metabolism Flashcards

(49 cards)

1
Q

storage of energy

A

in triglycerides & glycogen (carb storage)

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2
Q

anabolism

A

body energy stores replenished during & immediately after eating

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3
Q

glycogen

A

fine capacity (liver or skeletal muscle)

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4
Q

triglycerides

A

huge capacity (in adipose tissue)

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5
Q

catabolism

A

during fasting, triglycerides & glycogen broke down to provide continuous supply

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6
Q

hypothalamus & metabolism

A

regulates behaviours (hunger, satiety)

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7
Q

ARC (hypothalamus)

A

critical role in feeding behaviour, energy expenditure, senses metabolic hormones in blood

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8
Q

VMH (hypothalamus)

A

critical role in feeding behaviour, energy expenditure & reproduction

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9
Q

DMH (hypothalamus)

A

key role in adaptive thermogenesis & feeding behaviour

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10
Q

LH (hypothalamus)

A

reply bw ARC and VMH and higher centres involved in motivation and reward

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11
Q

PVH

A

controlling metabolism, GI renal and cardiovas functions

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12
Q

ME (hypothalamus)

A

circumventricular organ having permeable capillaries - interface bw neural and peripeheral endocrine systems

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13
Q

lesions in LH

A

caused weight loss (leaves them too satiated)

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14
Q

lesions on VMH

A

caused obesity (leave insatiable)

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15
Q

agrp / npy neurons

A

increase food intake
decrease energy expenditure

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16
Q

POMC neurons

A

decrease food intake
increase energy expenditure

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17
Q

tanycytes

A

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.

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18
Q

a1 and a2 tanycytes

A

along VHM & ARC surface
express GFAP

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19
Q

B1 and B2

A

B1 - lateral exterior of infundibular recess
B2 - floor of ventricles
B = contact capillaries

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20
Q

where are AgRP only found?

A

ARC
synthesised in NPY containing cell bodies in ARC

21
Q

what type of neurons increase after fasting?

22
Q

what does POMC gene encode for

A

MSHs ACTH B - endorphin

23
Q

agonists of MC4R receptor

A

a-msh b-msh y-msh

24
Q

what happens when someone doesnt have MC4R

25
mc4r in LH?
regulate feeding behaviour and motivated behaviour
26
mc4r in PVH
regulate energy stores
26
mc4r in PVH
regulate energy stores
27
what is an agonist / antagonist to mc4r
a-msh = agonist (not hungry from pomc) agrp = antagonist (hungry from agrp)
28
db/db
overproduce a satiety factor but dont respond to it have factor no receptor
29
ob/ob
respond to satiety factor have receptor but no factor
30
leptin
more fat = more leptin secreted
31
leptin receptor
encoded by db gene (three isoforms: long, short, secretory) leptin -> LepR activates STAT3 -> pSTAT3 -> regulate gene transcription
32
leptin -> agrp
inhibits
33
leptin -> pomc
activates
34
leptin -> pomc
activates
35
deletion of lepR in AgRP & POMC
increase BW & adiposity
36
insulin (what do signals to muscle/fat & liver mean?)
signals to muscle & fat TO uptake glucose form blood signals to liver TO stop glucogenesi
37
insulin on IR
phosphorylation of AKT -> gene transcription and neuronal excitability
38
deleted IR
increase BW and fat mass
39
exogenous insulin signals to ?
agrp & pomc in arc
40
endogenous insulin
insulin after a meal activated agrp neurons
41
ghrelin
hunger hormone activates agrp`
42
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
43
pomc & wat browning?
pomc activation = increase in browning
44
agrp & wat browning?
inhibition of agrp = increase in wat browning
45
PTP1B
negatively regulates LepR signalling
46
TCPTP
negatively regulates IR signalling
47
PTP1B & TCPTP + obesity?
increased
48
increased PTP1B & TCPTP = ? wat browning & HGP
WAT browning decrease & HGP increase