Name
Type of Action
Chemical Nature
Juxtracrine, paracrine, autocrine, endocrine, Peptide, amino acid or neurocrine, derivative, fatty acid or neuroendocrine, exocrine derivative, or steroid?
Thyroid Hormone (thyroxin)
Endocrine
Steroid-like, but not a steroid – is lipid-soluble, though
Where Made?
In what gland or tissue?
Thyroid gland
Target Cells
Mechanism of Signal Transduction
Actual Effect
Where does it act?
1. Location/type of receptor on target cells; 2. Type of signal transduction (e. g. second messenger); 3. Intracellular mode of action (e.g. change in enzyme activity/transcription)
1. Biochemically speaking (which target enzymes, proteins, or genes are affected; 2. Physiological end result (another hormone secreted, glycogen broken down, etc.); 3. what's the teleological point (e.g. homeostasis, response to stress, growth, maintenance of cycle, etc.)
Act, basically, everywhere...
INTRACELLULAR – receptor itself is a transcription factor (TF). Binding of TH causes activation of TF and transcription of gene --> protein.
Increase BMR (basal metabolic rate), increase heart rate, ventilation rate, cardiac output, and increases catabolism of proteins/carbohydrates Is necessary not only for BMR but also for 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)
Estrogen
Thyroid Stimulating Hormone (TSH) – aka thyrotropin
Endocrine
E nd nd oc oc riri ne ne ( tr tr op op ic ic )
Steroid
P ep ep titi de de
Some is made in the adrenal glands, but most is produced in the Uterus, breast (for our ovaries purposes)
A nt nt er er io io r P itit ui ui ta ta ry ry
Thyroid gland (only thyroid gland has TSH receptors)
INTRACELLULAR – binding of estrogen activates or inhibits transcription (depending on target cell, e.g. the uterus or breast)
BREAST: estrogen binding --> inhibit transcription of gene for prolactin r eceptors --> downregulation of prolactin receptors (this prevents lactation before birth, but when birth occurs, estrogen levels fall, and prolactin receptors can be produced again [becuase there is no more inhibition] to respond to signal to release milk).
G PROTEIN COUPLED RECEPTOR – TSH binds, activates GPCR, activates G protein, activates Adenyl Cyclase, generates cAMP, cAMP activates PKA, PKA phosphorylates target enzymes -> mutliple steps that cause production Causes the release of Thyroid Hormone 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)
Thyrotropin Releasing Hormone (TRH)
Endocrine (t ( tropic)
Peptide
Hypothalamus
Anterior Pituitary – travels via portal vessel
Cell surface receptors in Anterior Pituitary
An overproduction of TRH can can lead to overproduction of TSH --> overstimulation of thyroid --> goiter Phosphorylation leads to glycogen breakdown (metabolism) and glycogen synthesis.
Epinephrine
Endocrine
Peptide – catecholamine
Adrenal Medulla
G PROTEIN COUPLED RECEPTOR – epinephrine binds to GPCR --> AC Adrenergic receptors activation --> cAMP synthesis --> PKA (alpha and beta), acts activation --> PKA phosphorylates on nearly all bodily enzymes involved in glycogen tissue metabolism.
The enzymes for glycogen breakdown are stimulated by phosphorylation, and those enzymes for glycogen syntehsis are inhibited by phosphorylation. Is secreted in response to crisis and activates 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.
Growth Hormone
Endocrine (pseudotropic)
TYROSINE RECEPTOR KINASE – acts on TRK in the liver (and other tissues as well)
Peptide
Note: ILGFs are also released from other tissues, where they don't enter general 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)
Insulin
Endocrine
Peptide
Pancreas
TYROSINE RECEPTOR KINASE – Insulin activates multiple pathways; acts more like a typical growth factor Liver, skeletal muscle, than endocrine (is in same family as and adipose tissue Insulin-Like Growth Factors)
Other effects – inhibits breakdown of glucose "stores" in fat and glycogen, activates enzymes to synthesize stores (glycogen, fat, and/or 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)
Glucagon
Endocrine
Peptide
Pancreas
Liver (for glucose release, and primary physiological effect), G PROTEIN COUPLED RECEPTOR – muscle/adipose tissue triggers the cAMP pathway, activates (for lactate release) PKA
Unlike insulin (which is the ONLY substance known to be able to transport GLUT4 in skeletal muscle), many substances can mimick the effects of glucagon, which makes it an 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 Increases blood glucose levels via gluconeogensis, aids in metabolism of fat/protein/carbs, decreases bone formation.
