hormonal control of metabolism I Flashcards
by which system is metabolism regulated
the neuroendocrine system
briefly, how does the neuroendocrine system work
one cell senses a change in conditions and secretes small quantities of a chemical messenger that travels to a second cell and binds to a receptor to trigger changes in that second cell
what two things can messengers be
neurotransmitters or hormones
T or F: some molecules that are messengers can be both NTs and hormones
true
give an example of a chemical messenger that is both an NT and a hormone
epinephrine
describe endocrine hormone secretion
they’re secreted by endocrine cells and travel to a target cell in a distant tissue via the blood
describe paracrine hormone secretion
secreted by paracrine cells and act on nearby cells. They don’t enter the bloodstream
describe autocrine hormone secretion
they’re secreted by autocrine cells and act on the cell that secreted it. they don’t enter the bloodstream
list 5 things that can change upon a hormone binding to a receptor
second messenger concentration, RTK activity, membrane potential, adhesion properties of ECM/cytoskeleton, gene expression
what are the two main classes of hormones
water soluble and lipid soluble
which hormone types are water soluble
peptide + amide
which hormone types are lipid soluble
steroid + thyroid
what do water soluble hormones do
quickly induce conformational changes in their receptor on the cell surface
what do lipid soluble hormones do
cross the bilayer + have receptor proteins in the nucleus to slowly alter gene expression
in which two groups can water soluble hormones be further divided
those that bind a metabotropic or a ionotropic receptor
what does a metabotropic receptor result in
changes in pre-existing enzymes or enzyme transcription
what does an ionotropic receptor result in
change in membrane potential
list some examples of peptide hormones
insulin, glucagon, and all hormones of the hypothalamus and pituitary
briefly, how are peptide hormones synthesized
as prohormones + are only activated after proteolytic cleavage
T or F: many peptide hormones can be transcribed by a single gene
true
describe the steps of insulin synthesis
synthesized in the pancreas as the inactive single-chain precursor preproinsulin with an N term signal sequence to direct it to secretory vesicles. The signal sequence is cleaved and disulfide bridges are added on route to secretory vesicle to form proinsulin. When blood glucose levels are high, proteases cleave the peptide and mature insulin is released into the blood via exocytosis
describe the structure of preproinsulin
inactive, single-chain, has an N terminal signal sequence to direct it to secretory vesicles
list 3 catecholamines
dopamine, norepinephrine, and epinephrine
how are catecholamines synthesized
by decarboxylating tyrosine
T or F: during catecholamine synthesis, tyrosine is decarboxylated and the amino group is lost
false; tyrosine IS decarboxylated, but the catecholamines retain the amino group (hence the name)
list 2 key thyroid hormones
T3 and T4
how are thyroid hormones synthesized
by attaching iodines to two tyrosine residues
steroid hormones are derivatives of ___
cholesterol
where in the body are steroid hormones made
adrenal cortex
list 2 examples of steroid hormones
glucocorticoids and mineralocorticoids
what do glucocorticoids do
regulate carb metabolism
what do mineralocorticoids do
regulate concentration of electrolytes in the blood
list 9 endocrine glands
hypothalamus, pituitary, thyroid, parathyroid, adipose, adrenals, pancreas, ovaries, testes
what does the hypothalamus do
receives sensory signals and coordinates the endocrine response
where does the hypothalamus receive all sensory messages from
the central nervous system
what is the top down system
the hypothalamus signals the pituitary to release hormones that travel to many ultimate target organs
describe how the anterior pituitary and hypothalamus interact
hypothalamus releases hormones which travel through portal veins to anterior pituitary which then releases its own separate hormones
describe how the posterior pituitary and hypothalamus interact
neurosecretory cells originating in the hypothalamus have synapses that can release hormones in posterior
which pituitary releases its own separate signals
anterior
T or F: top down hormone pathways include signal amplification
true
T or F: top down hormone pathways can include negative feedback inhibition
