Energy Flashcards

1
Q

What is metabolism?

A

We derive all energy and many macromolecules we need from the food we eat.​ We use this energy to:​
keep warm
establish ion gradients ​
synthesise new molecules ​
perform mechanical work​​
Collectively these processes are termed metabolism

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2
Q

What are the types of metabolic processes?

A

Catabolic processes - the breakdown of complex molecules to release ATP. ATP has a high energy phosphate bond which yields energy when broken.

Anabolic processes - synthesis of new molecules from less complex components

Catabolic processes produce precursors which are used in anabolic processes.​ These complex molecules will be used for processes like growth, repair, movement and new tissue synthesis.

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3
Q

Why is the study of metabolism important?

A

Disease like diabetes, atherosclerosis and gall stones have a metabolic basis​
To understand a disease you need to know how the body normally deals with nutrients ​
Changes in metabolites can aid diagnosis and follow treatment

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4
Q

How much ATP do we use and need?

A

Total energy available from ATP hydrolysis is 65kj/mole​
We use 40Kg/24hour ​at rest and 0.5Kg/minute during exercise.
The body only has 100g of ATP so meet the demands of the body it must re-synthesise ATP from ADP

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5
Q

Describe cofactors central to metabolism

A
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6
Q

What is step one of glycolysis?

A

step 1 is the phosphorylation of glucose to form glucose six phosphate. This needs energy from the hydrolysis of ATP, and this step is irreversible.
This step is regulated by hexokinase.​

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7
Q

Why is G-6-P formed/what is the purpose of the phosphorylation step?

A

G-6-P maintains the glucose gradient, so glucose conc within the cell is kept low compared to the outside.​

The 2nd function of the phosphorylation step is that it traps the glucose within the cell- G-6-P is unable to be transported out of the cell.​

G-6-P also inhibits hexokinase so that unnecessary glucose metabolism doesn’t occur.​

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8
Q

Outline the 2nd step of glycolysis

A

G-6-P is converted to Fructose 6 phosphate which is phosphorylated again to form fructose-1,6-bisphosphate. This is regulated by phosphofructokinase.​

Fructose bisphosphate splits into 2 3C molecules: Dihydroxyacetone phosphate and Glyceraldehyde 3 phosphate which are in eqm (lies toward the glyceraldehyde).​

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9
Q

Outline the 3rd step of glycolysis

A

The glyceraldehyde undergoes a series of reactions to form phosphoenol pyruvate which is then converted to pyruvate.
The pyruvate conversion in step 3 is regulated by pyruvate kinase (in the liver only!!!)

First half of glycolysis consumes 2 ATP’s, second part of glycolysis produces two ATP’s and one NADH molecule but this is x by 2.​
So the overall products are: 2 ATP, 2 NADH and 2 pyruvates​

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10
Q

What regulates glycolysis

A

Enzymes catalysing irreversible reactions= potential regulation sites
Activity of these enzymes can be regulated by: ​
reversible binding of allosteric effectors ​
covalent modification ​
transcription

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11
Q

How and why do muscle cells regulate glycolysis?

A

Important for muscle to protect from excessive lactate production during anaerobic respiration.
Glycolysis is inhibited by low pH as low pH kills muscle cells
High ATP concs inhibit PFK enzyme​ by lowering the affinity of ​Fructose 6 phosphate for it.
Inhibition of PFK also leads to inhibition of hexokinase

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12
Q

How is regulation of glycolysis different in the liver?

A

Hexokinase is inhibited by G6P. But the liver also has glucokinase which is not inhibited by G6P.
This means glycolysis regulation in liver cells is different compared to other non hepatic.​

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13
Q

Draw a diagram to describe the metabolism of galactose and fructose.

A
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14
Q

How does glycolysis differ in hard exercising muscles?

A

Normally the pyruvate formed in glycolysis is converted to acetyl CoA and will undergo oxidative phosphorylation in the mitochondria. ​
In exercising muscle, ATP demand exceeds the capacity of the of the mitochondria. So, pyruvate is converted to lactic acid which leads to NAD+ generation.
This NAD+ produced is used to generate more NADH in step 1, allowing glycolysis to continue.
Unlike oxidative phosphorylation this doesn’t need 02 but lactate buildup leads to pain and fatigue.

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15
Q

How do tumours grow to rely on anaerobic respiration?

A

As tumour size increases, so does need for blood supply.​
The tumour produces angiogenic factors which stimulate the endothelial cells of a nearby vessel to proliferate and migrate to form a vascular network.​

But, the rate at which a tumour grows often out strips the ability of these newly formed vessels to deliver sufficient 02 to it.​ Cells w/in this this mass are in a hypoxic state.
Low 02 stimulates HIF-1 alpha. HIF-1α stimulates expression of glycolytic enzymes. Tumour cell metabolism reverts to glycolysis

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16
Q

Describe the TCA cycle

A

Takes place in the mitochondrial matrix​
​In the presence of 02, pyruvate is converted to acetyl CoA (2C) and enters the citric acid cycle​

Acetyl CoA reacts w Oxaloacetic acid (4C) to form citrate (6C)​
​Citrate undergoes a series of reactions resulting in the loss of 2CO2 ​

3 NADH and 1 FADH2 molecules are formed per cycle​. 1 GTP molecule is formed​. ATP is not produced

17
Q

Draw the TCA cycle

A
18
Q

What regulates entry into the TCA cycle?

A

Pyruvate dehydrogenase converts pyruvate-> acetylcoA. It’s inhibited by NADH, ATP and Acetyl CoA​
Acetyl CoA formation from pyruvate is irreversible ​

Also, PD phosphatase converts PD into the active form.
PD Kinase converts PD into the inactive form.

19
Q

What stimulates PD phosphatase?

A

In muscle PD phosphatase is stimulated by Ca2+​

​In liver adrenalin increases Ca2+ by activation of alpha adrenergic receptors and IP3​

In liver and adipose tissue, insulin (which signifies the fed state) stimulates PD phosphatase

20
Q

Which other enzymeps regulate the TCA cycle?

A

PD is inhibited by NADH, ATP and Acetyl CoA​. It is stimulated by ADP and pyruvate

Citrate synthase is inhibited by citrate
Isocitrate ​dehydrogenase​ is inhibited by ATP and NADH, but is stimulated by ADP

α-Keto glutarate ​dehydrogenase is inhibited by NADH, ATP, Succinyl CoA

21
Q

Describe the ETC and oxidative phosphorylation

A

H atoms are removed from NADH + FADH2​ (oxidation)
​H atoms enter the ETC and each is split to give an electron and a proton ​
​The e- passes through a series of cytochrome enzymes which releases energy. This energy moves H+ ions from the mitochondrial matrix into the intermembrane space, creating a steep electrochem gradient.
H+ diffuse down this gradient via protein channels joined to ATP synthase. H+ ions change the enzyme a.s, allowing ADP and phosphate ions to bind. ADP is phosphorylated to ATP, catalysed by ATPsynthase

W/in the matrix, H+ and e-s recombine to form H2. These combine w 02 to form 2H20. 02= final e acceptor

22
Q

What is the difference between brown and white fat?

A

Brown fat contains many mitochondria and is used to generate heat as new born babies haven’t yet developed the shivering reflex.​

The mitochondria in brown fat in brown expresses a UCP-1 protein. This diverts the flow of protons away from ATP generation and instead to heat generation