Hormone

ORIGIN

STRUCTURE

MECHANISM

FUNCTION

NOTE 1

Melatonin

Pineal gland

Tryptophan (serotonin
deriv)

IP3-DAG

Drowsiness; used to treat jet lag

Synthesis: Serotonin > N-acetyltransferase > hydroxyindole-O-Methyltransferase > Melatonin

Serotonin

Enterochromaffin cell

Tyrptophan

EPI

Chromaffin cell in Adr. Medulla

Tyrosine derivative
(catecholamine)

NE

Chromaffin cell in Adr. Medulla

DA (Dopamine)

ARC, Substantia Nigra

CRH

PVN in hypothalamus

ACTH

Corticotrope of AP

Cortisol

Zona Fasciculata of Adr. Cortex

a-MSH

Melanotroph of AP (from POMC)

TRH

(PVN) Medial neurons of

Paraventricular Nuclei in
hypothalamus

TSH

Thyrotropes of AP

T4, Thyroxine

Follicular cells of thyroid gland

T3 (3,3',5triiodothyronine)

Follicular cells of thyroid gland

Renin

Justaglomerular (granular) cells

TARGET

Tyrosine derivative
(catecholamine)
Tyrosine
(catecholamine)
Protein
MC2 Receptor in Adrenal
Cortex (Fasicullata)

Protein
Steroid (glucocorticoid)

MC1 Receptor in Skin

Melanocytes

Peptide

Tripeptide
Glycoprotein
(alpha/beta)
Tyrosine (fused)
Tyrosine (fused)

Peptide

Angiotensin (II)
Aldosterone

Zona Glomerulosa of adrenal cortex

ANP / Atrial Natriuretic

Hormone

Atrium of Heart

Steroid
(mineralocorticoid)
Peptide
Arachidonic acid
derivatives

Prostaglandins
Endothelin
Adrenomedullin

Affects mood and appetite

cAMP or IP3-DAG

fight/flight, inc O2 supply, inc bp, inc glycolysis, inc lipolysis

Storage: secretory granules, triggered by Ca, half life 10 secs

Note: degraded by MAO/COMT

cAMP or IP3-DAG

Same effects as EPI including increased [glycemia + FFA (due to lipolysis) + lactate]; bronchodilation

Storage: secretory granules, triggered by Ca, half life 15 secs

Note: degraded by MAO/COMT

Inc heart rate, BP / Inhibits PRL / functions as neurotransmitter in brain and associated with learning

Note: DA cannot cross BBB. Therefore L-Dopa used to treat Parkinsons because L-Dopa can cross BBB.

cAMP

Stimulates ACTH release

Stimulated by: Deviation from Homeostasis | Inhibited by: Cortisol

cAMP

Stimulates corticoid release

Inhibited via neg. feedback loop of Cortisol to Hypothalamus and AP

transcription

Gluconeogenesis; catabolism; permissive effect on GH; inc lipolysis

Inhibited via cortisol, CRH, high glucose Note: anti-inflammatory effects Synthesis: p450c11beta adds hydroxyl group to carbon 11 of 11-deoxycortisol
Note: corticosteroid binding globulin (CBG) is a transport protein for cortisol in the blood Note: slow effects (30 mins)

cAMP

Hyperpigmentation; melanogenesis; inhibits appetite

IP3-DAG
Gs>AC>cAMP>CREB
Gq>PLC>IP3-DAG

AVP/ADH

Nonapeptide

Calcium

PTH

Synthesis: iodine trapping by Na-Iodide symporter > in presence of H2O2, thyroid peroxidase oxidizes iodide, which reacts with tyrosine to produce MIT and
DIT > two DITs fuse together to form T4 Storage: extracellularly stored as thyroglobulin
Inhibits TRH via neg. feedback loops
Synthesis: Type II iodothyronine deiodinase cleaves iodine from T4 Note: rT3 is inactive

Mediates vasoconstriction by cleaving angiotensinogen

cAMP or IP3-DAG

Potent vasoconstrict (inc bp) / inc Aldosterones secretion / Thirst

Note: renin is inhibited by Calcium Note: renin is stimulated by decrease in perfusion pressure, sensed by JGA baroreceptor
Note: Angiotensin II acts on glomerulus Synthesis: Kidney releases renin. Renin binds substrate angiotensinogen(from liver) to produce angiotensin 1. Lung
releases ACE to convert AT-I into AT-II. Note: stimulates SCCE and 18-hydroxylase Note: stimulates contraction via Ca by using IP3 pathway Note:
stimulates catecholamine release

transcription

Reabsorb Na -(at Distal Convuluted Tubule) > inc blood volume > inc blood pressure

