Cell metabolism II Flashcards

1
Q

What are some examples of lipids?

A

Free fatty acids, triacylglycerols, phospholipids, glycolipids and steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the properties of triglycerides?

A

Long hydrocarbon tails are hydrophobic, insoluble in water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the properties of saturated lipids?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why are triglycerides good for waterproofing?

A

Hydrophobic nature of lipids reduces water loss through evaporation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why are triglycerides good insulators?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the product of B-oxidation?

A

Acetyl-CoA molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where does b-oxidation occur?

A

Mitochondria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the sources of fats?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is de novo synthesis?

A

Synthesis of complex molecules from simple molecules.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What vitamins does bile salts assist in the absorption of?

A

Vitamin A,D,E & K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What results from a bile salt deficiency?

A

Fat passing through the gut undigested and unabsorbed resulting in steatorrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the benefits or orlistat?

A

Can be used to treat obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are lipoproteins?

A

Lipids are transported in the plasma by lipoproteins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the role of chylomicrons?

A

Dietary fat transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the role of VLDLs?

A

Endogenous fat transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the role of IDLs?

A

LDL precursor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the source of VLDLs?

A

Liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the role of LDLs?

A

Transport of cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the role of HDLs?

A

Reverse cholesterol transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

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

A

Enterocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are stored within chylomicrons?

A

Triglycerides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What do high-density lipoproteins donate to chylomicrons?

A

Apoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How are fatty acids transported within the blood?

A

As albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Describe the life cycle of chylomicrons?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What forms the monolayer of lipoproteins?

A

Cholesterol, and phospholipids

Apoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What does the lipoproteins encapsulate?

A

Cholesterol esters and triacylglycerides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Where does lipoprotein synthesis occur?

A

Occurs within the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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