Lipids Flashcards

1
Q

Name the three classes of lipids.

A

Fatty acid derivatives
Hydroxy-methyl-glutaric acid derivatives
Vitamins

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2
Q

How are triacylglycerides formed?

A

They are formed from a glycerol backbone and three fatty acid molecules. They are a product of esterification reactions.

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3
Q

Give properties of TAG and state where in the body it can be found.

A

TAG is a hydrophobic molecule which is stored in its anhydrous form in adipose tissue.

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4
Q

What are the products of TAG breakdown and where are they metabolised?

A

Glycerol –> Liver. Metabolised by glycolysis.

Fatty Acids –> Adipose / Target Tissues. Fatty Acid oxidation releases energy.

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5
Q

What enzyme in the small intestine catalyses breakdown of TAG?

A

Pancreatic lipase.

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6
Q

What are the two tissues/ cells where Fatty acid oxidation cannot be used to release energy?

A

Red Blood Cells (these have no mitochondria) and the brain (cannot pass the blood-brain barrier)

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7
Q

Name two hormones which can activate fat mobilisation.

A

Adrenaline and Glucagon.

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8
Q

Explain why when there is low Extracellular glucose, FA are oxidised.

A

When glucose is low, there is less substrate for TAG synthesis (glycerol-1-phosphate) being produced from glycolysis, so this leads to an accumulation of FA in the tissues. These are oxidised to release energy.

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9
Q

Why are some fatty acids essential?

A

Fatty acids with a double bond after C9 cannot be synthesised by the body and therefore they must be sourced from the diet.

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10
Q

Where does activation of fatty acids occur and what is the enzyme responsible for this?

A

Activation occurs in the cytoplasm.

Fatty acyl coA synthase.

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11
Q

What transporter protein is used to transport activated fatty acids into the mitochondria for B oxidation?

A

Carnitine shuttle

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12
Q

Name the substance which inhibits the Carnitine shuttle to prevent breakdown of newly synthesised FA.

A

Malonyl~coA

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13
Q

When a Cn fatty acid enters B oxidation, what is the product?

A

A C(n-2) molecule and also a C2 which is acetyl~coA and enters the TCA cycle.

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14
Q

What is the enzyme which converts glycerol from TAG breakdown into glycerol phosphate?

A

Glycerol kinase.

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15
Q

Acetyl~coA is a useful intermediate for anabolism and catabolism. What anabolic processes is it a precursor for?

A

Hydroxymethylglutaric acid derivatives including Ketone Bodies and Cholestrol.
Fatty Acids

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16
Q

Name three ketone bodies

A

Acetoacetate, acetone and B hydroxybuturate.

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17
Q

How do statin drugs lower Cholestrol?

A

Statin drugs lower Cholestrol formation by inhibiting HMG~coA reductase which is a step in the metabolic pathway for Cholestrol synthesis.

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18
Q

How is production of ketone bodies regulated?

A

Ketone body production is regulated because the starting molecule is acetyl~coA which is diverted from the TCA cycle. When NADH is high this leads to product inhibition, and so acetyl~coA is diverted to alternative pathways.

19
Q

What is the name of the enzyme which catalyses the reaction from HMG~coA to acetoacetate?

A

Lyase. This is inhibited when Insulin to Glucagon ratio is high as HMG~coA is used for Cholestrol synthesis. When this ratio is low, lyase is activated and ketone bodies form.

20
Q

How does muscle protein breakdown provide glucose for the brain?

A

Protein - amino acids, Pyruvate, gluconeogenesis glucose

21
Q

In prolonged starvation what fuel molecules do muscles use and why?

A

Fatty acids and ketone bodies. The prevent usage of glucose which is reserved for the brain.

22
Q

What is a common condition seen in starvation and also in type one diabetes?

A

Ketoacidosis. This occurs because acetoacetate and B hydroxybuturate are both relatively strong acids. Ketouria will also be seen because ketone bodies are above the renal threshold.

23
Q

What happens during fatty acid oxidation if the carbon chain has an odd number of carbons?

