endocrine physiology Flashcards
What are the classes of hormones
- peptides: largest group
- amines: catecholamines; thyroid hormones
- steriod
- others
What are factors that influence hormones
-rate of hormone secretion
-rate of metabolism or excretion
-quantity of transport proteins
-changes in plasma volume
down-regulation and up regulation of receptors
-the receptors that hormones bind to will be up-regulated if the hormone is used a lot or down regulated if it is not used
what are the general actions of hormones
-alter DNA activity to modify protein synthesis
-use “second messengers” to activate special proteins
change membrane transport mechanics
What does the posterior pituitary gland release
ADH and oxytocin
Role of ADH
-controls water balance by causing water retention
-osmoreceptors send info based on extracellular osmorlarity top the para-ventricular nucleus and supra-optic nucleus
-changes in blood volume are also detected by baroreceptors
role of Oxytocin
stimulates uterine contactions, milk ejection and maternal behavior
thyroid gland
-releases calcitonin, Thyroxine (t4) and triiodothyronine (T3)
-thryoid homrone receptors are all through the body
-increases metabolic rate
-increase hepatic glucose production through gluconeogenesis
what type of hormones are made in the medulla of the adrenal gland
- catecholamines: epinephrine and norepinephrine
- peptides: somatostatin and substance P
What is made in the Zona reticularis layer of the cortex of the adrenal gland
Androgens: estrogen and testosterone
What is made in the zona fasciculata of the adrenal cortex of the adrenal gland
glucocorticoids: cortisole and cortisone
What is made in the zona glomerulosa of the adrenalcortex of the adrenal gland
mineralocorticoids: aldosterone and corticosterone
What are catecholamines and describe
-released by adrenal medulla but controlled by preganglionic sympathetic neurons
-epinephrine: major endocrine product
-norepinephrine: major sympathetic neurotransmiter
What reactions do catecholamines cause in the cell
-depends on the receptor type
-Aphla1 = increase in intracellular Ca in cells
-alpha2 = suppress cAMP response
-Alpha 1,2,and 3 = increase cAMP
short term response of caetcholamines
-increased cardiac output, bronchodilation, and elevation of blood glucose
Aldosterone functions
-maintains normal extracellular volume
-stimulates Na reabsorption and K excretion
Pancrease: what hormones does it secret and from what cells
- alpha cells: secrete glucogon
- beta cells: secrete insulin, proinsulin and C peptide
-gamma cells: secrete somatostatin
what does insulin do, what does it effect and what stimulates its release
-increases after meals and reduces glucose, amino acids, fatty acids and ketones
-effects the liver, skeletal muscle and adipose tissue
-release stimulated by rising blood glucose levels and plasma concentration of arginine, leucine, or lysine amino acids
what does glucogon do, what does it effect and what stimulates its release
-increase glucose and ketone production by the liver
-targets the liver
-stimulated by hypoglycemia and inhibited by hyperglycemia and by eating a protein rich meal
Explain the initial rapid phase of insulin release
-when plsma glucose increases; depletes cells of insulin; beigins in 1 minute and lasts about 10 minutes
explain the slow phase of insulin releas
begins 10-15 minutes and lasts until lucose levels recedes
-depends on the synthesis of new hormone through transcription, protein synthesis and post translational processing
What stimulates glucose production into the plasma and what inhibits it
- glucogone, cortisol, growth hormone and catacholamines,
- insulin
what stimualtes blood glucose into glucose that is used and what inhibits that
- insulin
- cortisole and growth hormone
What does growth hormone stimulate
-stimulates protein synthesis
-stimulates gluconeogenesis in the liver
-blocks glucose entry into adipose
Feedback mechanisms that regulate GH
-GH inhibits secretion once levels get too high
- IGF-1 inhibits GH at somatotropes and inhibtis hypothalamic GHRH
-IGF inhibits hypothalamic release of somatostatin
Insulin like growth factos effecs and what is it stimulated
effects are similar to GH and it can be stimualted also by contractin muscles
cortisol
-affects many cell types
-involved in plpasma glucose regulation
-binds to glucocorticoid receptors
-secreted in response to stress
-mobilizes glucose, Amino acids, and fatty acids
-antagonist against inflammatory and immune response
Leptin
-tells you you are full and done eating
-released from fat
-makes cells more sensitive to insulin and therefore the body is more effective at using its insulin
-as you increase adipose tissue you become leptin resistant
Adiponectin
increase insulin sensitivity
-as fat increases adiponectin decreases and it can cause insulin resistant and possibly type 2 DM
Parathryoid gland function
-secretes parathyroid hormone (PTH)
-importnat in regulation of Ca and phosphate
-stimulates bone reabsorption, renal reabsorption of CA in the ascending and distal tubule of the kidney and renal phosphate excretion
-controlled secretion by plasma free Ca concentration, plasma phosphate (inversely related to Ca levels) and vitamin` D
What is the primary fuel at the onset of exercise and during strenuous activity?
