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metabolism > extremes of metabolism > Flashcards

extremes of metabolism Flashcards

1
Q

what are the two types of muscle fibres?

A

type 1 slow twitch

type 2 fast twitch

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2
Q

how to type 1 muscle fibres make energy?

A

oxidative metabolism from glucose

fatty acids in the longer term

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3
Q

what is an adaptation of type 1 slow twitch muscles?

A

lots of mitochondria

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4
Q

how do type 2 muscle fibres make energy?

A

glycolysis to make lactate

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5
Q

what is the main fuel of type 2 muscle fibres?

A

glycogen

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6
Q

what are the subtypes of type 2 muscle fibres?

A

A - contain myoglobin - aeorbic

B - anaerobic

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7
Q

what causes the balance of the type 2 muscle fibre subtypes to change?

A

levels of exercise

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8
Q

how much can ATP demand increase in exercise in skeletal muscle?

A

100x

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9
Q

what energy sources are used in exercise and in what order?

A

phosphocreatine –> muscle glycogen –> blood glucose/fatty acids

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10
Q

how do the levels of ATP, ADP and AMP change with the intensity of exercise?

A

as intensity increase
ATP decreases
ADP and AMP increase

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11
Q

what does AMP signal for during exercise?

A

increases glucose uptake in the short term and FA oxidation in the long term

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12
Q

what vitamin is needed for muscle contraction?

A

calcium

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13
Q

what activates phosphorylase kinase?

A

calcium bound to calmodulin

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14
Q

what does Pyruvate dehydrogenase complex do?

A

controls entry to TCA

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15
Q

what enzymes control pyruvate dehydrogenase complex and what effect do they have on it?

A

PDH kinase - inactivates PDC by phosphorylation in response to low NADH and ATP

PDH phosphatase - activates PDC in response to calcium

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16
Q

what enzymes are allosterically controlled by calcium?

A

alpha-ketoglutarate dehydrogenase

isocitrate dehydrogenase

17
Q

how does AMP promote glycogen breakdown?

A

activates enzymes such as glycogen phosphorylase (when its not phosphorylated) and
phosphofructokinase-1

increases number of GLUT4 channels

18
Q

what allosterically inhibits phosphofructokinase?

A

high levels of ATP

19
Q

explain the mechanism in the heart to activate PFK1

A

PFK2 produces F-2,6-BP which is an allosteric activator of PFK1 - controlled by phosphorylation via AMP kinase

20
Q

explain the structure of AMP dependent protein kinase

A

heterotrimeric

3 subunits - 2 regulatory and 1 catalytic

21
Q

what is the function of AMPK?

A

sensor for energy status
Detects levels of AMP – when AMP is high, AMPK is activated –> increases no. of GLUT4

activating the carnitine shuttle

22
Q

how does AMPK sense AMP levels?

A

specific domain on its gamma subunit

23
Q

what controls AMPK?

A

phosphorylation on the Thr172 of the alpha subunit –> not dependent on AMP

24
Q

how does AMPK activate the carnitine shuttle?

A

phosphorylates Acetyl-CoA carboxylase
stops acetyl-CoA from building up
malonyl-CoA is therefore made
inhibits CPT-1 which activates the carnitine shuttle

25
Q

what happens to muscles in muscle fatigue?

A

running out of glycogen
depletion of phosphocreatine
excessive conversion of glycogen to glucose to lactic acid –> decreases pH and inhibits glycolysis
inefficient mitochondria

26
Q

how does exercise affect the density of mitochondria

A

increases the density

27
Q

what is ethanol metabolised to in the body?

A

acetyl-CoA

28
Q

what are the 3 stages of alcohol metabolism in the body?

A

ethanol –> acetylaldehyde
Acetylaldehyde + NAD+ –> Acetate + NADH
ATP + Acetate + CoA –> AMP + PPi + Acetyl-CoA

29
Q

in what ways can ethanol be converted to acetylaldehyde?

A

alcohol dehydrogenase - makes NADH
catalase - makes water
microsomal ethanol oxidising system - makes NADP and water

30
Q

what is the function of Antabuse and how does it work?

A

inhibits acetaldehyde dehydrogenase so you get more acetylaldehyde. Makes you feel sick sooner when you start drinking –> stops you from drinking alcohol.

31
Q

what is another name for Antabuse?

A

disulfiram

32
Q

what are the biochemical effects of alcohol on the body?

A

High levels of Acetyl-CoA = excess FA synthesis and excess ketone bodies

high levels of NADH = inhibition of the TCA cycle. =more pyruvate is converted to lactate as NAD+ needs to be regenerated –> lactic acidosis

33
Q

why does the immune system have a variable energy demand?

A

needed to produce ROS to kill microbes
energy to make antibodies
energy is required in phagocytosis

34
Q

why does the immune system require NADPH?

A

to make ROS

35
Q

how is NADPH needed by the immune system made?

A

from the pentose phosphate pathway

converting malate to pyruvate in the cytoplasm

36
Q

what is the Warburg effect?

A

regardless of how much O2, cancer cells have major up regulation of glycolysis (due to mutations of Hif protein)

37
Q

why do cancer cells have increased use of amino acids?

A

to feed into the TCA cycle to increase energy production

metabolism (23 decks)

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