metabolism Flashcards
storage of energy
in triglycerides & glycogen (carb storage)
anabolism
body energy stores replenished during & immediately after eating
glycogen
fine capacity (liver or skeletal muscle)
triglycerides
huge capacity (in adipose tissue)
catabolism
during fasting, triglycerides & glycogen broke down to provide continuous supply
hypothalamus & metabolism
regulates behaviours (hunger, satiety)
ARC (hypothalamus)
critical role in feeding behaviour, energy expenditure, senses metabolic hormones in blood
VMH (hypothalamus)
critical role in feeding behaviour, energy expenditure & reproduction
DMH (hypothalamus)
key role in adaptive thermogenesis & feeding behaviour
LH (hypothalamus)
reply bw ARC and VMH and higher centres involved in motivation and reward
PVH
controlling metabolism, GI renal and cardiovas functions
ME (hypothalamus)
circumventricular organ having permeable capillaries - interface bw neural and peripeheral endocrine systems
lesions in LH
caused weight loss (leaves them too satiated)
lesions on VMH
caused obesity (leave insatiable)
agrp / npy neurons
increase food intake
decrease energy expenditure
POMC neurons
decrease food intake
increase energy expenditure
tanycytes
subtype of ependymal cells (extend into hypothalamic tissue)
contact with neurons, reaching fenestrated network (tight junctions between = prevent diffusion into CSF)
controlling energy
balance and play a crucial role in regulating the access
of peripheral metabolic signals to the ARC.
a1 and a2 tanycytes
along VHM & ARC surface
express GFAP
B1 and B2
B1 - lateral exterior of infundibular recess
B2 - floor of ventricles
B = contact capillaries
where are AgRP only found?
ARC
synthesised in NPY containing cell bodies in ARC
what type of neurons increase after fasting?
agrp / npy
what does POMC gene encode for
MSHs ACTH B - endorphin
agonists of MC4R receptor
a-msh b-msh y-msh
what happens when someone doesnt have MC4R
obesity
mc4r in LH?
regulate feeding behaviour and motivated behaviour
mc4r in PVH
regulate energy stores
mc4r in PVH
regulate energy stores
what is an agonist / antagonist to mc4r
a-msh = agonist (not hungry from pomc)
agrp = antagonist (hungry from agrp)
db/db
overproduce a satiety factor but dont respond to it
have factor no receptor
ob/ob
respond to satiety factor
have receptor but no factor
leptin
more fat = more leptin secreted
leptin receptor
encoded by db gene
(three isoforms: long, short, secretory)
leptin -> LepR activates STAT3 -> pSTAT3 -> regulate gene transcription
leptin -> agrp
inhibits
leptin -> pomc
activates
leptin -> pomc
activates
deletion of lepR in AgRP & POMC
increase BW & adiposity
insulin (what do signals to muscle/fat & liver mean?)
signals to muscle & fat TO uptake glucose form blood
signals to liver TO stop glucogenesi
insulin on IR
phosphorylation of AKT -> gene transcription and neuronal excitability
deleted IR
increase BW and fat mass
exogenous insulin signals to ?
agrp & pomc in arc
endogenous insulin
insulin after a meal activated agrp neurons
ghrelin
hunger hormone
activates agrp`
ghrelin & BBB
ghrelin cant diffuse across BBB
so in fed state: no fenestrations = no ghrelin = no hunger
fasting state: expand brain windpw = ghrelin can enter = hunger
pomc & wat browning?
pomc activation = increase in browning
agrp & wat browning?
inhibition of agrp = increase in wat browning
PTP1B
negatively regulates LepR signalling
TCPTP
negatively regulates IR signalling
PTP1B & TCPTP + obesity?
increased
increased PTP1B & TCPTP = ? wat browning & HGP
WAT browning decrease & HGP increase