true
give an example of a molecule that turns off preceding parts of the top down hormone pathway (negative feedback inhibition)
cortisol
what are bottom-up systems
send signals back to the brain: tell the brain how the body is doing, not what to do
in bottom-up systems, where are the hormones produced (3)
digestive tract, muscle, adipose tissue
what is the normal blood glucose range
70-100 mg/100ml
list the symptoms found at 40-60 mg/100 ml blood glucose
subtle neurological signs like hunger, release of glucagon/epinephrine/cortisol, sweating, trembling
list the symptoms found at 20-40 mg/100 ml blood glucose
lethargy, convulsions, coma
list the symptoms found at 0-10 mg/100 ml blood glucose
permanent brain damage, death
T or F: the pancreas is both an endocrine and exocrine gland
true
describe the exocrine function of the pancreas
relates to sending digestive enzymes from acini cells
describe the endocrine function of the pancreas
relates to maintenance of blood sugar levels through islet cells
what are the endocrine cells of the pancreas called
pancreatic islets
list 5 types of pancreatic islets
Alpha, beta, delta, epsilon, F
what do alpha cells of the pancreas release
glucagon
what do beta cells of the pancreas release
insulin
what do delta cells of the pancreas release
somatostatin
what do epsilon cells of the pancreas release
ghrelin
what do F cells of the pancreas release
pancreatic polypeptide
what is somatostatin
inhibitor of glucagon and insulin secretion
__% of the pancreas is acini cells for digestion
99%
describe the location of the islets of Langerhans in the pancreas
scattered randomly amongst the acini
where are GLUT2 transporters located
on the membranes of B cells and on hepatocytes
pancreas tracking blood glucose: what happens to glucose after a carb-rich meal (hint: GLUT2)
there is rapid, passive transport of glucose into B cells and hepatocytes until [glucose] in the cell is equal to [glucose] in the blood
pancreas tracking blood glucose: what process occurs in the cells after the influx of glucose + what does this process make a lot of
cellular respiration = high ATP levels
pancreas tracking blood glucose: due to high ATP levels from cellular respiration, what occurs in the cell
ATP-gated K+ channels close, depolarizing the membrane
pancreas tracking blood glucose: what happens once the membrane is depolarized
voltage-gated Ca2+ channels open = influx of cytosolic Ca2+
pancreas tracking blood glucose: what is the result of having high intracellular Ca2+ levels
causes the release of even more Ca2+ into the cytosol from the ER
pancreas tracking blood glucose: what is the result of having high Ca2+ from both cytosol and ER
induces exocytosis of insulin granules
how many subunits do the B cell ATP-gated K+ channels have
8
describe the structure of the B cell ATP-gated K+ channels
octamers: 4 SUR1 subunits and 4 Kir 6.2 subunits
what is Kir
a subunit type of B cell ATP-gated K+ channels. Kir = inwardly rectifying K+ channel
what is SUR
a subunit of B cell ATP-gated K+ channels. SUR = sulfonylurea receptor
mutations in the B cell ATP-gated K+ channels can cause ______________
neonatal diabetes
which subunits of the B cell ATP-gated K+ channel forms the actual channel? what is the structural function of the other subunit
Kir forms the channel, SUR subunits surround the Kir subunits
which two molecules can bind to Kir
ATP and PIP2
what does ATP do to Kir
promotes closing
what does PIP2 do to Kir
promotes opening
which two molecules can bind to SUR
ADP and sulfonylurea drugs
what does ADP to do SUR
promotes opening
what do sulfonylurea drugs to do SUR
promote closing
how can sulfonylurea drugs be used to treat type II diabetes
they bind to the B cell ATP-gated K+ channel and encourage it to close = promotes insulin release (you get more insulin)
fed state: what enzyme is activates upon insulin release
glycogen synthase
where is glycogen synthase located
liver
fed state: why is glycogen synthase activates/what is the purpose of this
it will help us store excess glucose that’s incoming
fed state: what enzyme does insulin inhibit
glycogen phosphorylase
fed state: purpose of glycogen phosphorylase inhibition?
reduces glycogen breakdown (because when there’s lots of glucose we want to be building glycogen)
fed state: insulin stimulates glucose uptake by which 2 tissue types
muscle and adipose tissue
fed state: how does insulin stimulate glucose uptake by muscle and adipose tissue?
