Name Type of Action Chemical Nature Where Made?

Target Cells Mechanism of Signal Transduction Actual Effect

1. Biochemically speaking (which target
enzymes, proteins, or genes are affected; 2.
1. Location/type of receptor on target Physiological end result (another hormone
Juxtracrine, paracrine, cells; 2. Type of signal transduction (e. secreted, glycogen broken down, etc.); 3.
autocrine, endocrine, Peptide, amino acid or g. second messenger); 3. Intracellular what's the teleological point (e.g. homeostasis,
neurocrine, derivative, fatty acid or In what gland or mode of action (e.g. change in enzyme response to stress, growth, maintenance of
neuroendocrine, exocrine derivative, or steroid? tissue? Where does it act? activity/transcription) cycle, etc.)
Increase BMR (basal metabolic rate), increase
heart rate, ventilation rate, cardiac output, and
INTRACELLULAR – receptor itself is a increases catabolism of proteins/carbohydrates
Steroid-like, but not a transcription factor (TF). Binding of TH
Thyroid Hormone steroid – is lipid-soluble, Act, basically, causes activation of TF and Is necessary not only for BMR but also for
(thyroxin) Endocrine though Thyroid gland everywhere... transcription of gene --> protein. normal altertness and reflexes
Estrogen controls production of receptors for
other hormones. During pregnancy, estrogen
controls production of oxytocin receptors (in
uterus) and prolactin receptors (in breast).

UTERUS: estrogen binding --> activate

transcription of gene for oxytocin receptors -->
produce new oxytocin receptors (receptors to
oxdytocin are needed in the uterus to respond
to the signal for contractions to give birth --
oxytocin)

BREAST: estrogen binding --> inhibit

transcription of gene for prolactin receptors -->
downregulation of prolactin receptors (this
Some is made in prevents lactation before birth, but when birth
the adrenal INTRACELLULAR – binding of occurs, estrogen levels fall, and prolactin
glands, but most is estrogen activates or inhibits receptors can be produced again [becuase
produced in the Uterus, breast (for our transcription (depending on target cell, there is no more inhibition] to respond to signal
Estrogen Endocrine Steroid ovaries purposes) e.g. the uterus or breast) to release milk).
G PROTEIN COUPLED RECEPTOR –
TSH binds, activates GPCR, activates
G protein, activates Adenyl Cyclase,
Thyroid Stimulating generates cAMP, cAMP activates PKA,
Thyroid gland (only PKA phosphorylates target enzymes --
Hormone (TSH) – aka thyroid gland has > mutliple steps that cause production Causes the release of Thyroid Hormone
thyrotropin Endocrine (tropic) Peptide Anterior Pituitary TSH receptors) and release of TH (thyroxine) from the thyroid glands
Causes release of TSH (thyrotropin) from the
anterior pituitary

Production is negatively inhibited by TH

(although TH's primary negative feedback
effect is in the AP, where it reduces response
to TRH)

Anterior Pituitary – An overproduction of TRH can lead to

Thyrotropin Releasing travels via portal Cell surface receptors in Anterior overproduction of TSH --> overstimulation of
Hormone (TRH) Endocrine (tropic) Peptide Hypothalamus vessel Pituitary thyroid --> goiter
Phosphorylation leads to glycogen breakdown
(metabolism) and glycogen synthesis.

The enzymes for glycogen breakdown are

G PROTEIN COUPLED RECEPTOR – stimulated by phosphorylation, and those
epinephrine binds to GPCR --> AC enzymes for glycogen syntehsis are inhibited
Adrenergic receptors activation --> cAMP synthesis --> PKA by phosphorylation.
(alpha and beta), acts activation --> PKA phosphorylates
on nearly all bodily enzymes involved in glycogen Is secreted in response to crisis and activates
Epinephrine Endocrine Peptide – catecholamine Adrenal Medulla tissue metabolism. the fight or flight response.
Name Type of Action Chemical Nature Where Made? Target Cells Mechanism of Signal Transduction Actual Effect
Stimulates production of secretions, but not
from endocrine glands.

GH stimulates secretion of ILGFs (insulin-like

growth factors), ILGF 1 and 2, in the liver. The
ILGFs are released from the liver into the
bloodstream, where they act as endocrines.

TYROSINE RECEPTOR KINASE – Note: ILGFs are also released from other
Endocrine (pseudo- acts on TRK in the liver (and other tissues, where they don't enter general
Growth Hormone tropic) Peptide tissues as well) circulation but instead act as paracrines.
Considered body's main anabolic (breakdown)
enzyme.

Effectors increase both uptake and utilization

of glucose:
1. Increase of glucose uptake by membrane
transporters
2. Breakdown of glucose to provide energy
3. Conversion of glucose to "stores" (fat,
glycogen—and breakdown of storage
molecules inhibited)
4. Increasing phosphorylation of glucose to
G6P, trapping it inside cells

In resting skeletal muscle/adipose tissue –

mobilizes GLUT4 (insulin transporter) for
facilitated diffusion of G, no other protein can
do this.

In liver – liver (and brain) can take up glucose

without insulin (don't use GLUT4). GLUTs are
located permanently in membrane. In liver,
insulin promotes glucose uptake by increasing
phosphorylation (trapping) of G.