Muscle glycogen
What activates glycogenolysis
- plasma epinephrine: stimulates cyclic AMP formation by binding to Beta adrenergic receptors
-Ca from contracting muscles binds to calmodulin
Describe the pathway that occurs when epinephrine is released and stimulates the breakdown of muscle glycogen (glycogenolysis)
- epinephrine binds to Beta receptors (adrenergic) and causes formation of cyclic AMP
- cAMP causes phosphorylase B to turn into phosphorylase A
- Phosphorylase A is necessary for glycogen break down
- therefore glycogen breaks down into glucose-1-PO4 which then enters glycolysis
escribe the pathway that occurs when the cisternae release Ca (glycogenolysis)
- cisternae of SR releases Ca
- Ca binds to calmondulin which causes phosphorylase B to turn into phosphorylase A
- phosphorylase A causes glycogen breaks down into glucose-1-PO4 which then enters glycolysis
Where do we get energy once glycogen stores are depleted
- mobilize glucose from liver glycogen stores
- mobilize plasma FFA from adipose tissue
- synthesize new glucose in the lover by gluconeogenesis
- block glucose entry into the cells
What are permissive and slow acting hormones
- thyroid hormones
- cortisol
- growth hormone
Thryoid hormone
- allows epi to mobilize FFA from adipose tissue
- exercise effects: T3 is removed by tissue faster than it is replenished by the thyroid
- the more you exercise and deplete T3/T4 the body will up regulate the receptors to use the hormones more efficiently (the rate at which people use T3/T4 varies)
Cortisol
- concentration doesn’t change much during low-intensity, long duration exercise
- direct and permissive effects
- when glucose decreases, cortisol causes an increase glucagon and decrease in insulin
- need to stress the body to get cortisol to increase
Growth hormone
- works to preserve plasma glucose but takes time
- increase is related to intensity
role of cortisol in plasma glucose levels
- muscle: proteins are broken down into amino acids that enter gluconeogenesis in the liver by combining with glycerol; the glucose then enters the bloodstream
- adipose tissue: triglycerides are broke into FFA and glycerol; the glycerol enters the liver to undergo gluconeogenesis while the FFA enter the bloodstream
- tissues: increase FFA oxidation and cortisol blocks glucose from entering the cells
Role of growth hormone in plasma glucose levels
- increases gluconeogenesis in the liver
- increases the breakdown of triglycerides into FFA and glycerol
- increases FFA oxidiation and blocks glucose entry
Role of epinephrine and norepinephrine in the substrate mobilization
- increases liver breakdown of glycogen to glucose
- increases adipose tissue breaking down triglycerides into FFA and glycerol
- increases tissue FFA oxidiation and blocks tissue taking in glucose from the blood
Role of insulin/glucagon in substrate mobilization after a meal
- increase in insulin and decrease in glucagon (decreases G/I ratio)
- that causes an increase storage of glycogen , fat, and protein
- which causes decrease plasma glucose, amino acids and fatty acids
Role of insulin/glucagon in substrate mobilization during fast/exercise
- decreased insulin and increase glucogon (increases the G/I ratio)
- hydrolysis of glycogen, fat, and protein
- increase in gluconeogenesis
- increase in plasma glucose, amino acids and fatty acids
Long term exercise effects
- plasma insulin decreases and plasma glucose increases (do not want a lot of insulin floating around if you are not using it)
- net effect: FFA mobilized from adipose and glucose mobilized from liver for gluconeogenesis maintains plasma glucose concentration
- Endurance training: increases mitochondria and decreases lactate concentration so more FA can be used for energy and limited carbohydrate stores can be spared (improves preformance)
Describe what happens with Epinephrine/norepinephrine bind to alpha cells in the pancreas
- alpha cells have beta adrenergic receptors and when Epi/Norepi bind alpha cells increase glucagon production
- the increase in glucagon causes an increase in plasma glucagon causing the liver breaks down glycogen into glucose
describe what happens when epi/norepi bind to beta cells in the pancreas
- the beta cells have alpha receptors that when epi/norepi bind, it decreases insulin production
- that will decrease plasma insulin which causes the liver to break down glycogen into glucose
effects of exercise on glucose uptake
- increases glucose uptake by increase blood flow
- the increase in blood flow causes an concentration gradient for glucose to diffuse across the membrane through channel proteins
- sensitivity to insulin increase as a result of increased membrane transportation
- therefore you require less insulin to get glucose into the cells
Changes in glucose transporters with exercise
- high intramuscular Ca concentration causes a reduction in the bodies insulin resistance which causes diabetes
- exercise also causes the release of protein kinases, nitric oxide, AMP activated protein kinase
Horomonal response to graded exercise
- epinephrine, norepinephrine, growth hormone, cortisol and glucagon increase
- insulin decreases until about 80% VO2 max when it starts to increase again
hormonal response to prolonged exercise
- epinephrine, norepinephrine, growth hormone, cortisol and glucagon increase
- insulin decreases during prolonged exericse