Note: Aldosterone release stimulated by high [K+] / Angiotensin II Synthesis: cholesterol converted to pregnenolone by SCCE. Pregnenolone converted
through several enzymes and then finally by 18 hydroxylase to produce aldosterone. Note: Also stimulates ACTH release

cGMP (No G-protein involved)

Vasodilation; reduces water in circulation thereby dec BP

Autocrine or paracrine, not

endocrine

Induce pain; regulation of constractions and relaxations of muscle tissues.

Paracrine

Vasoconstrictor

Paracrine

Vasodilator

cAMP (V2 receptor) or IP3DAG (V1 receptor)

Note: inhibits Na reabsorption by inhibiting ADH release

Note: PGE1 is a vasodilator used for men with erectile dysfunction Note: PGF2alpha is used to induce luteolysis and labour
Note: PGD2 causes asthma by
constricting bronchial airways Note: PGE2 causes bone resorption by osteoclasts and fever.. Synthesis: Cyclooxygenase (COX) is the enzyme involved in
prostaglandin synthesis)

Vasodilator

Note: Inhibited by ACE

Vasodilator

Note: Predominates during inflammation

Water retention in kidney (phosphorylates/activates AQP-2, inserts AQP-2 in DCT)

Note: Not enough AVP = Diabetes Insipidus Note: stimulates release of ACTH / Inc BP through vasoconstriction / Inc Na reabsorption in thick ascending loop
of henle Note: stimulated by voltage gated calcium channels Inhibited by: High BV, High Blood Osomlarity

cAMP inhibition

Inhibit PTH secretion

Protein

cAMP or IP3-DAG ( osteoblast

activity > RANK-Ligand >
osteoclast activity
)
transcription
( Vit-D

Inc calcemia, stimulates Vit. D synthesis in Kidney; stimulate osteoblast via RANK2--> stimulate
osteoclasts--> bone degradation

Note: mobilizes phosphate from bone (dec phosphataemia, makes kidney excrete phosphates (doesnt reabsorb it at proximl tubule), reabsorb Ca in the
kidney Note: makes the active form of vit D by converting 25OHD into 1,25OHD3
Note: osteoclasts dont have receptors for PTH, which is why they have
to work through osteoblasts
Inhibited by: Hypercalcemia

Steroid

receceptor forms heterodimer

with retinoid-x (RXR) dimer HRE > binds PTH promotor >
transcription )

Inc calcemia by absorption of Ca in gut, Inc. Phosphates

Inhibited by: Hypercalcemia, High Blood Phosphate conc.

cAMP

Dec calcemia, constructs bone, inhibits PTH

Note: Activates Vit-D / Dec Blood-Phosphate and Ca Reabsorption in kidney

Chief cells of parathyroid gland

Vit-D (Active: 1,25dihydroxycholecalciferol

or calcitriol)

Inhibited by: T3/T4 (t3 and t4 inhibit trx. of TSHsubunit mRNA), Leptin, NPY, a-MSH

Inc BMR (basal metabolic rate); inc oxygen consumption

cAMP

Peptide
supraoptic nuclei in hypothalamus /
Magno cells in posterior pituitary

Inhibited by: T3/T4 (t3 and t4 inhibit trx. of TSHsubunit mRNA)

Stimulates uptake of iodine, synthesis & secretion of T4/T3, secretion of FSH, LH

Increase trx. of Na/K pump, Inc BMR; Inc. Glucose metabolism --> Inc. O2 consumption, development:
transcription (retinoid-x dimer) induce myelination of neurons

Kinin
Bradykinin

Stimulates production and release of TSH; stimulates PRL release as well

or

transcription

Gut, Bones, Kidney

Calcitonin

Parafollicular cells (c-cells) of thyroid

gland

Protein

GnRH

ARC in hypothalamus

Peptide

IP3-DAG

Inc FSH and LH (Low Freq- FSH | High Freq - LH)

FSH

Gonadotrope of AP

Peptide (alpha/beta)

cAMP

Prep for Reprod. - 1. Follicle maturation. 2. Spermatogenesis

LH

Gonadotrope of AP

cAMP

Syn & Secretion of Sex Hormones - 1. Inc P4. 2. In Women, Ovulation & secretion of estrogen and
progesterone. 3. In men T production

