Hormones

College of Arts and Sciences

Norzagaray College
 Amino Acids
Target
Name Abbreviation Tissue Cells Receptor Effect
Tissue

CNS and
pineal melatonin circadian
Melatonin MT peripheral
gland receptor rhythm
tissue

nearly
thyroid increased
Triiodo peripheral every cell
T3 hormone metabolis
thyronine tissue in the
receptor m
body
similar
thyroid effect as
thyroid
Thyroxine T4 hormone T3 but
gland
receptor much
weaker
 Eicosanoid
Name Abbreviation Tissue Cells Receptor Target Tissue Effect

vasodilation,
Broncho-
prostaglandin
Prostaglandins PG seminal vesicle constriction,
receptor
platelet
aggregation

G protein- increase
white blood
Leukotrienes LT coupled vascular
cells
receptors permeability

prostacyclin
Prostacyclin PGI2 endothelium
receptor

Broncho-
thromboxane constriction,
Thromboxane TXA2 platelets
receptor Vaso-
Constriction
 Peptide
Name Abbreviation Tissue Cells Receptor Target Tissue Effect
slowing down gastric
Amylin (or Islet emptying, inhibition
Amyloid IAPP pancreas pancreatic β-cells amylin receptor of digestive
Polypeptide) secretion, and
reducing food intake
Anti-Müllerian Inhibit release
hormone (or of prolactin and TRH
AMH testes Sertoli cell AMHR2
Müllerian inhibiting fromanterior
factor or hormone) pituitary
adiponectin
Adiponectin Acrp30 adipose tissue
receptors
synthesis
of corticosteroids (gl
Adrenocorticotropic
ACTH receptor → ucocorticoidsand an
hormone (or ACTH anterior pituitary corticotrope
cAMP drogens)
corticotropin)
in adrenocortical
cells
vasoconstrictionrele
ase
Angiotensinogen an angiotensin
AGT liver of aldosterone from
dangiotensin receptor → IP3
adrenal
cortexdipsogen.
Parvocellular
neurosecretory retention of water
Antidiuretic
neurons in in kidneys
hormone(or
hypothalamus moderate vasoconst
vasopressin, ADH posterior pituitary several
Magnocellular riction
arginine
neurosecretory Release ACTH in ant
vasopressin)
cellsin posterior erior pituitary
pituitary
Atrial-natriuretic
ANP
peptide (or ANP heart
receptor→ cGMP
atriopeptin)

(To a minor degree

than ANP)
reduce blood
Brain natriuretic pressure by:reducing
BNP heart Cardiac myocytes NPR
peptide systemic vascular
resistance, reducing
blood water, sodium
and fats

Construct bone,
Calcitonin CT thyroid gland parafollicular cell CT receptor→ cAMP
reduce blood Ca2+

Release of
digestive enzymes fr
om pancreas
Cholecystokinin CCK duodenum CCK receptor Release
of bile from gallblad
der
Hunger suppressant

Corticotropin- Release ACTH from a

CRH hypothalamus CRF1 → cAMP
releasing hormone nterior pituitary

Enkephalin Kidney Chromaffin cells Opioid receptor Regulate pain

Smooth
Vascular muscle contraction
Endothelin Endothelial Cells ET receptor
Endothelium of medium sized
vessels

Extraglomerular Stimulate erythrocyt

Erythropoietin EPO kidney EpoR
mesangial cells e production
 In female: stimulates
maturation of Graafian
follicles in ovary.In
Follicle-stimulating FSH receptor→ male: spermatogenesis
FSH anterior pituitary gonadotrope , enhances production
hormone cAMP
of androgen-binding
protein by theSertoli
cells of the testes

