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DIG > Digestion and Absorption of Fat > Flashcards

Digestion and Absorption of Fat Flashcards

1
Q

What properties of lipids make them the most suitable storage of energy?

A

They are non polar and can be stored in an anhydrous state.

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2
Q

Why does the ‘apple shape’ distribution of fat pose a higher risk of weight-related health problems?

A

There is more visceral fat and less subcutaneous fat with the apple shape than with the pear shape.

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3
Q

What are the RQ values for carbohydrates, lipids and proteins?

A

Carbohydrates: 1

Proteins: 0.8

Lipids: 0.7

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4
Q

What are the 4 steps of b-oxidation?

What is the starting molecule for the cycle?

A

1 - Oxidation.

2 - Hydration.

3 - Oxidation.

4 - Cleavage.

Starting molecule is fatty acyl-CoA.

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5
Q

What is the function of acyl-CoA synthetase?

A

To convert fatty acids into fatty acyl-CoA.

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6
Q

Summarise The ATP production of beta oxidation.

A
  • 1 ATP required for initial step.
  • Step 1: FAD -> E.T.C produces 2 ATP.
  • Step 4: NAD+ -> E.T.C produces 3 ATP.
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7
Q

What is the primary product of beta oxidation?

A

Acetyl CoA.

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8
Q

How many carbons are removed form the fatty acid chain per turn of the b-oxidation cycle?

A

2.

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9
Q

Which vitamins are fat soluble?

A

A, D, E and K.

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10
Q

List 6 symptoms of vitamin A deficiency.

A

1 - Night blindness.

2 - Corneal drying (xerosis).

3 - Corneal degeneration and blindness (xerophthalmia).

4 - Impaired immunity.

5 - Hypokeratosis.

6 - Keratosis pilaris (bumps on the skin).

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11
Q

List 9 symptoms of a vitamin A overdose.

A

1 - Hair loss.

2 - Nausea.

3 - Jaundice.

4 - Irritability.

5 - Vomiting.

6 - Blurred vision.

7 - Headaches.

8 - Muscle pain.

9 - Abdominal pain.

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12
Q

Where can vitamin D3 be synthesised?

What can result in vitamin D deficiency?

A

In the skin.

Inadequate sunlight exposure + inadequate dietary intake can lead to vitamin D deficiency.

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13
Q

List 2 dietary sources of vitamin D3.

A

Egg yolk and fish oil.

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14
Q

What is vitamin E otherwise known as?

What is its function?

A

Tocopherol.

Acts as an antioxidant. Has a role in protection against cardiovascular disease and cancer.

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15
Q

List 3 sources of vitamin E.

A

1 - Vegetable oils.

2 - Corn.

3 - Soybean.

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16
Q

What are the signs of vitamin E deficiency?

A

Neurological problems (due to poor nerve conduction).

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17
Q

Where can vitamin K be obtained from other than dietary sources?

A

Vitamin K is produced by intestinal bacteria.

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18
Q

What is the function of vitamin K?

A

Involved in the carboxylation of glutamate side chains in proteins to form gamma carboxyglutamate residues.

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19
Q

What are the 3 functions of gamma carboxyglutamate residues?

A

Usually involved in binding calcium.

Involved in the regulation of:

1 - Blood coagulation.

2 - Bone metabolism.

3 - Vascular biology.

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20
Q

Considering the functions of gamma carboxyglutamate, list 3 symptoms of vitamin K deficiency.

A

1 - Risk of uncontrolled internal bleeding.

2 - Cartilage calcification.

3 - Malformation of developing bone.

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21
Q

List 7 functions of fatty acids such as:

  • Linoleic acid.
  • Linolenic acid.
  • Arachidonic acid.

Where must these fatty acids come from?

A

1 - Formation of healthy membranes.

2 - Development and function of the nervous system.

3 - Production of eicosanoids, e.g. PGs.

4 - Regulation of blood pressure.

5 - Regulation of blood viscosity.

6 - Regulation of vasoconstriction.

7 - Regulation of immune and inflammatory responses.

  • Must come from diet as cannot be derived endogenously.
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22
Q

What makes up > 90% of dietary fat?

A

Triglycerides.

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23
Q

How do sphingolipids differ from other membrane phospholipids?

A

They have a serine rather than a glycerol backbone.

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24
Q

List 4 lipids that are found in bile.

A

1 - Phospholipids (mostly phasphatidylcholine).

2 - Unesterified cholesterol.

3 - Membrane lipids from desquamated cells.

4 - Lipids derived from dead colonic bacteria.

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25
Q

What is phosphatidylcholine?

A

A phospholipid head group.

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26
Q

Where in the intestine does lipid hydrolysis occur?