P4 (Progesterone)

Granulosa cells of ovary, granulosa

lutein cells of corpus luteum

transcription

1. inhibits basal GnRH. 2. stimulates alveolar gland dev. 3. Preps endometrium by calming it through
reduced contractions

transcription

Secondary sex chars in female

Anabolic growth, male charachteristics

Note: augments GH secretory episodes and frequencyNote: 5-alpha reductase converts testosterone to DHT (a more potent hormone as compared to
Testosterone)

Peptide

transcription
JAK2/STAT (Tyr Kinase,
cytosolic)

Stimulates milk production

Note: stimulated by TRH, inhibited by P4

Steroid

transcription

Potent form of testosterone

Note: Major secretory hormone from adrenal gland

Dimeric Glycoprotein

Inhibits growth of mullerian ducts via apoptosis to make a male

Peptide (alpha/beta)
hypothalamus, uterus,
mammary gland

Steroid

E2 (Estradiol - a type of Granulosa (Female) or sertoli (Male)

estrogen)
cells

Steroid

T (Testosterone)

Leydig cells in testes

Steroid

PRL, Prolactin

Lactotrophes of AP

DHEA

Adrenal gland

AMH (Antimullerian
Hormone aka MIF)

Sertoli cells during embryogenesis

PGF2alpha

Uterine endometrium

Oxytocin

Magno cells, PVN of hypothalamus,

large luteal cells in CL of ovary

Inhibin

Sertoli Cells

cuboidal cells

Peptide
Arachidonic acid
derivatives
Nonapeptide

Luteolysis
IP3-DAG

gonadotrophes

1. Milk ejection (milk letdown) 2. contraction of cervix (uterine contraction) 3. Luteolysis

Note: stimulated by: suckling, nipple stimulation, cervical dilation

Synthesis: FSH binds sertoli cells > secrete inhibin- Note: NFB on FSH production

Relaxin

ARC in hypothalamus (lesser in VMN

of Hypothalamus)

GHRH
GH (somatotropin or
STH)

Protein
Protein

cAMP
JAK2/STAT (Tyr Kinase,
cytosolic); MAP for bone
growth

Stimulates release of GH

Note: Stimulated: Ghrelin | Inhibited: SS (increased by IGF-1)

Stimulates release of IGF-1 from liver, increases bone plate growth

Metabolic Effects: mobilize fatty acids (ketone bodies produced > inc acidity ) , inhibit glucose metablism (thereby causing diabetes)
(increased via IGF-1), GHRH, hypoglycemia

inhibits GH and TRH

Note: Stimulated: IGF-1

SS (somatostatin)

Somatotropes
of AP
Delta
cells of pancreas
/
periventricular nucleus of
hypothalmus

IGF-1 (somatomedin-C)

Hepatocytes of liver

Protein

cAMP
Intrinsic Tyr Kinase

Glucagon

Alpha cells of pancreas

Protein

cAMP > CREB

Gluconeogenesis in liver, ureogenesis, ketogenesis, glycogenolysis

Note: actvates phosphorylase kinase > activates glycogen phosphorylase

Insulin

Beta cells of pancreas

Protein

Intrinsic Tyr Kinase (not JAK2)

Intake of glucose; glycolysis in liver

Note: fat storage by FA synthesis (inhibit FFA oxidation)

NPY

stomach, expressed in ARC

Peptide

Induce hunger, dec energy expenditure

Note: upregulated during fasting

a-MSH(cocaine and
CART
amphetamine reg
transcript)

POMC

Peptide

Inhibits food intake

Leptin

Adipocytes

Peptide

Insulin-like effects; growth

Inhibits NPY thereby inhibiting food intake

Peptide

JAK2/STAT3

Counters NPY, thereby inhibitiing food intake. Promotes a-MSH

Stimulate ATP synthesis by inc glucose availability, conserves ATP by switching to fatty acid oxidation
for energy

Gastrin

G-cells of Antrum

Peptide

IP3-DAG

Stimulates ECL to secrete His, which acts on Parietal (Oxyntic) cells to release acid

CCK

I cells of Duodenal Jejunum Mucosae

Peptide

IP3-DAG

Gall bladder contraction; induces satiety

Somatostatin

D-cells in Antral Mucosa

Secretin

S cells of Duodenum

Peptide

cAMP or IP3-DAG

GLP-1 (Incretin)

