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POM Y1 Imperial > Cell metabolism II > Flashcards

Cell metabolism II Flashcards

1
Q

What are some examples of lipids?

A

Free fatty acids, triacylglycerols, phospholipids, glycolipids and steroids

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2
Q

What is the structure of triacylglycerols?

A

Consists of a molecule of glycerol chemically bonded through a condensation reaction forming ester bonds to 3 fatty acids
Occurs between hydroxyl group of glycerol, and the carboxyl group of the fatty acids.

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3
Q

What are the properties of triglycerides?

A

Long hydrocarbon tails are hydrophobic, insoluble in water

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4
Q

What are saturated lipids?

A

Saturated lipids have single carbon bonds, this means that they have reached the maximum amount of hydrogen bonds. Each carbon atom is bonded to the adjacent one with a single covalent bond.

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5
Q

What are the properties of saturated lipids?

A

Saturated lipids have higher melting points ,being solid at room temperature.

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6
Q

What are unsaturated lipids?

A

Unsaturated lipids have double carbon bonds, meaning that they have the ability to bond to more hydrogen atoms, through a hydrogenation reaction.

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7
Q

What is the biological significance of triglycerides?

A 
Energy storage molecules
Waterproofing
Thermal insulation 
Protection of internal organs
Source of metabolic water
Buoyancy
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8
Q

Why are triglycerides good energy storage molecules?

A

Hydrocarbon tail of fatty acids contain a lot of chemical energy, thus a lot of energy is released when oxidised during cellular respiration
store twice as much energy per gram

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9
Q

Why are triglycerides good for waterproofing?

A

Hydrophobic nature of lipids reduces water loss through evaporation

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10
Q

Why are triglycerides good insulators?

A

Thick layer reduces SA:V ratio, reducing heat loss. Stored within adipose tissue

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11
Q

What is the product of B-oxidation?

A

Acetyl-CoA molecules

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12
Q

Where does b-oxidation occur?

A

Mitochondria

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13
Q

What are the sources of fats?

A

The diet, de novo biosynthesis, and storage deposits in adipose

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14
Q

What is de novo synthesis?

A

Synthesis of complex molecules from simple molecules.

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15
Q

What are bile salts?

A

Salts generated by the liver and stored within the gallbladder. Secreted from the bile duct into the intestine emulsifying fats to increase surface area, assisting digestion

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16
Q

What vitamins does bile salts assist in the absorption of?

A

Vitamin A,D,E & K

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17
Q

What results from a bile salt deficiency?

A

Fat passing through the gut undigested and unabsorbed resulting in steatorrhea

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18
Q

Describe the mechanism of action of Orlistat?

A

Potent inhibitor of gastric and pancreatic lipase, behaves as a competitive inhibitor of lipase.
Prevents lipids and reduces fat absorption

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19
Q

What are the benefits or orlistat?

A

Can be used to treat obesity

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20
Q

What are lipoproteins?

A

Lipids are transported in the plasma by lipoproteins.

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21
Q

What is the role of chylomicrons?

A

Dietary fat transport

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22
Q

What is the role of VLDLs?

A

Endogenous fat transport

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23
Q

What is the role of IDLs?

A

LDL precursor

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24
Q

What is the source of VLDLs?

A

Liver

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25
Q

What is the role of LDLs?

A

Transport of cholesterol

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26
Q

What is the role of HDLs?

A

Reverse cholesterol transport

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27
Q

What cells lining the brush border of the small intestine absorb dietary fat?

A

Enterocytes

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28
Q

What are stored within chylomicrons?

A

Triglycerides

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29
Q

What do high-density lipoproteins donate to chylomicrons?

A

Apoproteins

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30
Q

What is the fate of chylomicrons?

A

Lipoprotein lipases located on endothelial cells enzymatically hydrolyse the triglycerides into fatty acids and glycerol, these enter into adipocytes.

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31
Q

What occurs within adipocytes to fatty acids and glycerol?

A

Formed into triglycerides and stored within adipocytes
beta oxidation
Hormone sensitive lipase regulates the storage of triglycerides within adipocytes

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32
Q

How are fatty acids transported within the blood?

