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Metabolism > Extremes of metabolism > Flashcards

Extremes of metabolism Flashcards

1
Q

Name the two types of muscle fibers

A

Type 1- slow twitch

Type 2- Fast twitch

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2
Q

Describe the properties of slow twitch muscle fibers

A

Short term energy supply- Oxidative metabolism from glucose

Long term energy supply- Fatty acids

Rich in mitochondria

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3
Q

Describe the properties of fast twitch muscle fibers

A

Short term- anerobic metabolism- (glycolysis to lactate)
Main fuel glycogen

Long term- Main fuel blood is glucose

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4
Q

What are the subtypes of fast twitch muscles? What is the difference between the two?

A

2 subtypes
A- contains myoglobin (aerobic)
B- anaerobic

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5
Q

Can the properties of the muscles fibers change? If so how?

A

Yes, depending on the type of exercise/ training

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6
Q

During exercise where do you muscles seek energy?

A

Blood glucose
Glycogen
Fatty acids
Phosphocreatine

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7
Q

What is the use of AMP during exercise?

A

It increases during exercise

This stimulates increased glucose uptake short term and fatty acid oxidation long term

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8
Q

How does calcium cause increased muscle contraction?

A 
Phosphorylase kinase (CAMKinase) a is activated by a calcium subunit calmodulin. 
Phosphorylase kinase then breaks down glycogen to produce glucose

More calcium= more muscle contraction

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9
Q

What is the name of the calcium sub unit responsible for muscle contractions

A

Calmodulin

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10
Q

What is the purpose of pyruvate dehydrogenase complex?

A

Controls the entry to the TCA cycle

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11
Q

How is pyruvate dehydrogenase complex regulated?

A

It is controlled by the phosphorylation of PDH kinase in response ATP and NADH levels.
PDH phosphotase is activated by calcium. It reverses the effects of PDH kinase on PDC (keeping it active).
PDC is allosterically activated by low NADH and ATP and high ADP and NAD concentrations

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12
Q

Which enzymes in the TCA cycle are controlled by calcium? What else controls these enzymes?

A

Isocitrate dehydrogenase and
alpha-ketoglutarate dehydrogenase

NAD levels also controls the enzymes

Maintaining high ATP production

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13
Q

How does AMP regulate metabolic activity during exercise

A

During excerise ATP is low and AMP increases.
AMP allosterically activates glycogen phosphorylase (when not phosphorylated)
This promotes glycogen break down providing more fuel.

It in general allosterically activates enzymes (PFK-1) at the start of glycolysis and glycogenolysis.

Increase GLUT4 membrane channels so more glucose uptake

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14
Q

What is the structure of AMP kinase?

Which part of the structure senses energy status?

A

3 subunits- alpha, beta, gamma
2 regulatory
1 catalytic
Gamma subunit

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15
Q

How is AMP kinase controlled?

A

Phosphorylation on the Thr172 on alpha subunit

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16
Q

Name one effect of AMP Kinase. Which other molecule does the same thing?

A

Promotes movement of GLUT4 to the membrane of muscle cells

Insulin does the same

17
Q

What is the difference between phosphofructokinase1 and phosphofructokinase2

A

1- tissues

2- heart

18
Q

How is phosphofructokinase1 regulated?

A

Allosterically inhibited by high levels of ATP

Activated by ADP and AMP

19
Q

How is phosphofructokinase2 regulated?

A

Firstly it produces F-2,6-BP from F6P. This is allosterically activated by PFK1 and controlled by phosphorylation using AMP kinase

20
Q

Which molecule mediates the transition from glucose to fatty acid metabolism during prolonged exercise? How does it do this?

A

AMP kinase mediates this transition.

It phosphorylates acetyle-CoA carboxylase
making it inactive. This stops the production of malonyl coA which inhibits carnintine shuttle

This activates the carnintine shuttle which transports fatty acids into the mitochondria for break down to make ATP

21
Q

During long periods of exercise what happens to the PH and what effect does this have on other metabolic processes?