L cells of Ileum

Peptide

cAMP

VIP

Vagal neurons

Peptide

GIP (Incretin)

K cells of Duodenum

PACAP

Vagal neurons

Neurotensin

AMPK (enzyme)

Note: acts on hypothal. More adipo = more leptin. Stimulated by insulin, Inhibits insulin in return. Inc angiogenesis.
fertility at hypothalamic level Note: Stimulates POMC, aMSH, CRH, CART; inhibits NPY, orexin, AGRP, and MCH
Note: stimulated during exercise

Note: Stimulated by fat, protein. Synergistic with Secretin to act on SS

Inhibit G-cells
Releases HCO3 from pancreatic acinar cells
Paul Revere hormone; releases Insulin; dec. acidity; slows gastric emptying; Involved in Ileal Break
mechanism

Note: Synergistic with CCK to act on SS; PKA activates HCO3/Cl antiport

Induces fullness; Relaxes smooth muscle; synchronizes SCN to stimulate GnRH

Note: VIP-1 Receptor located in Gut; VIP-2 Receptor located in Brain

Peptide

cAMP
cAMP (targets pancreatic Bcells)

Paul Revere hormone; releases insulin; dec acidity

Note: Induced by AA, FA

Peptide

cAMP

N cells of jejunum, ileum

Tridecapeptide

IP3-DAG

Stimulates ECL to secrete Histamine

Inhibits gastrc acid secretion; slows gastrc emptying; involved in the Ileal Break mechanism;
stimulates bile secretion

Note: stimulated by FA

Motilin

M cells in duodenal endocrine cells

Peptide

IP3-DAG

Induces gastric motility; secreted between meals

Note: stimulated by cholinergic neuronal inputs from enteric nerves. Has both paracrine and endocrine function

Ghrelin
PPP (Pancreatic Poly
Peptide)

oxyntic A/X cells

Peptide

IP3-DAG

Stimulates hunger, motility, and gastric emptying

Note: inter-digestive periods; stimulates GH

F-cells in panc. islets

inhibit gastric acid

Peptide YY

L cells of ileum

inhibit gastric acid; slows chime motility; involved in Ileal Break mechanism; induces satiety

Note: Inhibited: SS

Note: induced by amino acids and fatty acids

Note: stimulated by FA

Derived from tyrosine residues (the Y represents tyrosine)

Note: Leptin receptor in gonad promotes

PATHOLOGIES
NAME

PATHOPHYSIOLOGY

SYMPTOMS

Neurogenenic diabetes insipidus Not enough AVP released

Diabetes mellitus type 1

Not enough insulin production; death of beta cells; autoimmune

Diabetes mellitus type 2

Problems with GLUT-t4 receptor

Addison's Disease

Hypersecretion of ACTH (because not enough cortisol to negatively inhibit ACTH) -> B-MSH & Clip produced -> darkFatigue, lightheadedness, dark skin

Cushing's Syndrome

Hypersecretion of Cortisol; problem with pituitary gland

Chronic Fatigue Syndome

Cortisol is not released properly according to circadian rhythm

Pheochromocytomas (exam2)

Hypertention from tumored Adrenal Medulla. Cure = TOH inhibitor

hyperPTH

Secondary pathology due to low Calcium. Result of chronic renal disease or from hypoVitD

Hypercalcemia

Parathyroid failure; elevated PTH

Hypocalcemia / osteoperosis

Parathyroid failure

Cretinism (hypothyroid infant)

Not enough thyroid hormone in perinatal period

Mentally handicapped infant

Hyperthyroidism

Too much thyroid hormone secretion due to excess TRH or excess TSH

Heat intolerance (due to too much uncoupling protein); cardiac arrythmia

Hypothyroidism

Too little thyroid hormone due to insufficient TSH or TRH

Cold intolerance, slow, myxedema

Acromegaly

Excess GH

wide face or lower jaw

Taking Testosterone

Tiny testes b/c testosterone has a negative feedback on gonads

Cholera

G-protein continuously working -> water release -> diarreah

Hypertension

genetic: decrease in renal kalikrein system (vasodilators) / overactivity of RAS

Secondary Hyperaldosteronism

renal artery stenosis > JGA mistakenly detects low BP > inc renin > inc ATII > inc ALDO > inc potassium loss > inc hypertension

Fat redistribution, hypertension, glucose intolerance, stunted growth, moon face

if elevated PTH -> weak bones; kidney stones