Energy Flashcards

1
Q

Give 4 processes for which energy is required?

A

Synthesis of new molecules
Establishing ion gradients
Mechanical work
Keeping warm

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2
Q

What is catabolism?

A

The breakdown of complex molecules to release energy or carry out mechanical work

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3
Q

What is anabolism?

A

The synthesis of new molecules from less complex components

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4
Q

What are catabolic processes important for in the body?

A

Catabolic processes degrade components of our diet such as carbohydrates and fats and generate heat, CO2 and the precursors for anabolic processes

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5
Q

What are anabolic processes involved in in the body?

A

Growth, movement and repair

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6
Q

What are the 4 major oxidative pathways?

A

Glycolysis
Citric acid cycle
Electron transport coupled to oxidative phosphorylation
Fatty acid oxidation

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7
Q

What is the simplest description of glycolysis?

A

The conversion of glucose (6C) to pyruvate (3C)

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8
Q

How is glycolysis regulated?

A

By enzymes catalysing irreversible reactions. The enzyme activity can be regulated by reversible binding of allosteric factors, covalent modification and transcription

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9
Q

What’s the most important control point in glycolysis?

A

Phosphofructokinase (PFK).
High concentrations of ATP inhibit PFK by lowering the affinity for fructose-6-phosphate. PFK is also inhibited by low pH. Inhibition of PFK leads to inhibition of hexokinase

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10
Q

What regulates hexoinase?

A

G6P concentration

As G6P accumulates in a cell, hexokinase activity decreases

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11
Q

What regulates PFK?

A

ATP, citrate and H+.

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12
Q

How does ATP regulate PFK activity?

A

High ATP content in a cell down regulates PFK activity. This is an allosteric regulation

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13
Q

How does AMP regulate PFK?

A

AMP positively regulates PFK activity

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14
Q

What’s the function of PFK?

A

PFK catalyses the formation of fructose-1,6-bisphosphate and ADP from fructose-6-phosphate and ATP

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15
Q

What’s the function of hexokinase?

A

Hexokinase phosphorylates glucose to glucose-6-phosphate

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16
Q

How can galactose be used in glycolysis?

A

Galactose can be converted to glucose-6-phosphate in 4 steps. First, galactokinase converts galactose to galactose-1-phosphate. Galactose-1-phosphate then acquires a uridyl group from uridine diphosphate glucose in a reaction catalysed by galactose-1-phosphate uridyl transferase, to form UDP-galactose and glucose-1-phosphate. UDP-glucose is then reformed from UDP-galactose via UDP-galactose 4-epimerase. Glucose-1-phosphate is then isomerised to glucose-6-phosphate by phosphoglucomutase

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17
Q

How can fructose be used in glycolysis?

A

Fructose can be phosphorylated to fructose-6-phosphate by fructokinase, to then be phosphorylated to fructose-1,6,-bisphosphate and eventually form pyruvate.

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18
Q

Why is AMP a better indicator of energy state than ADP?

A

ATP can be made from ADP by adenylate kinase. 2ADP gives ATP + AMP, so production of ATP from ADP will also produce AMP, making AMP a signal for low energy state

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19
Q

Why will glycolysis have to stop after extended periods of exercise?

A

A muscle cell’s NAD stores will get depleted

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20
Q

How do muscle cells get around depleted NAD stores?

A

Muscle cells produce lactate from the pyruvate formed in glycolysis

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21
Q

What’s the problem with lactate production as a solution to depletion of NAD stores?

A

Lactate is acidic and inhibits glycolysis at the level of phosphofructokinase.

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22
Q

How is the problem of lactate acidity overcome?

A

There’s a cycle where lactate is secreted into circulation and transported back to the liver to allow the metabolism in skeletal muscle to continue. Pyruvate can also be converted to acetyl CoA

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23
Q

How does the liver regulate PFK?

A

PFK is regulated by ATP in the same way as in muscle. Low pH isn’t a problem as the liver doesn’t normally produce lactate.

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24
Q

What inhibits glycolysis in the liver?

A

Citrate. High levels of citrate indicate the precursors of biosynthesis are abundant

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25
Q

What inhibits PFK in the liver?

A

Citrate

26
Q

What inhibits hexokinase in the liver?

A

G6P

27
Q

What enzyme does the liver have that’s not inhibited by G6P?

A

Glucokinase

28
Q

What does low oxygen stimulate the expression of?

A

Many glycolytic enzymes

29
Q

What happens when tumours outgrow their blood supply?

