of eicosanoids
15-hydroxyprostaglandin dehydrogenase
Arachidonic acid +
1. Lipoxygenase = Leukotriene
2. Epoxygenase (p450) = Epoxides
3. PGH Synthase/COX1-2 = Prostaglandins OR Thromboxanes
4. Free Radicals = Isoprostanes
Prostaglandins are the precursors of what?
Both Thromboxanes and Prostacyclins
How can you block synthesis of ALL eiconsanoids?
1. Corticosteroids synthesize lipocortins (inhibitors of phospholipase A2)
2. Lipocortins block release of arachidonic acid
3. Game, set, match
How does aspirin block prostaglandins? How do ibuprofen and acetaminophen block prostaglandins?
Irreversible binding to COX Ser residue in catalytic site. Competitive binding.
What are the three steroid hormones (non-gonadal) and what do they do?
1. Mineralcorticoids: metabolism
2. Glucocorticoids: Salt-retention
3. Androgens: Sex hormones
Precursor of all steroids
The cortico-steroid-binding protein?
First enzyme in all three steroid synthesis pathways
P450ssc makes Pregnolone from cholesterol
The steroid-synthesizing precursor in the mitochondria?
3 part degradation of steroids?
1. Deydrogenases
2. Reductases
3. Urinary clearance of sulfate esters and glucuronides
2 glucocorticoids
Cortisol (major, metabolic UP)
Corticosterone (minor, intermediate betwee pregnolone and
The 4 functions of glucocorticoids.
1. Up gluconeogenesis/up protein breakdown
2. Inhibit glucose uptake in muscles and adipose tissue
3. Increase blood pressure
4. Supress immune system
Again, how does glucocorticoid inhibit inflammation?
Produce phospholipase inhibitory proteins (lipocortins) that prevent the release of arachidonic acid for synthesis of eicosanoids. KNOW
How long do steroids live?
hours and sometimes days.
What hormone from the pituitary stimulates glucocorticoid synthesis?
ACTH - works within minutes
Three main mechanisms of neuroendocrine control
1. Episodic secretion of ACTH (circadian)
2. Stress reponse
3. Feedback inhibition of pituitary ACTH secretion via cortisol.
What does cortisol feedback inhibit? What is special about this mechanism, as opposed to other feedbacks we've studied? What does that suggest about feedback receptors?
ACTH at pituitary and CRH at hypothalamus. This is NOT concentration dependent, but RATE OF INCREASE dependent. Can shut off very fast. Therefore, the receptors are not cytosolic but right there on the membrane.
If the GC concentration is prolonged, what happens to ACTH secretion?
It diminishes and eventually becomes unresponsive.
What happens if GC is prolonged for a VERY long time?
No ACTH means the cells of the adrenal cortex will atrophy. Response to stress will become nil. This means the LONG feedback pathway is a cytosolic receptor pathway, and the cells will stop expressing the precursors to ACTH
When is cortisol at it's lowest? When does it spike? When does it rise incrementally?
1. late in the evening if awake
2. 3-5 hours of sleep, it rises. Between 6-8 hours of sleep it peaks.
3. As we eat and exercise, cortisol increases
What is the disease of glucocortoids? Why?
Stress. The prolonged use of cortisol will diminish ACTH, the adrenals will atrophy, no circadian rhythm
Treatment for stress
Exercise, reassurance, therapy, doctor's evaluation.
What is the principal mineralcorticoid? What is it's principle function? Where is it produced?
Aldosterone, electrolyte regulation, zona glomerulosa
Flow of Renin Angiotensin system from kidneys to angiotensin II
1. Hypoxia in kidneys
2. Kidneys secrete Renin
3. Renin cleaves angiotensinogen to make angiotensin I (weak vasoconstrictor)
4. Angiotensin converting enzyme (ACE) in lungs changes angiotensin I to angiotensin II (strong vasoconstrictor)
Flow of Renin Angiotensin system from angiotensin II to increase blood pressure
5. ATII stimulates aldosterone production in adrenal cortex
6. Aldosterone turns on Na-K-ATPase in kidney
7. FATE of K: more in urine, less in blood
8. FATE of Na: reabsorbed, taking water in with it
9. increase in blood volume, decrease in urine
10. Increase in blood volume = increase in blood pressure
What two receptors can bind ATII? What do they do?
AT1: systemic vasoconstriction (to increase b.p.) and inhibit platelet formation
AT2: vasodilation and apoptosis. THIS IS BAD.
Primary disease of mineralcorticoids?
In addition to vasoconstriction and aldosterone production, what else does ATII do? Is this good or bad?
1. Stimulates ADH from neurohypophysis to tell kidneys to retain water.
2. Stimulates thirst
3. Promotes release of norepi without uptake, enhancing sym nervous system
4. Stimulates cardiac and vascular hypertrophy

Ultimately bad. You will die from continued ATII stimulation
Treatment of hypertension
ACE inhibitor and ATII receptor blockers
What is an androgen?
Any compound (mostly steroids) that masculinize an organism
Other names for androgens? They are the precursor to what? What's the best known androgen?
1. androgenic hormones, testoids.
2. All estrogens
3. Testosterone
Name 4 androgens and their characteristics
1. DHEA - precursor of all sex steroids (DHEA-S is just the sulfated form)
2. Andro - parent of estrone
3. Androstanediol - gonadotropin regulator
4. Androsterone - weak testosterone
How is DHEA produced?
Two cytochrome p450 enzymes from cholesterol precursor
Life-cycle of human DHEA production
1. High in fetal
2. Low in childhood
3. Rise in puberty
4. Peak in young adulthood
5. Decline to end of life.
Primary disease of mineralcorticoids?
In addition to vasoconstriction and aldosterone production, what else does ATII do? Is this good or bad?
1. Stimulates ADH from neurohypophysis to tell kidneys to retain water.
2. Stimulates thirst
3. Promotes release of norepi without uptake, enhancing sym nervous system
4. Stimulates cardiac and vascular hypertrophy

Ultimately bad. You will die from continued ATII stimulation
Treatment of hypertension
ACE inhibitor and ATII receptor blockers
What is an androgen?
Any compound (mostly steroids) that masculinize an organism
Other names for androgens? They are the precursor to what? What's the best known androgen?
1. androgenic hormones, testoids.
2. All estrogens
3. Testosterone
Name 4 androgens and their characteristics
1. DHEA - precursor of all sex steroids (DHEA-S is just the sulfated form)
2. Andro - parent of estrone
3. Androstanediol - gonadotropin regulator
4. Androsterone - weak testosterone
How is DHEA produced?
Two cytochrome p450 enzymes from cholesterol precursor
Life-cycle of human DHEA production
1. High in fetal
2. Low in childhood
3. Rise in puberty
4. Peak in young adulthood
5. Decline to end of life.