central nervous
modulation and
system and GALR1,GALR2,
Galanin GAL inhibition of action
gastrointestinal andGALR3 potentialsin neurons
tract
stomach,duodenu Secretion of gastric
Gastrin GRP G cell CCK2 acid by parietal cells
m
Stimulate appetite,secr
etion of growth
Ghrelin stomach P/D1 cell ghrelin receptor hormone from anterior
pituitary gland
glycogenolysis and gluc
Glucagon oneogenesis in liver
Glucagon GCG pancreas alpha cells increases blood
receptor → cAMP
glucose level
Release
Gonadotropin- GnRH receptor →
GnRH hypothalamus of FSH and LH from ant
releasing hormone IP3 erior pituitary.
Growth hormone- GHRH receptor → Release GH from anteri
GHRH hypothalamus or pituitary
releasing hormone IP3
inhibits iron export
Hepcidin HAMP liver ferroportin from cells
promote maintenance
of corpus
luteum during
Human chorionic syncytiotrophoblas LH receptor→
hCG placenta beginning of pregnancy
gonadotropin tcells cAMP Inhibit immune respon
se, towards the human
embryo.
 increase production
of insulin and IGF-
Human placental
HPL placenta 1increase insulin
lactogen
resistance and carbohy
drateintolerance
stimulates growth and
cell reproductionReleas
Growth hormone GH or hGH anterior pituitary somatotropes GH receptor
e Insulin-like growth
factor 1 from liver
Sertoli cells of testes
Inhibit production
Inhibin testes, ovary, fetus granulosa cells of ovary anterior pituitary
of FSH
trophoblasts in fetus
Intake
of glucose, glycogenesi
s and glycolysisin liver a
nd muscle from
insulin receptor,IGF-
Insulin INS pancreas beta cells bloodintake
1, IGF-2
of lipids and synthesis
of triglycerides inadipo
cytes Other anabolic ef
fects
insulin-like
Insulin-like growth
effectsregulate cell
factor (or IGF liver Hepatocytes insulin receptor,IGF-1
growth and
somatomedin)
development
decrease
of appetite and
Leptin LEP adipose tissue LEP-R
increase of
metabolism.
lipolysis and steroidoge
nesis,
Lipotropin LPH anterior pituitary Corticotropes
stimulates melanocyte
s to produce melanin
In female: ovulationIn
male: stimulates Leydig
Luteinizing hormone LH anterior pituitary gonadotropes LHR → cAMP
cell production of
testosterone
Melanocyte anterior pituitary/pars melanocortin melanogenesis by mela
MSH or α-MSH Melanotroph
stimulating hormone intermedia receptor → cAMP nocytes in skin and hair
Motilin MLN Small intestine Motilin receptor stimulates gastric activity

wakefulness and
increased energy
Orexin hypothalamus OX1, OX2 expenditure, increased
appetite

release breast
milkContraction
of cervix and vagina Invol
Magnocellular ved inorgasm, trust
posterior OXT receptor →
Oxytocin OXT neurosecretory between people.
pituitary IP3 and circadian
cells homeostasis (body
temperature, activity
level, wakefulness).

Self-regulation of
pancreatic secretions
pancreatic (endocrine and exocrine).
Pancreatic
Pancreas PP cells polypeptide It also affects hepatic
polypeptide glycogen levels and
receptor 1 gastrointestinal
secretions.

•increase
blood Ca2+:indirectly
stimulate osteoclasts
•Ca2+ reabsorption
in kidney
Parathyroid parathyroid parathyroid PTH receptor→ •activate vitamin D
PTH (Slightly) decrease
hormone gland chief cell cAMP blood phosphate:
•(decreased reuptake
in kidney but increased
uptake from bones
•activate vitamin D)

lactotrophs of milk production

in mammary glands
anterior anterior pituitary
Prolactin PRL PRL receptor sexual
pituitary,uterus Decidual cells of gratification after sexual
uterus acts
Prolactin releasing Release prolactin from anterior
PRH hypothalamus
hormone pituitary
Relaxin RLN uterus Decidual cells RLN receptor Unclear in humans
Activates the renin-angiotensin
system by
Renin Kidney Juxtaglomerular cells
producing angiotensin
I of angiotensinogen

Secretion
of bicarbonate from liver, pancr
eas and duodenal Brunner's
Secretin SCT duodenum S cell SCT receptor
glandsEnhances effects
of cholecystokinin Stops
production of gastric juice

Inhibit release
of GH and TRH from anterior
pituitary
Suppress release
of gastrin, cholecystokinin(CCK)
, secretin, motilin, vasoactive
intestinal peptide (VIP), gastric
delta cells in islets inhibitory
hypothalamus, islets Neuroendocrince polypeptide(GIP), enteroglucag
of cells of Somatostatin on in gastrointestinal system
Somatostatin SRIF
Langerhans,gastroint the Periventricular receptor Lowers rate of gastric
estinal system nucleus in emptyingReduces smooth
hypothalamus muscle contractions and blood
flow within the intestine
Inhibit release
of insulin from beta cells
Inhibit release
of glucagon from alpha cells
Suppress the exocrine
secretory action of pancreas.
Thrombo- liver, kidney, megakaryocyte produce platele
TPO Myocytes TPO receptor
poietin striated muscle s ts
Thyroid- secrete thyroxin
Thyrotropin
stimulating anterior e (T4)
TSH thyrotropes receptor → thyroid gland
hormone (or pituitary and triiodothyr
cAMP
thyrotropin) onine(T3)
Release thyroid
-stimulating
Thyrotropin- Parvocellular
anterior hormone(prima
releasing TRH hypothalamus neurosecretory TRHR → IP3
pituitary rily)
hormone neurons
Stimulate prola
ctin release