A

Oxygen delivery is reduced, so tumour cell metabolism reverts to glycolysis. A reduction of O2 leads the activation of the transcription factor HIF-1a, which regulates the expression of a number enzymes in the glycolytic pathway

30
Q

Give 4 properties of aerobic respiration

A

Only occurs in the presence of oxygen
Yields more energy in the form of ATP than anaerobic respiration
Requires the citric acid cycle and oxidative phosphorylation
Takes place in mitochondria

31
Q

Where does Krebs cycle take place?

A

The mitochondrial matrix

32
Q

What does Krebs cycle provide?

A

Most of the electrons for mitochondrial oxidative phosphorylation

33
Q

What enters the citric acid cycle?

A

Acetyl CoA (2C) derived from pyruvate (3C)

34
Q

What does acetyl CoA react with in the Krebs cycle?

A

Acetyl CoA reacts with oxaloacetate (4C) to form citrate (6C)

35
Q

What happens to citrate in the Krebs cycle?

A

Citrate undergoes a series of reactions resulting in decarboxylation and the release of 2CO2

36
Q

How many co-enzymes are made in a full Krebs cycle?

A

3 molecules of NADH and 1 FADH2 are formed

37
Q

What energy is released from a Krebs cycle?

A

1 GTP or ATP

38
Q

What is the aim of the Krebs cycle?

A

Oxidation to produce NADH and FADH2, which become substrates for the ETC

39
Q

What regulates entry into the Krebs cycle?

A

NADH and acetyl CoA, which inhibit the cycle

40
Q

What does build-up of NADH and acetyl CoA inform the enzyme?

A

Energy needs are being met or fatty acids are being broken down to produce NADH and acetyl CoA. This has the effect of sparing glucose

41
Q

What stimulates pyruvate dehydrogenase in muscle tissue?

A

Ca2+

42
Q

What enzyme catalyses formation of acetyl CoA from pyruvate?

A

Pyruvate dehydrogenase

43
Q

What does conversion of pyruvate to acetyl CoA commit the glucose carbon skeleton to and why?

A

The reaction is irreversible, so the glucose carbon skeleton is committed to either oxidation to CO2 and energy production, or fatty acid synthesis

44
Q

What increases Ca2+ concentration in the liver?

A

Adrenaline activates alpha-adrenergic receptors and IP3

45
Q

What does insulin stimulate in liver and adipose tissue?

A

Insulin stimulates phosphatase, which funnels glucose to fatty acid synthesis

46
Q

What does inhibition of isocitrate dehydrogenase and ketoglutarate dehydrogenase lead to?

A

Build-up of citrate, which is transported out of the mitochondria and inhibits PFK, stopping glycolysis. It also acts as a source of acetyl CoA for FA synthesis

47
Q

What is the condition ‘beriberi’?

A

A deficiency in thiamine (vitamin B1), characterised by cardiac and neurological symptoms.

48
Q

What is thiamine a prosthetic group for?

A

Thiamine is a prosthetic group for pyruvate and alpha-ketoglutarate dehydrogenase

49
Q

What’s the difference between wet beriberi and dry beriberi?

A

Wet beriberi affects the heart and circulatory system. Dry beriberi damages nerves and can lead to decreased muscle strength

50
Q

In who does beriberi mainly occur?

A

People with alcohol-use disorder and in countries where rice is a staple food

51
Q

What are some symptoms of wet beriberi?

A

Shortness of breath during physical activity, waking up short of breath, tachycardia and swollen lower legs

52
Q

What are some symptoms of dry beriberi?

A

Decreased muscle function, especially in the lower legs, pain, mental confusion, tingling or loss of sensation in the hands and feet, difficulty speaking, vomiting and involuntary eye movement

53
Q

How many protons are needed to generate 1 ATP and why?

A

4 protons

1 proton is consumed to transport ATP out of the matrix and 3 are needed to make ATP

54
Q

For every NADH, how many H+ are pumped out of the mitochondrial matrix?

A

10H+

55
Q

How many protons are pumped out of the mitochondrial matrix for every FADH2?

A

6H+

56
Q

What does the ETC do?

A

The ETC involves the removal of hydrogen atoms from oxidisable substrates, notably NADH and FADH2

57
Q

What happens to hydrogen atoms that enter the ETC?

A

They are split to give an electron and a proton

58
Q

What happens to the electron from a hydrogen atom in the ETC?

A

The electron passes through a series of enzymes called cytochromes and finally reacts with molecular oxygen

59
Q

What happens to the H+ from the hydrogen atom in the ETC?

A

The H+ is pumped across the IMM, forming a pH gradient transmembrane potential (proton motive force)

60
Q

What are OXPHOS diseases?

A

Common diseases caused by mutations in genes coding for proteins of the ETC. Symptoms include fatigue, epilepsy and dementia. Symptoms may be evident near birth or may become apparent in early adulthood, depending on the mutation. A metabolic consequence can be congenital lactic acidosis