U1: ch 16 the endocrine system

Second messenger system: used by

all amino acid hormones except thyroid hormones

cAMP signaling mechanism

amino acid based hormones: general

amino acid derivatives, peptides and proteins

steriods: mechanism

direct gene activation

steriods: general

synthesized from cholesterol, lipid soluble

second messenger systems w/ plasma membrane receptors

signaling mechanisms:

1. hormones (first messenger) binds to receptor

2. receptor activates G protein

3. G protein activates or inhibits effector enzyme adenylate cyclase

4. adenylate cyclase then converts ATP to cAMP → second messenger

5. cAMP activates protein kinases

• activated kinases phosphorylates various proteins leading to: activating some, deactivating others

second messenger system: process

G protein act as ‘switch’

1st & 2nd messenger → huge amplifications, one hormone molecule → millions of products

phosphodiesterase → fine regulation

result depends on: target cell, specific protein kinase, substrate of protein kinase

ex: glucagon → liver cells → glycogen breakdown

mechanism of hormone action: second messenger cAMP

each “hormone + receptor” complex activates MANY g proteins

AND

each adenylate cyclase converts MANY atp to cAMP

AND

each protein kinase can catalyze MANY reactions

PRODUCES…

cascading amplification (1 hormone molecule → millions of final products)

direct gene activation w/ intracellular receptors

1. hormones diffuse into target cells and bind with intracellular receptors

2. receptor-hormone complex enters the nucleus

3. receptor-hormone complex binds to specific region of DNA

4. this prompts DNA transcription to produce mRNA

5. mRNA directs translation, producing a polypeptide (protein)

direct gene activation: summary/short

building of hormone + receptor complex to DNA acts as switch and turns on gene

exception: thyroid hormone, receptor is always bound to DNA

target cell: specificity

must have specific receptors to which hormone binds

ex: ACTH receptors found only on certain cells of adrenal cortex

target cell: activation

3 factors:

1. blood levels of hormones → negative feedback

2. relative number of receptors on or in target cell

3. affinity (strength) of binding between receptor and hormone

interaction of hormones at target cells: antagonism

one or more hormones oppose the action of another homrone

ex: insulin and glucagon

interaction of hormones at target cells: synergism

more than one hormone produces same but amplified effects on target cells

ex: glucagon, epinephrin, and cortisol

interaction of hormones at target cells: permissiveness

one hormone cannot exert its effects without another hormone being present

ex: thyroid and epinephrine

hypothalamus&pituitary gland: relationship

hypothalamic hypophyseal tract: connected to hypothalamus via neuronal connection

STORAGE area for hormones (stores antidiuretic hormone and oxytocin)

pituitary gland: posterior pituitary

neurohypophysis

nerve fibers and supporting cells

pituitary gland: anterior pituitary

adenohypophysis

glandular tissue

hypothalamus and pituitary gland: genera;

hypothalamus acts as control center, pituitary acts as messenger gland

hypothalamus/pitutiary gland: control of posterior pituitary

hypothalamus produces oxytoxin and ADH (antidiuretic hormone)

travels down neurons and stored and released by posterior pituitary

hypothalamus makes → posterior pituitary releases

hypothalamus and pituitary: control of anterior pituitary

hypothalamus secretes releasing and inhibiting hormones into hypophyseal portal system

these hormones regulate what anterior pituitary secretes (like GH, TSH, ACTH)

hypothalamus signals → anterior pituitary produces and releases hormones

adrenal medulla: composure

composed of nervous tissue, part of sympathetic nervous system

adrenal medulla: produces

catecholamines: epinephrine and norepinephrine

adrenal medulla: short or long term response

short term response

adrenal cortex: composition

3 layers of glandular tissues producing corticosteroids

adrenal cortex: produces

corticosteroids:

zona glomerulosa → mineralocorticoids

zona fasciculata → glucocorticoids

zona reticularis → gonadocorticoids (adrenal sex hormone)

adrenal cortex, mineralocorticoids: general

produced by zona glomerulosa, regulates electrolyte (Na+ and K+) in blood

aldosterone: most potent mineralocorticoid

1. stimulates Na+ reabsorption and water retention by kidneys → results in increased blood volume and blood pressure