Cortisol
Endocrine
Steroid – glucocorticoid
Arenal Cortex
Multiple effects/targets, e.g. supressing immune system
Regulates long-term stress response after epinephrine wears off INTRACELLULAR – acts as TF
Production controlled by ACTH 1. Required for the release of release of milk from the mammary glands
Oxytocin
Endocrine --> Uterus
Peptide – only differs from Hypothalamus – ADH / vassopressin by released by TWO amino acids posterior pituitary
Mammary glands and uterus
2. Required for the muscular contractions that allow for birth Aldosterone affects Na+ reabsorption 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 ACTH)
Adrenal Cortex
Aldosterone
Endocrine
Steroid – mineralocorticoid
Trigger – inadequate blood flow through kidney
The distal convoluted tubule and the beginning of the coll collec ectin ting g duc ducts ts
STER STEROI OID D – a mine minera ralo loco corti rticoid c oid..
Adrenal Cortex (glucocorticoid production, e.g. cortisol)
Stimulates release of cortisol (glucocorticoid) from the adrenal cortex (note that it does not G PROTEIN COUPLED RECEPTOR – control the production of mineralocorticoids like and the cAMP pathway (like all tropic aldosterone or sex steroids in the Adrenal hormones) Cortex)
ACTH (adrenocorticotropic hormone)
Endocrine (tropic)
Peptide
Anterior Pituitary (stim. by CRH – corticotropin releasing hormone)
FSH, LH (folliclestimulating hormone, lutenizing hormone) – aka Gonadotropins
Endocrine (tropic)
Peptide
Anterior Pituitary ( st st im im . by by G nR nR H) H)
Endocrine Endocrine (pseudotr (pseudotropic) opic) Peptide de
Anterior Pituitary (controlled by inhibiting factor from HT called PIH)
Endocrine
Anterior Pituitary – all are made from the same peptide precursor (proopio-melanocortin, or pomC), that is cut up to give ACTH, MSH, etc. (Alternative processing of protein, protein, not RNA).
Prolactin
Melanocyte Stimulating H (MSH), endorphins, and enkephalins
Peptide
Aldosterone's effects are slower slower than ADH's becuase aldosterone requires the synthesis of new proteins (e.g. Na+ transporters) instead of the activation of pre-existing channels
G on on ad ad s
G PROTEIN COUPLED RECEPTOR – and the cAMP pathway (like all tropic Development, growth, and pubertal maturation hormones) of reproductive system
Mammary glands
TYROSINE RECEPTOR KINASE – acts on TRK in t he exocrine (mammary) gland
Stimulates mammary gland (exocrine) to produce milk—note that oxytocin is required to secrete that secrete that milk.
Relatively obscure function; MSH may be involved in body weight control and pigmentation.
Name
Type of Action
Chemical Nature
Where Made?
Target Cells
Mechanism of Signal Transduction
Hypothalamus – released by posterior pituitary (PP)
Actual Effect
Directly affects water reabsorption, primarily for water volume control Released in response to high blood osmolarity
ADH (antidiuretic hormone), aka vasopressin
Endocrine
Peptide
Trigger – release stimulated by 1. Primarily – osmolarity receptors in the hypothalamus 2. Secondarily – by stretch receptors in the arteries that detect Collecting ducts of a drop in BP distal nephron
The osmolarity of filtrate will increase as it passes through collecting ducts if more ADH is released (causes reabsorption of water into blood)
G PROTEIN COUPLED RECEPTOR – using the CAMP pathway, ADH causes insertion of aquaporins into the collecting ducts.
Water flows out of the collecting ducts becuase of the high osmolarity (salt concentration) in the interstitial fluid that is created by the countercurrent multiplication system in the loop of Henle.
