Hormones

how is hormone when it comes to traveling around membrane

it can pass through since lipophilic

what is a hormone

given off by gland + travels through blood

what is hormone size compared to nt

much larger than nt

what is protein hormone and an example

long chain, ex. insulin

what is peptide hormone and an example

short chain ex. growth hormone

how are steroid hormones made

from cholesterol

what are examples of steroid hormones

sex hormones - androgens, estrogen, testosterone and glucocorticoids

what is another type of hormone

amine hormone

how is hormone different from nt in time wise

sticks around longer, gradually decreases

how does hormone affect a neuron differently to nt

change probability + intensity of a behavior/ ap

what is relationship between a stimuli/behavior and hormone

reciprocal and can influence each other

one hormone can have how many effects

several effects

one behavior can be affected by how many hormone

several hormones

what is the pattern of hormone release

pulsatile secretion - in bursts

some hormone vary with what and give an example

circadian rythmn, ex. melatonin

hormones can do what to each other

affect and interact

what is a similarity between hormone and nt

hormones can affect cells with receptor protein for that hormone

what are endocrine transmissions

endocrine and neuroendocrine communications

what is the pathway for endocrine communication

endocrine cell --> hormones to blood --> go to target cell receptor

where is endocrine cell housed in

gland

what is the pathway for neuroendocrine communication

nts --> neurons --> send hormones to blood --> target cell receptor

what are neuroendocrine cells

neurons that release hormones in blood

what is another name for neuroendocrine cell

neurosecretory

what are neuropeptides

peptide hormones used by neuron and can act as neuromodulator and change sensitivity to nts

how is hormone different from nt when it comes to effects

nt is rapid message, hormone is slow and long lasting effects

how is hormone different from nt when it comes to length of travel

nt travel only synaptic cleft, hormones travel across blood - over a meter

what are two ways hormones influence cell/neuron

bind to receptor on surface or steroid hormone pass through membrane and bind to inside receptors

how does bind to cell surface work for hormone

cause second messenger cascade --> change in cellular function/ multiple bio effects

cAMP is what related to hormones

second messenger that transmits
messages of many peptide and amine hormones

how does steroid hormone passing through membrane influence cell

hormone receptor complex acts as transcription factor inside as opposed to second messenger

hormone receptor complex is similar to

second messenger

what used to be master gland and what is now

pituitary gland; hypothalamus

what are the hormone systems

pitiutary gland and hypothalamus

where is anterior pitutiary gland

close to nose

where is posterior pitutiary

close to head back

what is anterior pitutiary made of

endocrine tissues/glands

what is posterior pitutiary made of

neural tissue- neurons and glial

what does anterior pitutiary make

six tropic hormones

what causes making of tropic hormones

hypothalamus order's through releasing hormones

how does anterior tropic hormones influence

releasing hormone causes tropic release --> travel through blood to influence endocrine glands in periphery such as thyroid, testes ex. crh (releasing hormone) --> acth (tropic hormone) --> corticosteroids

what do posterior pitutiary get projections from

hypothalamus

what does posterior pitutiary release

oxytocin + vasopressin (for bp)

what is the hypophyseal portal system

hypothalamus sending blood vessels to anterior pitutiary

what does hypothalamus send to pitutiary

blood vessel to anterior and axons projections to posterior

what do hypo release

releasing hormones

what is pathway for thyroid hormone

trh (releasing hormone) --> tsh (tropic hormone) --> thyroid --> thyroid hormones that go for metabolism

what regulates the amount of hormones in the system

negative feedback loop

what is autocrine feedback loop

endocrine cells release a
hormone whose presence feeds back on the
endocrine cells to inhibit further secretion

how is drinking related to hormone

maintain fluid + sodium levels around and inside cells

how can negative feedback loop be created

in many ways for ex. biological response itself causes suppression of hormone

what does insulin do

cause glucose to turn into glycogen

what does glucagon do

cause glycogen to turn into glucose

what is glucagon

hormone

what is similar of drinking and being awake

very important functions that have several ways to dictate and make sure these functions are kept in the body

