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Nutrition And energy > Week 4 & 5 > Flashcards

Week 4 & 5 Flashcards

0
Q

What are the epithelium and endothelium in the live separated by?

A

They are separated by the Space of Disse (contains collagen and stellate cells)

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1
Q

What is the blood supply to the liver?

A

75% portal vein from pancreas, small intestine, gall bladder and spleen.
25% hepatic artery
All output through hepatic vein.

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2
Q

What do Kuppfer cells do?

A

Kuppfer cells - sinusoidal lining macrophages. Old erythrocytes and bacteria phagocytosis.

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3
Q

What are Pit cells?

A

Pit cells are liver associated lymphocytes. Natural killer cells.

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4
Q

What are hepatic stellate cells?

A

Hepatic stellate cells are fat cells which store Vitamin A.

They are also control collagen synthesis and sinusoidal contractility.

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5
Q

How is bile formed?

A

Bile is formed in hepatocytes from cholesterol by hydroxylation. It is then coupled with glycine or taurine.

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6
Q

How much of the bile is recirculated?

A

95% of bile is recirculated.

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7
Q

What does cholestyramine do to bile?

A

Cholestyramine binds to bile acids in the gut, preventing recirculation. This increases bile acid synthesis, decreasing cholesterol levels.

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8
Q

What is Xenbiotic breakdown?

A

Xenbioiotic breakdown is where substances that are potentially toxic with no nutritional value are broken down. (drugs, additives, hormones, bilirubin, urea).

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9
Q

What are the two phases of xenbiotic breakdown?

A

Phase 1 is catabolic to a primary metabolite. (Oxidation, hydrolysis, hydroxylation, reduction.)

Phase 2 results in an inactive substance. (Conjugation, sulphation, and glucuronidation).

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10
Q

How does phase 1 of xenbiotic breakdown proceed?

A

Phase 1 is performed by cytochrome p450 enzymes. The reaction is catalysed by oxygen and NADPH as a cofactor.

They are inducible enzymes is only expressed under certain conditions. Enzymes can be inhibited by warfarin, contraceptive pill and cyclosporine.

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11
Q

How does phase 2 of Xenbiotic breakdown work?

A

Phase 2 involves conjugation by enzymes. Addition of glucuroynl, sulphate, methyl, acetyl and glycl groups.

This occurs in liver but also Lung and kidney.

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12
Q

Where are erythrocytes broken down in bilirubin metabolism?

A

Erythrocytes are phagocytosed by Kupffer Cells.

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13
Q

What is haem initially broken down into?

A

Haem is initially broken down into biliverdin (green).

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14
Q

What is biliverdin broken down into?

A

Biliverdin is broken down into the yellow/orange bilirubin.

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15
Q

Which enzyme does the first part of haem metabolism involve?

A

Cytochrome p450 enzyme.

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16
Q

What is bilirubin conjugated with in the liver?

A

Bilirubin is conjugated with glucaronic acid in the liver.

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17
Q

Conjugated bilirubin is secreted into the gut, what happens there?

A

Bilirubin is converted to urobilinogen in the gut.

Urobilinogen is then converted into urobilin for urine excretion or stercobilin for faecal excretion

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18
Q

What is jaundice?

A

Jaundice is bilirubin deposition in tissue due to a problem with haem degradation.

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19
Q

If there is too much haem, why does jaundice occur?

A

If there is too much haem, the liver can’t conjugate it all.

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20
Q

What is Gilbert’s Syndrome?

A

Gilbert’s is a genetic condition which can lead to jaundice. Usually asymptomatic.

Causes reduced activity of enzyme which conjugated bilirubin in liver.

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21
Q

What do muscle cells use as a short term energy source?

A

Phosphocreatine is used with ADP to form ATP via creatine kinase.

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22
Q

What do cells convert 2ADP to?

A

Cells convert 2ADP to ATP and AMP via adenylate kinase.

AMP regulates metabolic enzymes.

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23
Q

What are carbohydrates?

A

Carbohydrates bind lots of water, glucose stored as polymers (glycogen) in liver and muscle.

Rapid but short lived energy store.

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24
Q

What are fats as an energy store?

A

Fats are a dense store with little water. Energy release takes a while and can’t be synthesised back to glucose.

Fats do not pass through the liver.

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25
Q

How good are proteins as an energy store?

A

Proteins are not ideal as they can impair cellular function.

Alanine and glutamine can be exported for gluconeogenesis (conversion of amino canids to glucose).

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26
Q

What is the lower threshold for glucose concentration in the brain?

A

If glucose conc falls below 3mM this leads to unconsciousness and death.

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27
Q

How much of cardiac muscle is mitochondria?

A

40% mitochondria.

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28
Q

What are the characteristics of type 1 skeletal muscle?

A

Type 1 muscle is similar to cardiac muscle. Highly aerobic and good for long modest activity.