A

As albumin

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33
Q

Describe the life cycle of chylomicrons?

A

Nascent chylomicrons with triglycerides –> HDL transfers apoproteins –> Chylomicrons releases NEFA & glycerol –> Recycled in liver

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34
Q

What forms the monolayer of lipoproteins?

A

Cholesterol, and phospholipids

Apoproteins

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35
Q

What does the lipoproteins encapsulate?

A

Cholesterol esters and triacylglycerides

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36
Q

Where does lipoprotein synthesis occur?

A

Occurs within the liver

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37
Q

What are cholesterol esters formed from?

A

Formed from cholesterol and the dactyl chain of phosphatidylcholine by lecithin cholesterol acyltransferase

38
Q

How are cholesterol molecules transported in the blood?

A

Converted into cholesterol esters, and stored within LDLs

39
Q

Why is cholesterol converted into cholesterol esters?

A

Ester linkages remove hydroxyl group, decreasing the water solubility

40
Q

What is the function of HDLs?

A

Extracts cholesterol from cell surface membrane, converting them into cholesterol esters via LCAT
reverse cholesterol transport, transports to liver, and reduces total serum cholesterol

41
Q

What is the initial stage of beta oxidation?

A

Conjugation with coenzyme A in the cytosol by acyl CoA synthetase forming an acyl-Coa species

42
Q

What is the function of beta-oxidation?

A

Reduced hydrogen carriers (NADH, FADH2) used in ATP synthesise by oxidative phosphorylation
Acetyl-CoA used as a substrate in the TCA cycle

43
Q

How are fatty-acyl-CoA molecules transported into the inner mitochondrial membrane?

A

Carnitine shuttle, modified by carnitine palmitoyl transferase -1 to acyl carnitine

44
Q

What cytosolic enzyme converts carnitine into acyl carnitine?

A

Carnitine acyltransferase-1

45
Q

What transports acyl carnitine across the inner mitochondrial membrane?

A

Carnitine translocase

46
Q

What is the destination of acyl carnitine within the matrix?

A

Acyl carnitine is cleated by Carnitine acyltransferase-II into carnitine and acyl-CoA

47
Q

What is the fate of acyl-CoA?

A

Acyl-CoA undergoes beta oxidation

48
Q

What type of disorder is primary carnitine deficiency?

A

Autosomal recessive disorder

49
Q

What does the mutation in the gene SLC22A5 cause?

A

Reduced ability to intake acylcarnitine into matrix for beta oxidation

50
Q

When does beta-oxidation end?

A

Until acetyl-CoA forms

51
Q

Palmitoyl-CoA is a 16 carbon compound, how many acetyl-CoA potentially forms?

A

8 Acetyl-CoA molecules, 16 carbon compound is consecutively decarboxylated to remove 2 carbons from acyL-CoA, forming acetyl-CoA

52
Q

How many cycles of beta-oxidation is required to generate 8 acetyl-CoA molecules?

A

7

53
Q

What is the fate of acetyl-CoA?

A

Oxidised in the TCA cycle provided oxaloacetate is present; used for lipogenesis; and the formation of ketone bodies.

54
Q

What are the products of one cycle of beta oxidation?

A

1 ATP, 1 FADH2, 1NADH, x acetyl-CoA

55
Q

How many molecules does acetyl-CoA yield?

A

12 ATP
3NADH = 3 x 3 = 9
FADH2 = 2
+ ATP.

56
Q

How many high energy bonds are utilised in beta oxidation?

A

2 ATP –> AMP

57
Q

How many ATP molecules does 16 Carbon molecule yield?

A

129

58
Q

What occurs during hypoglycaemia?

A

Ketone body formation,

59
Q

What does acetyl-CoA form during ketone body formation ?

A

Acetyl CoA forms acetoacetate, beta-hydroxybutyrate and acetone (ketone bodies); ketogenesis occurs in liver mitochondria.

60
Q

What organs do ketone bodies supply?

A

Brain, heart, skeletal muscle

61
Q

What is lipogenesis?

A

Lipogenesis is the metabolic formation of fat; utilising two enzymes: acetyl CoA carboxylase and fatty acid synthase.