stimulates cont
ractility in the
heart, causes
vasodilation,
increases glyco
gut, pancreas,
Vasoactive genolysis,
Vasoactive and supra-
intestinal lowers
intestinal VIP chiasmatic
peptide arterial blood
peptide nuclei of the
receptor pressure and
hypothalamus
relaxes the
smooth muscle
of trachea,
stomach
and gall bladder
 Chemical class Name Abbreviation
Steroids
Tissue Cells Receptor Target Tissue Effect

libido, Anabolic:
growth of muscle
mass and
strength,
increased bone
density, growth
and
strength,Virilizin
androgen Testosterone testes Leydig cells AR
g: maturation of
sex organs,
formation
of scrotum,
deepening of
voice, growth
of beard and axill
ary hair.

Zona fasciculata
and Zona
reticularis cells
Dehydroepiandr testes,ovary,kidn of kidney Virilization, anab
androgen DHEA AR
osterone ey theca cells of olic
ovary
Leydig cellss of
testes
adrenal Substrate
androgen Androstenedione AR
glands,gonads for estrogen
 5-DHT or DHT is a
male reproductive
hormone that targets
the prostate gland,
bulbourethral gland,
seminal vesicles, penis
and scrotum and
promotes
growth/mitosis/cell
maturation and
Dihydrotestoster
androgen DHT multiple AR differentiation.
one
Testosterone is
converted to 5-DHT by
5alpha-reductase,
usually with in the
target tissues of 5-DHT
because of the need
for high
concentrations of 5-
dht to produced the
physiological effects.

Increase blood
volume by
adrenal reabsorption of
mineralocor cortex (zona sodium in kidney
Aldosterone MR
ticoid glomerulosa s (primarily)
) Potassium and H
+ secretion in

kidney.
 Females:Structural:
•promote formation of female secondary
sex characteristics
•accelerate height growth
•accelerate metabolism (burn fat)
•reduce muscle mass
•stimulate endometrial growth
•increase uterine growth
•maintenance of blood vessels and skin
•reduce bone resorption, increase bone
formation
Protein synthesis:
•increase hepatic production of binding
proteins
Coagulation:
females: •increase circulating level
females: granulosa of factors 2,7, 9, 10, antithrombin III, plas
minogen
ovary, cells, •increase platelet adhesiveness
estrogen Estradiol E2 ER Increase HDL, triglyceride, height growth
males: males: Decrease LDL, fat deposition Fluid
balance:
testes Sertoli •salt (sodium) and water retention
•increase growth hormone
cell •increase cortisol, SHBG
Gastrointestinal tract:
•reduce bowel motility
•increase cholesterol in bile
Melanin:
•increase pheomelanin, reduce
eumelanin
Cancer: support hormone-
sensitive breast cancers Suppression of
production in the body of estrogen is a
treatment for these cancers.
Lung function:
•promote lung function by supporting
alveoli.
Males: Prevent apoptosis of germ cells.
 granulosa
estrogen Estrone ovary cells,Adipocyt ER
es
syncytiotroph
estrogen Estriol E3 placenta ER
oblast

