Intergration of metabolism Flashcards

1
Q

what is the metabolic feature of the brain

A

can metabolise only glucose ( and partially ketone bodies ) can’t metabolise FA

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2
Q

what diseases arise from imbalanced glucose in diet

A

hypoglycaemia –> coma + fainting

hyperglycaemia –> irreversible brain damage

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3
Q

what does skeletal muscle metabolise

A

FA, carbs, ketone bodies ( depending on level of ex )

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4
Q

what does heart muscle metabolise

A

FA, Ketone bodies, glucose

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5
Q

what does excess G6P get turned into

A

glycogen by the liver

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6
Q

what does excess acetylCOA get turned into

A

FA –. adipose tissue

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7
Q

when and where is lactate produced

A

anaerbobic respiration
in mucles
from pyruvate

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8
Q

what are the 3 uses of acetyl coA

A

making ketone bodies
going into TCA
making FA/cholesterol

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9
Q

how are AA created

A

from pyruvate / from TCA substrates

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10
Q

how are nucleotides created

A

from pyruvate/TCA substrates –> AA–> nucleotides

from G6P via pentose phosphate pathway

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11
Q

what does the creation of nucleotides via the pentose pathway create

A

NADPH for anabolic reaction

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12
Q

describe the process of gluconeogensis

A

pyruvate ( latctate/AA)pyruvate carboxylase –> oxaloacetate ( AA) -phosphoenolpyruvate carboxylase -> phosphoenolpyruvate –> D3P ( DHAP added from glycerol) –> F16bisP–> F6P( fructose 1,6 bisphosphotase) –>G6P–>glucose ( glucose phosphotase)

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13
Q

how is lactate used in gluconeogensis

A

taken up by liver regenerated into pyruvate via LDH via cori cycle

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14
Q

how do FA provided energy via gluconeogensis

A

FA –> B oxidation

glycerol –> DHAP in gluconeogensis

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15
Q

what 3 reactions catalysed by enzymes are irreversible and must be skipped in glycolysis for gluconeogenesis

A

glucose –> G6P ( hexokinase )
G6P –> F6P phosphofructokinase
phosphoenolpyruvate –> pyruvate ( pyruvate kinase )

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16
Q

what enzymes / pathways do glyconeogenesis use instead

A

pyruvate –> oxaloacetate ( pyruvate decarboxylase)
oxaloacetate–> phosphenolpyruvate ( phosphoenolpyruvate decarboxylase)
F1,6bisP–>F6P ( fructose 1,6 phosphotase)
gG6P–> glucose ( glucose phosphotase)

17
Q

what happens in areobic respiration

A
main aim is to keep ETC going 
increase ATP demand 
increase glucose transport 
increase muscle glycolisis 
increase gluconeogenesis 
FA release
18
Q

what happens in anaerobic respiration

A

want to continue glycolysis and gluconeogenesis
increase latacte prodcution
lactate taken up by liver turned back into puruvate

19
Q

Control of metabolic pathways

A

product inhibition / signalling molecules

20
Q

how does hexokinase differ in the muscle and liver

A

mucel heoxkinase I liver hexokinase IV

hexokinase for opperates most effectvely at high glucose conc + less sensitive to inhibition by G6P

21
Q

what is michaelis constant

A

conc of substance when enzyme vmax

22
Q

what hormones regulate the metabolic pathway

A

insulin
glucagon
adrenalin
glycocorticoids

23
Q

function of insulin

A

increase uptake of glucose into cells

24
Q

function of glucogon

A

increase glucose synthesis

25
function of adrenalin
increases glycogen breakdown + gluconeogenesis | stimulates release of FA from adipose
26
function of glucocorticoids
steriods increases synthesis of enzymes increases glucose availability
27
how are type 1 and type II diabetes different
type 1 B cells fail to secrete insulin | type II cells have insulin resistance
28
what are the implications of diabetes
cell can't take up glucose so think they are starving
29
symptoms of diabetes
hyperglycaemia --> tissue damage hypoglycaemia --> coma acidosis increase ketone bodies cardiovarsular disease