In brain – liver does not affect G uptakle in

brain

Working skeletal muscle – insulin not required

for uotake of G in working skeletal muscle
(exercise mobilized GLUT4)
TYROSINE RECEPTOR KINASE –
Insulin activates multiple pathways; Other effects – inhibits breakdown of glucose
acts more like a typical growth factor "stores" in fat and glycogen, activates enzymes
Liver, skeletal muscle, than endocrine (is in same family as to synthesize stores (glycogen, fat, and/or
Insulin Endocrine Peptide Pancreas and adipose tissue Insulin-Like Growth Factors) protein), promotes breakdown of G for energy
Primary physiological effect is on the liver –
promotes production/release of glucose, not
it's utilization

Glucose produced by breakdown of glycogen

(liver cells) and build up from lactate (also
occurign in liver cells but w/ lactate from the
glycolysis of muscle/adipose tissue via
gluconeogensis)

Liver (for glucose Unlike insulin (which is the ONLY substance

release, and primary known to be able to transport GLUT4 in
physiological effect), G PROTEIN COUPLED RECEPTOR – skeletal muscle), many substances can mimick
muscle/adipose tissue triggers the cAMP pathway, activates the effects of glucagon, which makes it an
Glucagon Endocrine Peptide Pancreas (for lactate release) PKA unlikely candidate for disease.
Name Type of Action Chemical Nature Where Made? Target Cells Mechanism of Signal Transduction Actual Effect
Involved in energy metabolism regulation, not
just in response to stress. Increases blood
glucose levels via gluconeogensis, aids in
metabolism of fat/protein/carbs, decreases
bone formation.

Multiple Regulates long-term stress response after

effects/targets, e.g. epinephrine wears off
supressing immune
Cortisol Endocrine Steroid – glucocorticoid Arenal Cortex system INTRACELLULAR – acts as TF Production controlled by ACTH
1. Required for the release of milk from the
mammary glands
Peptide – only differs from Hypothalamus –
ADH / vassopressin by released by Mammary glands and 2. Required for the muscular contractions that
Oxytocin Endocrine --> Uterus TWO amino acids posterior pituitary uterus allow for birth
Aldosterone affects Na+ reabsorption (and K+
secretion) in the distal convoluted tubule and
beginning of the collecting ducts—which
indrectly encourages H2O reabsoprtion.

Stimulates virtually all steps of Na+

reabsorption (e.g. the number of sodium
transporters in the epithelial cells that line the
distal convoluted tubule)

Regulation not under HT/AP axis (not under

Adrenal Cortex ACTH)

Trigger – The distal convoluted Aldosterone's effects are slower than ADH's
inadequate blood tubule and the becuase aldosterone requires the synthesis of
Steroid flow through beginning of the new proteins (e.g. Na+ transporters) instead of
Aldosterone Endocrine – mineralocorticoid kidney collecting ducts STEROID – a mineralocorticoid. the activation of pre-existing channels
Anterior Pituitary Stimulates release of cortisol (glucocorticoid)
(stim. by CRH – Adrenal Cortex from the adrenal cortex (note that it does not
corticotropin (glucocorticoid G PROTEIN COUPLED RECEPTOR – control the production of mineralocorticoids like
ACTH (adrenocorticotropic releasing production, e.g. and the cAMP pathway (like all tropic aldosterone or sex steroids in the Adrenal
hormone) Endocrine (tropic) Peptide hormone) cortisol) hormones) Cortex)
FSH, LH (follicle-
stimulating hormone,
G PROTEIN COUPLED RECEPTOR –
lutenizing hormone) – aka Anterior Pituitary and the cAMP pathway (like all tropic Development, growth, and pubertal maturation
Gonadotropins Endocrine (tropic) Peptide (stim. by GnRH) Gonads hormones) of reproductive system
Anterior Pituitary
(controlled by
inhibiting factor TYROSINE RECEPTOR KINASE – Stimulates mammary gland (exocrine) to
from HT called acts on TRK in the exocrine produce milk—note that oxytocin is required to
Prolactin Endocrine (pseudotropic) Peptide PIH) Mammary glands (mammary) gland secrete that milk.
Anterior Pituitary –
all are made from
the same peptide
precursor (pro-
opio-melanocortin,
or pomC), that is
cut up to give
Melanocyte Stimulating H ACTH, MSH, etc.
(Alternative Relatively obscure function; MSH may be
(MSH), endorphins, and processing of involved in body weight control and
enkephalins Endocrine Peptide protein, not RNA). pigmentation.
Name Type of Action Chemical Nature Where Made? Target Cells Mechanism of Signal Transduction Actual Effect
Hypothalamus –
released by
posterior pituitary Directly affects water reabsorption, primarily for
(PP) water volume control

Released in response to high blood osmolarity

Trigger – release
stimulated by The osmolarity of filtrate will increase as it
1. Primarily passes through collecting ducts if more ADH is
– osmolarity released (causes reabsorption of water into
receptors in the blood)
hypothalamus
2. Secondarily – Water flows out of the collecting ducts becuase
ADH (antidiuretic by stretch G PROTEIN COUPLED RECEPTOR – of the high osmolarity (salt concentration) in
receptors in the using the CAMP pathway, ADH causes the interstitial fluid that is created by the
hormone), aka arteries that detect Collecting ducts of insertion of aquaporins into the countercurrent multiplication system in the loop
vasopressin Endocrine Peptide a drop in BP distal nephron collecting ducts. of Henle.