Stimulation
of gluconeog
enesisInhibiti
on of glucose
uptake in
muscle and
adipose tissu
e
adrenal
Mobilization
cortex (zona
of amino
Gluco- fasciculata
Cortisol GR acidsfrom ext
corticoid and zona
rahepatic tiss
reticularis
ues
cells)
Stimulation
of fat
breakdown in
adipose
tissue anti-
inflammatory
and immuno
suppressive
 •Support pregnancy
Convert endometrium to secretory
stage
•Make cervical mucus permeable to
sperm
•Inhibit immune response, e.g. towards
the human embryo.
•Decrease uterine smooth
musclecontractility
•Inhibit lactation
•Inhibit onset of labor
•Support fetal production
of adrenalmineralo- and glucosteroids
Other:
•Raise epidermal growth factor-1 levels
•Increase core temperature during
ovary,adren
ovulation
al Granulosa cells
•Reduce spasm and relax smooth
progestogen Progesterone glands,plac theca cells of PR
muscle (widen bronchi and regulate
enta(when ovary
mucus)
pregnant)
•Anti-inflammatory. Regulate immune
response
•Reduce gall-bladder activity
•Normalize blood clotting and vascular
tone, zinc and copper levels, cell
oxygen levels, and use of fat stores for
energy
•Assist in thyroid function and bone
growth by osteoclasts
•Resilience in bone, teeth, gums, joint,
tendon, ligament and skin healing by
regulating collagen
•Nerve function and healing by
regulating myelin
•Prevent endometrial cancer by
regulating effects of estrogen
 Active form
of vitamin
D3Increase
absorption
of calcium
Calcitriol (1
skin/proxim andphosph
,25-
secosteroid al tubule of VDR ate from ga
dihydroxyvi
kidneys strointestin
tamin D3)
al tract and
kidneys
inhibit
release
of PTH

Calcidiol (2 Inactive
skin/proxim
5- form
secosteroid al tubule of VDR
hydroxyvita of vitamin
kidneys
min D3) D3
 SOURCES HORMONE MAJOR ACTION
•Corticotrophic
Releasing Hormone
•Thyrotropin
Releasing Hormone •Control the
release of
HYPOTHALAMUS •Growth Hormone
Releasing Hormone pituitary hormone
•GnRH
•Somatostatin
•Inhibits GH and
TSH
SOURCES HORMONE MAJOR ACTION

•Growth Hormone •Stimulates

growth of bone
abd muscle
•TSH •Synthesis and
ANTERIOR secretion of TH
PITUITARY •ACTH •Synthesis and
secretion of
adrenal cortical
hormone
 SOURCES HORMONE MAJOR ACTION

•LH •Female:
development of
corpus luteum,
release of oocyte,
production of P &
ANTERIOR E
PITUITARY •Male: stimulates
secretion of
testosterone, dev’t
of interstitial
tissue of testes
 SOURCES HORMONE MAJOR ACTION

•FSH •Female:
Stimulates growth
of ovarian follicle,
ovulation
ANTERIOR •Male: stimulates
sperm production
PITUITARY
•Prepares female
breast for breast
feeding
•Prolactin
SOURCES HORMONE MAJOR ACTION

POSTERIOR •Anti Diuretic •Water and Na

PITUITARY Hormone retention
•Oxytocin •Stimulates
contraction, milk
ejection

ADRENAL •Mineralocorticoster •Na retain, K

CORTEX oid – Aldosterone release
•Glucocorticoids – •Decreases
cortisol stress, anti
inflammatory
efffect, regulates
blood glucose
 SOURCES HORMONE MAJOR ACTION

•Epinephrine and •Neurotransmitter

ADRENAL Norepinephrine – has
MEDULLA symphathetic
effect

•T3 and T4 •Increases

THYROID metabolic rate,
( follicularcells) necessary for
fetal and infant
growth
SOURCES HORMONE MAJOR ACTION

•Calcitonin •Lower blood Ca

THYROID C- and Phosphate
cells level when there
is increase
amount\in the
blood

PARATHYROID •Parathormone •Regulates

PTH serum Ca
SOURCES HORMONE MAJOR ACTION

•Insulin – Beta cells •Lowers blood

glucose
PANCREAS •Glucagon – Alpha •Increases blood
cells glucose
•Somatostatin •Delays intestinal
absorption of
glucose
•Renin •Activates RAAS

KIDNEY •Erythropoietin •Increases RBC

production
SOURCES HORMONE MAJOR ACTION

OVARIES •Estrogen •Development of

sex organ and
2nd sex
characteristics
•Progesterone •Maintains
pregnancy

TESTES •Androgen - •Development of

testosterone sex organ and
2nd sex
characteristics,
sperm production
Hormonal
disorders
 GROWTH
HORMONE
DEFICIENCY
DESCRIPTION:

