Flashcards in regulation and integration of metabolism Deck (45):
direct signaling for nervous system control of organ function
autonomic nervous system
indirect signaling for nervous system control of organ function
hypothalamus direct control
autonomic: innervation of pre-ganglionic neurons
both sympathetic and parasympathetic
hypothalamus indirect control
hormonal: release of pituitary and adrenal cortex hormones
what are the three parts of the autonomic nervous system
enteric nervous system
neurotransmitter of parasympathtic
both pre and post ganglionic use acetylcholine
neurotransmitter of sympathetic
pre uses acetylcholine
post use norepinephrine
autonomic control of cardiac function
carotid body detects O2/CO2 composition (chemoreceptors) CNIX
baroreceptors in heart detect blood pressure
the enteric nervous system characteristics
mesh of neurons in the gut
both parasympathetic and sympathetic
can function independently of the CNS
the neuroendocrine system the key players
**diffuse, system wide endocrine signaling
anterior pituitary uses what type of system
the substances released from the hypothalamus are called what?
the substances released from the pituitary are called what?
under stress what hormone does the hypothalamus release?
corticotropin releasing hormone (CRH)
under stress what hormones does the ant. pit. release
adrenocorticotropic hormone (ACTH)
under stress what hormone is released from adrenal cortex?
what nervous system is directly connected to the adrenal glands?
what is an example of an eicosanoid?
PGE2, from arachidonate acid
what is an example of a peptide hormone
epinephrine, dopamine, serotonin
what things does the liver do
amino acid content
lipid formation and mobilization
first pass metabolism
what things does the pancreas do
small intestine buffering
glucose-6-phosphate fate in liver
glycolysis to pyruvate to CAC
made into glucose and released into blood via glucose-6-phosphatase in ER
enter pentose phosphate pathway ->NADPH
when pyruvate is enters the matrix of mitochondria what can happen?
fatty acid synthesis
what is the cori cycle
under demanding activity
glycogen->lactate->blood lactate->enters liver->made into glucose->released into blood as blood glucose
why is NADPH important?
fatty acid synthesis
free radical degredation
how do AAs get into the liver
from the blood as glutamate or glutamine or alanine
once glutamine is in the liver what happens
enters the urea cycle which forms urea (two amine groups)
how does alanine get into the liver
pyruvate from muscle is converted into alanine by taking the amine group from glutamate
-travels in the blood to the liver
-once in the liver alanine donates the amine group to alpha ketogluterate and makes glutamate and pyruvate
-pyruvate is then converted to glucose and released into the blood
**glutamate is not used to transfer amine groups because it takes carbon backbones from the CAC
once AAs are in the liver what happens to them?
fatty acid syn
fatty acid liver metabolism
how do they get there?
once in the liver what happens to FAs
beta oxidation (makes NADH)
cholesterol formation (acetyl CoA) only in liver
ketone bodies (acetyl CoA) no glycerol
when adipose tissue reaches its capacity it releases what hormone?
what does leptin do?
goes to hypothalamus to eat less and metabolize more
what does ghrelin go?
tells you to eat more and metabolize less
what do insulin and satiety signals do?
tells you to eat less and metabolize more by turning off the ghrelin pathway
does leptin inhibit/activate fat synthesis and does it inhibit/activate beta oxidation?
when glucose is high it enters GLUT2 channels in cells and in particular beta cells and inhibits potassium from leaking out by inhibiting ATP-gated K channels. this leads to what?
-depolarization of the membrane and calcium voltage gated channel to open
-this causes the release of insulin granules
-as glucose decreases this stops due to less glucose and ATP in the beta cells
alpha cells are inhibited by what?
insulin, GABA and somatostatin
T/F glucagon is constitutively released at low glucose levels
fates of glucose in a well fed state
glycolysis which leads to triglycerides and taken to adipose tissue via VLDL
fates of glucose in fasting state
fatty acid metabolism->ketone bodies->brain
what are ketone bodies important for?
maintaining neurological function during a fasting state
-body breaks down muscle which releases AAs
increased production of urea
-fatty acid release->beta oxidation->acetyl-CoA->ketone bodies or glucose via gluconeogenesis