Integration of Cell Metabolism Flashcards

1
Q

what molecules does muscle rely on?

A

carbohydrate and fatty acid oxidation

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2
Q

what can the brain not use as a fuel source?

A

fatty acids BUT can utilise ketone bodies

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3
Q

what is adipose tissue?

A

storage site for triglycerides

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4
Q

what molecules can the heart metabolise?

A

both fatty acids and carbohydrates, also ketone bodies

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5
Q

liver

A

site of many metabolic processes e.g transamination, ketone body formation (during fasting), glycolysis
body’s main carbohydrate store and a source of blood glucose

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6
Q

what if the brain gets too little glucose?

A

=hypoglycaemia which causes faintness and coma

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7
Q

what if the brain gets too much glucose?

A

=hyperglycaemia, can cause irreversible damage

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8
Q

during light contraction, what meets the muscles’ ATP requirements?

A

oxphos

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9
Q

vigorous contraction?

A

O2 becomes limiting factor, glycogen is broken down and lactate formed

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10
Q

can the heart respire anaerobically?

A

no

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11
Q

what can excess glucose-6-phosphate make?

A

glyogen in the liver

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12
Q

how does body avoid hypoglycaemia?

A

-breakdown liver glycogen stores
-release free fatty acids from adipose tissue
-convert acetyl CoA into ketone bodies via liver (the ketone bodies will be used instead of glucose, freeing up glucose for the brain)

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13
Q

gluconeogenesis?

A

basically inverse of glycolysis
generation of glucose from pyruvate

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14
Q

which molecules can enter gluconeogenesis?

A

lactate + some amino acids can form pyruvate
some amino acids can form oxaloacetate
glycerol can enter via DHAP

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15
Q

bypass reactions of gluconeogenesis?

A

some of the reverse reactions are irreversible.
we need to bypass the kinase-driven reactions,
we need 4 additional enzymes to do this

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16
Q

4 extra enzymes of gluconeogenesis?

A

pyruvate carboxylase (pyruvate to oxaloacetate)

phosphoenolpyruvate carboxykinase (oxaloacetate to phosphoenolpyruvate)

fructose-1,6- bisphosphatase ( fructose 1,6 bisp to glucose 6-phosphate)

glucose-6-phosphatase (glucose-6-phosphate to glucose)

17
Q

where do the gluconeogenesis reversal reactions occur?

A

pyruvate carboxylase in the mitochondria, rest are cytosolic

18
Q

how many phosphoanhydride bonds are needed to turn an energetically unfavourable process into an energetically favourable one?

19
Q

deamination of all 20 amino acids gives rise to how many molecules?

20
Q

glycogenic amino acids?

A

their skeletons can generate glucose via gluconeogenesis

21
Q

ketogenic amino acids?

A

carbon skeletons can’t make glucose but can make fatty acids and ketone bodies

22
Q

when fasting what can fatty acids be converted to?

A

ketone bodies

23
Q

when muscle contracts, what happens?

A

increased glucose transporters on muscle cell membranes

24
Q

what does adrenaline do?

A

increases rate of glycolysis in muscle by:
increasing gluconeogenesis by the liver
releasing fatty acids from adipoctyes

25
Q

point of lactate synthesis?

A

replenishes NAD+ levels so glycolysis can continue

26
Q

lactate in gluconeogenesis?

A

can be used to synthesize more glucose in the liver

27
Q

typical blood glucose concentration?

28
Q

isoform of HK in liver and muscle

A

Hk 1 in muscle
Hk 4 in the liver

29
Q

what is Michaelis constant?

A

concentration of substrate at which an enzyme functions at a half maximal rate (half of vMAX)

30
Q

Muscle Hk?

A

high glucose affinity, makes sense as muscle cells are constantly respiring
highly sensitive to G-6-P inhibition (if there’s too much the reaction will slow down)

31
Q

Liver Hk?

A

low glucose affinity so active at high glucose concentrations,
less sensitive to G-6-P inhibition

32
Q

complications of diabetes?