A

Production of lactic acid decreases PH. This inhibits glycolysis and oxidative phosphorylation

22
Q

What happens when you run out of energy?

A

1st: run out of phosphocreatine
2nd: run out of glycogen (700g of glycogen need for a marathon; body only has 500g in storage – 400g in muscle + 100g in liver)
3rd: Over-reliance on FA metabolism for energy: lipolysis has a max energy output of 60% so might not meet the energy needs
FA oxidation is slower, requires more oxygen than glycolysis and TCA
4th: lactic acid build up decreases the pH in muscles and slows glycolysis and oxidative phosphorylation

23
Q

What happens to mitochondria as you age? What else decreases your levels of mitochondria?

A

It decreases with age

It decreases with inactivity

24
Q

What are the steps of metabolic changes during starvation?

A
  1. Glucose levels fall; insulin goes down, glucagon goes up
  2. Glycogen break down begins and can sustain body for about 30 hours
  3. Switch to FA break down which can sustain body for 2-3 days
  4. After 2 days gluconeogenesis and production of ketone bodies becomes only source of glucose & energy.
  5. Last resort for glucose is breakdown of protein (muscle) to release amino acids for gluconeogenesis
25
Q

How is alcohol metabolised?

A

in liver- 3 ways

Most common- methanol—-> acetaldehyde (toxic) using alcohol-dehydrogenase

26
Q

What causes hangovers?

A

Acetaldehyde produced from methanol

27
Q

Which drug is used to treat alcoholics? How does it work?

A

Disulrifam (anatabuse)

ALDH2 activity

28
Q

Which ethnic groups is predisposed to having hang overs? Why is this?

A

People of Asian

- deficiency of acetaldehyde dehydrogenase (ALDH2) enzyme due to the rs671 polymorphism is 30-50% of pop.

29
Q

What are the biochemical effects of alcohol?

A
  1. High NADH and acetyl coA
  2. Inhibit GAPDH and pyruvate dehydrogenase enzymes (TCA cycle)
  3. Inhibit malate dehydrogenase (gluconeogenesis)
  4. Inhibit lactate dehydrogenase (increases lactic acid)
30
Q

Describe the key features in immune cell metabolism

A
  1. They have an increased requirement for NADPH
    Produced by the transport of glucose from glycolysis to the pentose phosphate pathway. This occurs in macrophages, neutraphils and activated dendritic cells.
31
Q

What do immune cells use NADPH for?

A

As a reducing agent (NADPH oxidase)
To generate ROS.
Oxygen is reduced to free radicals and peroxide

32
Q

What is respiratory burst?

A

When peroxide is used to kill engulfed pathogens

33
Q

What is Chronic Granulomatous Disease

A

When ROS can not be produced in immune cells?

34
Q

Name the intermediates from immune cell metabolism which are used in other pathways?

A

G6P—->pentose phosphate pathway
Succinly coA—->Heme—->ROS
Glutamate——>TCA—–>oxaloacetete

35
Q

Which cells are energy selfish and what does this mean?

A

Immune cells and brain cells

Take priority over other tissues regarding energy supply

36
Q

What is the WARBURG EFFECT/HYPOTHESIS and it implication in cancer metabolism?

A

Cancer cells take up much more glucose than normal cells ( basis of PET scan)
Glucose tends to be used for aerobic glycolysis rather than oxidative phosphorylation, which means cancer cells prefer generating ATP through glycolysis than through oxidative phosphorylation (TCA cycle) even in the presence of oxygen.
Leads to build up of lactic acid in cancer cells

37
Q

What are the consequences of the Warburg effect

A

Cancer metabolism takes away intermediates from the TCA cycle. These have to be replaced or the cycle is left incomplete

Because cancer only uses glycolysis it uses a lot of glucose to obtain energy

Metabolism (9 decks)

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