it permits GLUT4 transporters (hidden in cytosolic vesicles) to fuse with the PM
relate GLUT4 to type II diabetes
GLUT4 doesn’t respond to insulin in type II diabetes = glucose cannot enter cells through it
what enters the well fed liver from the pancreas
insulin
what enters the well fed liver from the intestines (from food we ate)
glucose, amino acids, TAGs from chylomicrons (dietary cholesterol)
what happens to glucose as it enters the well-fed liver
used to build glycogen or we can enter glycolysis to make acetyl-CoA. The acetyl-CoA can then enter the CAC to make ATP/CO2 or it can be used in FA synthesis = TAG formation
what happens to amino acids as they enter the well fed liver
some used for liver protein, if there are excess we will split off the ammonia to leave us with the carbon skeleton (urea cycle)
what leaves the well fed liver
glucose to the brain, CO2 to lungs to be exhaled, TAGs to adipose for storage (via LDL and LDL), urea to the kidneys
what is coming into the fasting liver
glucagon from pancreas, TAGs mobilized from adipose tissue, amino acids from protein degradation in the muscle
what is leaving the fasting liver
glucose to the brain, ketones to the brain, urea to the kidneys
what is the primary source of fuel in the fasting liver
TAG breakdown
what is incoming to the starving liver
TAGs from adipose tissue, amino acids from protein degradation
what is leaving the starving liver
glucose (from GNG) to brain, ketones to brain, excess ketones to kidneys, urea to kidneys
starving liver: with amino acids from protein degradation in muscle, what can happen to them
they can have the NH4+ stripped off to enter the urea cycle. The carbon skeleton can then be used towards pyruvate or OAA, which can enter GNG to form glucose. OR the carbon skeleton can be used towards acetyl-CoA which is used to make ketones
how long into a fast do [ketones] start to rapidly increases
a couple of days
in a fast/starvation, why is the [FFA] in the blood increasing only slightly
because you’re constantly breaking them down in the liver, so the concentration in the blood will stay the same as we continuously take them from adipose and move them to the liver
in a fast/starvation, why doesn’t [glucose] plummet?
once we hit a day or two, GNG kicks in to produce glucose
what two pyruvate enzymes does acetyl-CoA affect
pyruvate dehydrogenase and pyruvate carboxylase
during starvation, how might acetyl-CoA regulate pyruvate dehydrogenase and pyruvate carboxylase
PD is responsible for acetyl-CoA production
PC is responsible for pyruvate –> OAA
the longer we’re in the starvation state, acetyl-CoA will downregulate PD and upregulate PC
when amino acids need to start being oxidized for fuel (during starvation), which amino acids will be degraded first
non-essential (because we can make these)
what triggers cortisol release
low blood glucose, fear, pain, infection, etc
what 3 parts of the body does cortisol act upon
muscle, adipose, liver
role of cortisol acting on muscle, adipose, and liver?
supplies the organism with fuel to withstand whatever stress is occuring
where is epinephrine secreted from
the adrenal medulla
when will epinephrine be secreted
by stress (fight or flight)
role of epinephrine on the muscle, heart, and lungs?
prepares them for a burst of activity, increases heart rate, BP, and vasodilation to get O2 to muscle
how do epinephrine, insulin, and glucagon interact
epinephrine inhibits inulin secretion from the pancreas and activates glucagon secretion
how does cortisol affect TAG breakdown in adipocytes + why
stimulates TAG breakdown = FFAs for fuel and glycerol for GNG
how does cortisol affect muscle protein degradation + why
stimulates muscle protein degradation = amino acids can be shipped to liver and their carbon skeletons used for GNG
how does cortisol affect PEP carboxykinase transcription in the liver + why
stimulates PEPC transcription in the liver = increases TAG cycle flix and FFAs in the blood = can use FFAs for fuel
T or F: the effects of cortisol are very beneficial in the long term
false; they’re only good in the short term. As time goes on, cortisol can damage muscle and bone + impair immune function
list the disease: underproduction of cortisol
Addison’s disease
addison’s disease symptoms
low blood sugar, low weight, fatigue, low appetite
list the disease: overproduction of cortisol
Cushing disease
cushing disease symtpoms
high blood sugar, high BP, weight gain