Growth hormone (GH)

deficiency (Hypopituitarism)
results from diminished or
deficient secretion of GH
from pituitary.
ETIOLOGY:
1. The cause is idiopathic in most cases.
2. Other causes include developmental
defects (aplasia or hypoplasia),
autoimmune hypophysitis, functional
deficiency, tumors (craniopharyngioma,
optic glioma, adenoma, astrocytoma,
and germinosm), septic-optic dysplasia,
empty sella(absent or small pituitary
gland that doesn’t fill the sella foramen),
radiation theraphy , and trauma.
 SYNDROME OF
INAPPROPRIATE
ANTIDIURETIC
HORMONE
DESCRIPTION:
SYNDROME OF
INAPPROPRIATE
ANTIDIURETIC HORMONE
(SIADH ) results from the
excessive production or release
of antidiuretic hormone (ADH)
(vasopressin)
ETIOLOGY:
1. SIADH usually occurs in childhood
and is caused by disorders affecting
the CNS , including infection ,
trauma , and brain tumors.
2. Transient but life-threatening .
SIADH may occur after surgery for
a brain tumor.
PRECOCIOUS
PUBERTY
DESCRIPTION:
1. Precocious puberty is the development of sexual
characteristics before the typical age of the onset of
puberty.
a. In white girls, precocious puberty occurs with breast and
pubic hair development before 7 years of age.
b. In black girls, precocious puberty occurs with breast and
pubic hair development before 6 years of age
c. In all boys, precocious puberty occurs with pubic hair
development before 9 years of age.
2. In boys, development of secondary sexual characteristics
before 9 years of age is considered precocious.
ETIOLOGY:
1. Gonadotropin - dependent precocious puberty may be
caused by a congenital anomaly, such as hydrocephalus; a
CNS tumor; an inflammatory condition, such as meningitis;
or trauma. It may also be idiopathic.
2. Gonadotropin - independent precocious puberty may be
caused by a human chorionic gonadotropin – secreting
tumor a gonadal condition, an adrenal disorder or
exogenous ingestion or absorption of steroids .
3. Combined Gonadotropin - dependent and . Gonadotropin –
independen precocious puberty may be caused by
congenital adrenal hyperplasia or an ovarian or adrenal
tumor.
hypothyroidism
Description:
• Hypothyroidism is a chronic condition
characterized by an inadequate amount
of thyroid hormone necessary to meet
metabolic needs.
• It may be congenital or acquired.
• Hypothyroidism is one of the most
common endocrine problems in
children.
Etiology:
• The most common cause of congenital
hypothyroidism is defective embryonic
development of the gland. Another cause is
maternal ingestion of goitrogens, such as
antithyroid drugs or large amounts of iodine.

• Hashimoto’s disease, an autoimmune thyroiditis, is

the most common cause of acquired
hypothyroidism in children. Autoimmune
thyroiditis is commonly assoiciated with other
endocrine disorders and chromosomal disorders.
• Other primary causes of acquired
hypothyroidism are surgical
thyroidectomy, radioactive iodine
therapy, and radiation treatment.

• Secondary hypothyroidism is caused

by a defect in either the
hypothalamus or pituitary.
CUSHING’S
SYNDROME
Description:
• Cushing’s syndrome is a cluster of clinical
abnormalities resulting from excessive
levels of adrenocortical hormones,
particularly cortisol, and to a lesser
extent, related corticosteroids,
androgens, and aldosterone.
Etiology:
• Infants and young children, the
most common cause are an
adrenocortical tumor.

• The common cause in older

children is steroid use.
Diabetes
mellitus
type 1
Description:
• DM is a chronic metabolic disorder that results from
either a partial or complete deficiency of insulin.

• Type 1 DM is characterized by pancreatic beta cell

destruction, leading to absolute insulin deficiency.

• Type 1 DM is the most common endocrine disease of

childhood.
• The primary long-term complications of DM are
nephropathy, retinopathy, and neuropathy.
Etiology:
• Type 1 DM is an autoimmune
disease that develops when a
genetically predisposed child is
exposed to a precipitating
factor, such as a viral infection.
Diabetes
mellitus
type 2
Description:

• Type 2 diabetes mellitus (DM) (formerly called

non-insulin-dependent diabetes mellitus and
type II diabetes mellitus) commonly result from
insulin resistance but may occur from
predominantly insulin resistance with relative
deficiency to a predominantly secretory defect
with insulin resistance

• Girls are nearly twice as likely to develop type 2

DM as boys.
Etiology:
• Type 2 DM is a complex disorder of various
causes with social, behavioral, and environmental
risk factors unmasking the effects of genetic
susceptibility

• Heredity is a strong component to the disorder,

and obesity is a significant risk factor for type 2
DM.

• Puberty appears to plays a significant role in the

development of type 2 DM, and the peak age of
onset in child coincides with midpuberty.