62
Q

How are fatty acids formed?

A

Elongation , reduction and dehydration

63
Q

What protein are developing fatty acyl groups linked to?

A

Acyl carrier protein

64
Q

Compare the carriers between lipogenesis and and beta oxidation?

A

Acyl carrier protein v CoA.

65
Q

What is the reduction power for lipogenesis?

A

NADP

66
Q

What is the reducing power for beta oxidation?

A

FAD/NAD+

67
Q

Where does lipogenesis occur within a cell?

A

Cytoplasm

68
Q

Where does beta oxidation occur within a cell?

A

Mitochondrial matrix.

69
Q

What is MCADD?

A

Medium chain acyl-CoA dehydrogenase deficiency

70
Q

What is the pathology of MCADD?

A

Prevents degradation of triacylglycerols and fatty acids, thus inhibiting B-oxidation, reducing ATP synthesis

71
Q

What are the recommendations for patients with MCADD?

A

Adhere to high carbohydrate diet, should not fast longer than 10-12 hours

72
Q

What are the metabolic features of the brain?

A

Requires continuous supply of glucose, cannot metabolise fatty acids
Ketone bodies used as a partial substitute

73
Q

What are the metabolic features of the heart?

A

Cardiac cycle and cardiac contraction designed for aerobic respiration.
Utilises Krebs cycles substrates
Cell necrosis and death

74
Q

What is gluconeogenesis?

A

The biochemical process, in which the respiratory substrate, glucose is synthesised from non-carbohydrate sources (amino-acids, lactate and glycerol)- the process mainly occurs in the liver and the cortex of the kidney; occurs when body carbohydrate levels are insufficiently low. Maintains blood glucose level.

75
Q

Which precursors enter gluconeogenesis?

A

Pyruvate, oxaloacetate, dihydroxyacetone phosphate

76
Q

What is the aim of the gluconeogenic pathway?

A

Lactate generated by skeletal muscle taken liver, lactate dehydrogenase through Cori cycle produce pyruvate

77
Q

What amino acids supply gluconeoegenesis?

A

Glucogenic amino acids

78
Q

What molecule is used to form dihydroxyacetone?

A

Glycerol backbone

79
Q

Which reaction must be bypassed first for gluconeogenesis?

A

Phosphoenolpyruvate + ADP –> Pyruvate + ATP (Pyruvate kinase)

80
Q

What is the first step of gluconeogenesis?

A

Pyruvate carboxylated into oxaloacetate, ATP required

Decarboxylated and phosphorylate to yield phosphoenolpyruvate

81
Q

How many additional high energy bonds required ?

A

Four

82
Q

What do ketogenic amino acids form?

A

Undergo ketogenesis to form ketone bodies

83
Q

Under anaerobic conditions what processes occur?

A

Cardiac glucose output increases, gluconeogenesis, glycogenolysis

84
Q

What are isoforms?

A

Different forms of hexokkinase within muscle and liver, maximally active at different concentrations of glucose

85
Q

What is Michaelis constant (KM)?

A

Concentration of substrate at which enzyme function at half-maximal rate (Vmax)

86
Q

What molecule is hexokinase sensitive to inhibition to?

A

Glucose-6-phosphate

87
Q

What happens under anaerobic conditions to hexokinase-1?

A

Accumulation of glucose-6-phosphate results in inhibition of activity

88
Q

What comparison of sensitive is hexokinase-1 in muscle compared to hexokinase-4 (liver)?

A

Higher km, less sensitive to glucose-6-phosphate (glycogen)

89
Q

What is glucose-6-phosphatase?

A

Found in liver, catalyses the reverse reaction of hexokinase, generating glucose from glucose-6-phosphate

90
Q

What is the function of glucagon?

A

Secreted during hypoglycaemic conditions; stimulates increased glucose cardiac output (glycognenolysis & gluconeogensis)

91
Q

Which cell secretes glucagon?

A

Alpha cells of the islets of Langerhans

92
Q

What effect does adrenaline have of glucose?

A

Increases rate of glycolysis, gluconeoegenesis and fatty acid release

POM Y1 Imperial (34 decks)

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