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29
Q

What are the characteristics of Type 2a.

A

Type 2a is an intermediate between type 2b and 1. It’s has some mitochondria and myoglobin.
Phosphocreatine and glycogen provide energy store. Glucose uptake through adrenalin or insulin.
They use fatty acids at lower exercise levels and release amino acids during fasting.

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30
Q

What are the characteristics of type 2b muscle? (Fast twitch)

A

Type 2b give an explosive response but are easily fatigued. They have few mitochondria and myoglobin.

Phosphocreatine replenishes ATP. Type 2b perform anaerobic glycolysis with glucose from glycogen store.
Insulin and adrenalin for glucose uptake.

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31
Q

Cortisol has what effect non glycogen and fats?

A

Cortisol redistributes glycogen to muscle, and redistributes fats to the abdomen.

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32
Q

What does TNF and IL-1 do to sugars, glycogen, proteins and fats?

A

Breaks them all down!

33
Q

Is fructose and galactose metabolism controlled by insulin?

A

No they are broken down to enter the same pathways as glucose.

34
Q

What is a standard glucose level?

A

Standard glucose level at 5mM.

3mM leads to coma and death.

8mM leads to vascular damage through glycation.

35
Q

Where is the majority of glucose stored after a meal?

A

Majority (25g) goes to muscle as glycogen.

17g goes to liver but at higher concentration.

Least goes to fats. 2g.

36
Q

Where does the majority of glucose go for ATP synthesis?

A

23g to muscle

15g to brain. (Brain totally reliant on glucose as fats don’t pass blood brain barrier)

8g to kidneys as lactate.

37
Q

What does the Krebs cycle produce?

A

Krebs produces reduced coenzymes (NADH) donating electrons to electron transport chain.

38
Q

How does the electron transport chain use energy from the electrons?

A

The ETC uses the energy to pump H+ over mitochondrial membrane.

This causes a H+ gradient driving ATP synthesis in mitochondria.

39
Q

What are the two phases of aerobic glycolysis?

A

Preparative phase: glucose to fructose 1, 6 phosphate.

Generating phase: fructose 1,6 phosphate to pyruvate. This generates ATP and NADH. 2ATP generated under anaerobic conditions.

40
Q

Under aerobic conditions how many more molecules of ATP are formed using NADH?

A

A further 3-5 ATP formed via oxidative phosphorylation.

41
Q

Why is the phosphorylation of glucose to glucose 6 phosphate important?

A

Conversion to glucose 6 phosphate prevents glucose from leaving the cell. This involves hexo/gluco kinase.

42
Q

Why is it important that fructose 1,6 biphosphate is split into glyceraldehyde 3 phosphate (6carbon to 2x 3carbon)

A

2 ATP can be produced per 3 carbon compound.

43
Q

What are the key points in the glycolysis pathway controlled by?

A

They are both controlled by irreversible enzymes. (Hexokinase for glucose to glucose 6 phosphate and phosphofructokinase for fructose 6 phosphate to fructose 1,6 biphosphate).

Pyruvate is formed from phosphoenolpyruvate via pyruvate kinase.

44
Q

What is the only way to get ATP through anaerobic glycolysis?

A

Pyruvate is converted to lactate. (Stops pyruvate from building up and continues Krebs.) this generates 2 molecules of ATP per glucose molecule.

NAD+ formed during conversion to lactate.

45
Q

How is glycogen synthesised?

A

Synthesis is controlled by glycogen synthase. Conversion of glucose 6 phosphate to glucose 1 phosphate.

Glycogenin is required as a primer. (UDP primer).

46
Q

How is glycogen broken down?

A

Glycogen phosphorylase removes glucose units.

Converts glucose 1 phosphate to glucose 6 phosphate which then either goes to glycolysis in muscle or is converted to glucose in the liver.

47
Q

If dietary supply of fats and lipids is insufficient, what happens to glucose?

A

Fats can be synthesised from glucose, uses include storage as triglycerides and lipid membrane synthesis.

Synthesised through cytosolic acetyl CoA, malonyl CoA until C 16 molecule formed.

48
Q

What does insulin do?

A

Insulin increases glycolysis expressing genes, decrease gluconeogenesis genes. High insulin, glycolysis stimulated. Glucose used by muscles.

49
Q

What does glucagon do?

A

Glucagon regulates level of fructose 1,6 biphosphate which activates glycolysis and inhibits gluconeogenesis.

Glucagon promotes phosphorylation and so glycogen breakdown through glycogen phosphorylase to glucose.

50
Q

What are the roles of fatty acids and lipids?

A

Fatty acids and lipids are used for phospholipids and cholesterol in cell membranes.

51
Q

What are omega 3 and 6 fatty acids used for?

A

Omega 3 and 6 are precursors to precursors for eicosanoids. (Inflammatory and anti inflammatories).

Eicosanoids (prostaglandins, leukotrienes and thromboxanes.)