what is long term energy / resevoir

fat (triglycerides)

what is short term resevoir

glucose

what are the ways weight is maintained

increased motivation to eat when reservoirs depleted and increase intake if more calories needed

what is natural selection favor when it came to eating and how do we know

weight gain not loss; strong signals to eat instead of not to eat

what starts a meal

stomach and metabolic signals

how does stomach signal hunger

stomach sends grelin hormone into blood

how do we know grelin is involved in starting a meal

grelin is increased during fasting, decreased after having a meal, in animals, grelin antagonists decrease hunger and in humans, feelings of hunger correlated with grelin

what causes grelin to be secreted from stomach

receptors in small intestine cause stomach to release grelin

how do we know small intestine causes grelin to release

gastric bypass of smaller small intestine has decrease grelin

what are the metabolic signals that start a meal

glucostat, lipostat, aminostat

increased insulin means

increased hunger

what is glucostat

detect level of glucose

how do we know glucostat exists

Injecting animals with insulin to cause glucoprivation stimulates eating

what is lipostat

Mercaptoacetate causes lipoprivation which stimulates eating

what is aminostat

not as evident because depriving of one amino acid doesn't really change much in animal

where are the receptors for glucose and fat

liver and brain

where in the liver is important for the receptors of glucose

hepatic portal vein that supplies blood to liver

how do we know liver has receptors for glucose

injecting insulin in hepatic portal vein stimulates hunger

when do liver receptors not signal

when vagus nerve between hepatic portal vein to brain is cut off

what other type of info does vagus nerve carry

lipoprivic hunger

where in brain are the receptors for sugar and fat

medulla

what are the satiety factors

head, intestine, stomach, liver

what does liver receptors sense

both glucose and lipid

what does brain receptors sense

only glucose

where are the receptors for head factors

eyes, nose, tongue + throat

how is head receptor sense satiety and ex,

taste and odor indicate calorice value of food ex. food through feeding tube is less fullness than soup fed by themselves

what does stomach factors monitor

amount of fullness

how does stomach detects fullness

through receptors and not just by fullness or physical expansion kinda thing; putting saline inside stomach doesn't decrease hunger meaning stomach can detect nutrients and drinking water doesn't decrease hunger.

what do intestine do satiety through

nutrient + taste receptors

what are the satiety peptide hormones in GI tract

CCK, PYY, GLP-1

what does duodenum do

controls how fast stomach gets emptied using CCK

when is CCK released

at the presence of fats

what functions do CCK do in GI

CCK causes gallbladder to inject bile into duodenum = breakdown food into fats AND causes pylorus to constrict hence keeping food inside stomach

what is CCK opposite of

grelin

where does CCK function for satiety

brain and GI tract

what does CCK do in brain

Injections of CCK into GI tract decrease eating unless cut vagus nerve (vagotomy) AND CCK KO’s (without CCK) become obese

when does PYY hormone work for satiety

released by GI tract after a meal that is proportional to number of calories consumed

where does PYY have receptors

in brain

when does GLP-1 work for satiety

interacts with insulin and receptors in brain to decrease appetite AND blocks ghrelin effects

how is GLP-1 related to weight loss

GLP-1 agonists causes weight loss in obese patients with not much side effects

how do we know liver is involved as a satiety factor as well

experiment infusing glucose + fructose in hepatic vein caused less food consumption. special: fructose can't cross blood brain barrier, hence liver must itself signal brain to stop eating

how is long term satiety done

detection of body fat through leptin,

what is long term satiety signal

leptin

how do we know leptin is involved in long term satiety

obese mice without leptin gene have low metabolism and were cured when given leptin

what releases leptin

fat cells

how do all satiety factors act

centrally - CNS