2. sitmulates secretion of K and elimination into urine

adrenal cortex, mineralocorticoids: factors regulating aldosterone secretion

low blood pressure → increase aldosterone

stress → incerase aldosterone

increased plasma K → increase aldosterone

high blood pressure → decrease aldosterone

adrenal cortex, glucocorticoids: general and function

produced by zona fasciculata

function:

influence metabolism of most cells and help resist stressors

keep blood glucose levels relatively constant

main BP by increasing action of vasoconstrictors

adrenal cortex, glucocorticoids: CORTISOL function

prime metabolic effect → gluconeogensis

• formation of glucose from fats and proteins

• promotes rises in blood glucose, fatty acids and amino acids

higher amounts suppress immune system (reduced inflammation)

adrenal medulla: catecholamines

epinephrine 80% and norepinephrine 20%

function:

involve in short term stress response (fight or flight)

blood diverted to brain heart and skeletal muscles

increased metabolism

increased HR

bronchial dilation

increased blood glucose levels

causes vasoconstriction leading to increased BP

adrenal medulla: catecholamines, homeostatic imbalance

hypersecretion → pheochromocytoma

tumor of adrenal medulla

symptoms: uncontrolled sympathetic NS like increased metabolic rate, rapid heartbeat, palpitations, hypertension, intense nervousness and sweating

adrenal medulla: catecholamines, hyposecretion imbalance

epinephrine and norepinephrine are not essential to life, no problems w hyposecretion

diabetes mellitus (homeostatic insulin imbalances): general and mechanism

due to hyposecretion or hypoactivity of insulin

mechanism:

less glucose transported from blood into cells

blood glucose rises but cells are starving for atp

cells use fat for ATP, producing ketones as byproduct

ketone causes blood pH to fall → ketoacidosis

diabetes mellitus (homeostatic insulin imbalances): 3 signs of diabetes

polyuria → huge urine output

• glucose in urine → water follows glucosei in urine

polydipsia → excessive thirst

• from water loss due to polyuria

polyphadia → excessive hunger and food consumption

• cells cannot take up glucose and are starving

types of diabetes: type I

most common in those younger than 20

immune system destroys pancreatic beta cells

low insulin levels in blood → less glucose transported from blood into cells → high blood glucose

types of diabetes: type II

most common in obsese populaitons older than 35

insulin receptors are unable to respond to insulin → insulin resistance

normal or high levels of insulin in blood BUT less glucose transported from blood into cells → high blood glucose

growth hormones GH

stimulates most cells, targets bone and skeleton

promotes protein synthesis and encourages use of fats for fuel

direct action → increase metabolism

indirect action → increased growth

prolactin (PRL)

stimulates milk production

antifiuretic hormone (ADH)

targets kidney

action → regulates bodys water balance by controlling how much water is ecreted in urine

oxytocin

taeget smooth muscle of uterus and breats

stretching of uterus and cervix stimulates oxytocin production

lactation → suckling, triggers milk ejection

thyroid hormone

metabolic hormone, effects all body cells

T4 (thyroxine) and T3 (triiodothyronine) iodine must for synthesis

direct gene activation, negative feedback control

function: calorigenic effect (increase metabolic rate and heat production), regulation of tissue growth and development, maintenance of blood pressure/heart rate

parathyroid hormone (PTH)

Ca2+ homeostasis

function: raises blood Ca+ levels by:

stimulating osteroclasts to digest bone matrix

enhancing reabsorption of Ca2+ by kidneys

promoting activation of vit D → increased absorption of Ca2+ by intestinal mucosa

negative feedback