A

In this case, the cycle continues until 3 carbons remain. Carboxylase catalyses carboxylation and the production of methylmalonyl~coA which is then rearrange to succinyl~coA, a Kreb cycle intermediate.

24
Q

When glucose is low, Pyruvate dehydrogenase is inhibited. How does this help to maintain glucose?

A

Inhibition of Pyruvate dehydrogenase slows acetyl~coA synthesis, and therefore acetyl~coA –> citrate which I inhibits phosphofructokinase. This leads to a build up of Glucose 6 phosphate which acts as product inhibition on hexokinase and so maintains glucose concentration.

25
Q

What is glycogen?

A

Glycogen is a glucose store which is used between meals to maintain glucose plasma concentration.

26
Q

What is the advantage of the branched structure of glycogen?

A

It means it can be broken down quickly when required for utilisation.

27
Q

What is the action of phosphoglycomutase and in which pathway can this be seen?

A

It converts glucose 6 phosphate to glucose 1 phosphate which can then be utilised to make glycogen in glycogenesis.

28
Q

Name the two enzymes responsible for adding UDP-glucose to Glycogen.

A

Glycogen synthase - (a1-4) bonds

Branching enzyme - (a1-6) bonds

29
Q

When glycogen is broken down, what does it initially form? What enzymes assist in this process?

A

It forms glucose 1 phosphate. Debranching enzyme and glycogen phosphotase are the two enzymes responsible for this breakdown.

30
Q

What is the difference between glycogen breakdown in the muscles compared to the liver?

A

In the muscles, it is converted to glucose 6 phosphate and this enters glycolysis. In the liver the enzyme glucose 6 phosphatase acts on glucose 6 phosphate and converts it back to glucose. This enzyme is not present in muscle.

31
Q

How is glycogenolysis and glycogenesis regulated?

A

The rate limiting enzymes are glycogen synthase and glycogen phosphorylase.
Glucagon phosphorylates both of these which inhibits synthase and activates phosphorylase. Insulin has the opposite action.

32
Q

In muscle stores, glucagon has no effect. In this case what is the activator of glycogen phosphorylase?

A

AMP which is a low energy signal.

33
Q

Are lipids soluble or insoluble?

A

Lipids are insoluble molecules made from C, H and O.

34
Q

Why do glycogen storage diseases arise and what are the consequences?

A

They occur due to deficiency or dysfunction of enzymes in glycogen metabolism. Excessive storage leads to tissue damage, whilst low glycogen stores lead to exercise intolerance and hypoglycaemia.

35
Q

Where does gluconeogenesis occur?

A

It occurs in the liver and in the kidney cortex.

36
Q

What are precursors for gluconeogenesis?

A

Lactate from anaerobic glycolysis, glycerol from TAG breakdown and amino acids (mainly alanine).

37
Q

Step 10 of glycolysis is irreversible

PEP – Pyruvate. What is the reverse of this in gluconeogenesis?

A

Pyruvate is converted to oxaloacetate by Pyruvate carboxylase. This is then converted to PEP by PEPCK.

38
Q

Describe how the action of PEPCK is regulated.

A

With increase Glucagon/ cortisol there is increased PEPCK and so this reaction is stimulated. With increased insulin, amount decreases and so does reaction rate.

39
Q

What is the action of fructose1,6, bisphosphotase? How is it regulated with glucagon/ insulin?

A

This converts fructose 1,6 bis phosphate into fructose 6 phosphate. Glucagon stimulates and increases activity. Insulin inhibits.

40
Q

Define Hyperplasia

A

Increase in the number of cells.

41
Q

Define hypertrophy

A

Increase in cell size.

42
Q

What is lipogenesis?

A

Fatty acid synthesis. Dietary glucose is used as a source of carbon.

43
Q

What enzyme is involved in lipogenesis?

A

Fatty acid synthase. It builds them by sequential addition of 2 carbon units provided by malonyl~coA.

44
Q

What enzyme catalyses the reaction of acetyl~coA to malonyl~coA? How is it regulated?

A

Acetyl~coA carboxylase.
It is activated by increased insulin or citrate
It is inhibited by glucagon/adrenaline or AMP