52
Q

What does cholesterol form?

A

Cholesterol forms bile salts, steroid hormones, vitamin D and cell membranes.

53
Q

What are cylomicrons?

A

Chylomicrons are formed in intestinal epithelium. They are released into lymph, then thoracic duct followed by subclavian vein.

No direct passage to liver.

54
Q

What is the first step of oxidation of fatty acids?

A

Activation to fatty acyl CoA in the cytosol. Beta oxidation takes place in mitochondria.

55
Q

What do long chain over 12C fatty acids require for transport?

A

Over 12C fatty acids require carnitine for transport.

56
Q

What does malonyl CoA do the the carnitine transport system?

A

Malonyl CoA inhibits the system to avoid cycling.

57
Q

What is produced at the end of each repeating cycle of beta oxidation?

A

Acetyl CoA is produced and the carbon chains shorten by 2C.

NADH and FADH are also produced which supply the electron transport chain.

58
Q

How many ATP’s does each molecule of palmitoyl CoA produce?

A

Each molecule of palmitoyl CoA produces 108 ATP.

59
Q

How is malonyl CoA formed?

A

Malonyl CoA is formed by acetyl CoA carboxylase. The first step of fatty acid synthesis.

60
Q

What does a high level of malonyl CoA concentration do?

A

High concentration of Malonyl CoA inhibits carnitine acyl-transferase-1. Transfers fatty acids into mitochondria.

Ensures fatty acid breakdown is inhibited when energy is plentiful

61
Q

Where are ketone bodies formed and what from?

A

Ketone bodies are formed from excess acetyl CoA which occurs in the mitochondria of liver cells.

62
Q

When are ketone bodies made?

A

Synthesis occurs only when the bonds is relying on fatty acids for energy.
Ketones are released into the blood to produce energy in peripheral tissues including brain tissue.

63
Q

What can high levels of ketone bodies lead to?

A

High levels of ketones can lead to ketoacidosis which can lead to coma and death. P

64
Q

How is cholesterol synthesised?

A

Cholesterol synthesis occurs in 4 steps.

First step is acetyl CoA to mevalonate (6C) and occurs in cytosol and smooth endoplasmic reticulum.

65
Q

How is the first step of cholesterol synthesis inhibited?

A

Acetyl CoA to mevalonate (6C) is inhibited by statins by stopping HMG CoA reductase activity. (Rate determining step)

66
Q

What is the second activation step of cholesterol synthesis?

A

Mevalonate to Phosphorylated isoprene units (5C)

67
Q

What does the third step of cholesterol synthesis involve?

A

The phosphorylate isoprene units (5C) are polymerised.

Using 6 units they are polymerised to from a 30C chain (squalene).

68
Q

What does the fourth and last stage of cholesterol synthesis do?

A

The fourth stage involves cyclisation to form a ring structure (lanosterol) then cholesterol.

69
Q

How is cholesterol synthesis controlled?

A

Cholesterol synthesis is inhibited by high cholesterol.

Insulin stimulates synthesis, glucagon inhibits.

70
Q

How is the activity of HMG CoA controlled?

A

HMG CoA reductase is controlled by phosphorylation. Enzyme inactivated when energy levels are low.

71
Q

What is serol regulatory binding protein? (SREBP)

A

When cholesterol levels fall SREBP is released from the ER.

SREBP codes for HMG reductass and LDL receptor.

72
Q

Can humans break down cholesterol?

A

Humans cannot break down cholesterol. It can only be excreted in the faeces. Less than 5% a day.

73
Q

What do saturated fats do to blood cholesterol?

A

Saturated fats raise LDL cholesterol.

74
Q

What do trans fats do to blood cholesterol?

A

Trans fats raise LDL and lower HDL levels

75
Q

What does dietary cholesterol do to blood cholesterol?

A

Dietary cholesterol raised LDLS

76
Q

What is familial hypercholesterolaemia?

A

Less LDL receptors so suffers are at increased risk of coronary disease.

77
Q

What is Tangier’s disease?

A

Tangier diseases is a lack of HDL. sufferers are at an increase risk of coronary disease.

78
Q

If fat accumulates in the liver, what can this lead to?

A

Fat accumulation can lead to inflammation and fibrosis –> steatohepatitis.

79
Q

What is alcoholic steatohepatitis?

A

Alcoholic steatohepatitis. This is where the balance of fatty acid synthesis and oxidation is disturbed, inhibiting fatty acid oxidation and activating excess triglyceride synthesis (cause by high NADH levels)

80
Q

What is non alcoholic steatohepatitis?

A

Non alcoholic steatohepatitis is caused by insulin resistance so there is more insulin secreted so there will be greater fatty acid synthesis.

81
Q

In both cases of steathepatitis what is the comment impairment?

A

In both cases triglyceride export is impaired.

Nutrition And energy (6 decks)

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