A

In the aqueous environment of the intestinal lumen.

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27
Q

List 4 processes that emulsify lipids (from dietary sources).

What is the purpose of emulsification?

A

1 - Food preparation (i.e. blending, cooking).

2 - Chewing and gastric churning.

3 - Squirting of gastric contents into the duodenum.

4 - Intestinal peristalsis.

  • Emulsification increases SA : Vol ratio and reduces lipid droplet size.
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28
Q

What prevents the lipid particles from coalescing?

A
  • Coating the droplets with membrane lipids, denatured protein, dietary polysaccharides, products of digestion and biliary phospholipids and cholesterol.
  • The polar groups project into the water, preventing coalescence of the micelles.
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29
Q

What is the core of lipid micelles composed of?

A

Triglyceride, which also contains cholesteryl esters and other non-polar lipids.

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30
Q

How do lingual and gastric lipases modify triglycerides?

A

They release a single fatty acid, leaving behind in tact diglycerides.

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31
Q

Why are the single fatty acids released by lipases not absorbed in the stomach?

A

They are insoluble at acidic pH, so remain in the core of the triglyceride droplets.

32
Q

What happens to medium and short chain fatty acids at gastric pH?

A

They are:

  • Ionised,
  • Remain in solution,
  • Passively absorbed across the gastric mucosa into portal blood.
33
Q

What proportion of fat digestion occurs in the stomach?

A

~15%.

34
Q

How do patients with pancreatic insufficiency compensate for fat malabsorption?

Give an example of a disease that may cause fat malabsorption.

A
  • Lingual and gastric lipase activity is extended in the duodenal lumen (lingual lipase has a low pH optimum).
  • Cystic fibrosis is an example of a disease that may cause pancreatic insufficiency.
  • CF Also causes a low pH in the duodenum.
35
Q

What is triggered in the duodenum when fatty acids are present?

A

The release of CCK from I cells in the duodenal mucosa.

36
Q

What two processes does CCK stimulate?

A

1 - The flow of bile into the duodenum by contraction and relaxation of the sphincter of Oddi.

2 - Secretion of pancreatic enzymes, including lipases and esterases from acinar cells.

37
Q

What is the function of the sphincter of Oddi?

A

Opens to allow bile and pancreatic juice to flow between the liver / pancreas and the duodenum.

38
Q

What is the papilla of Vater?

A

The sphincter of Oddi and its surrounding mucosa protruding into the duodenum.

39
Q

What is the strongest lipolytic enzyme?

A

Pancreatic lipase.

40
Q

Which 4 conditions must be met for full lipolytic activity of pancreatic lipase?

A

1 - Colipase (essential for ligand binding conformation).

2 - Alkaline pH.

3 - Bile salts.

4 - Fatty acids.

41
Q

What is colipase secreted as?

A

pro-colipase

42
Q

What are the 2 roles of colipase?

A

1 - Acts as an anchor for the binding of the lipase.

2 - Forms a colipase-lipase complex that can bind to the lipid interface.

43
Q

What are the products of pancreatic lipase acting on lipids?

A

Fatty acids
and
2-monoacylglyceride.

44
Q

What other pancreatic enzymes (other than lipase) hydrolyse lipid esters?

A

1 - Carboxyl ester hydrolase. AKA cholesterol esterase.

2 - Phospholipase A2.

45
Q

What does carboxyl ester hydrolase target?

A

A wide range of esters (low specificity).

46
Q

What does phospholipase A2 target?

What are the breakdown products?

A

Glycerophospholipids and their phosphatidylcholine head groups.

Releases a single fatty acid to yield lysophosphatidylcholine.

47
Q

Which bond does PLA2 target?

Under which conditions is it active and most effective?

A

Sn-2 acyl bonds of phospholipids.

Most effective at alkaline pH and required bile salts for activity.

48
Q

Why are in tact triglycerides rarely found in the stools?

A

Due to the presence of bacterial lipases, which are far more amenable than other lipases.

49
Q

How do lipolytic products contribute to the mechanisms of lipid breakdown?

A

By acting as additional emulsifiers to the emulsion droplets.

50
Q

How does the emulsion droplet change over the course of its breakdown?

A

Emulsion droplet -> multilamellar vesicle -> unilamellar vesicle -> mixed micelle (composed of bile salts and mixed lipids).

51
Q

What thins out multilamellar vesicles into unilamellar vesicles?

A

Addition of bile salts.

52
Q

Which 3 barriers must lipolytic products overcome to enter enterocytes?

A

1 - The mucous layer that lines the intestinal epithelial surface.

2 - The unstirred water layer.

3 - The apical membrane of the enterocyte.

53
Q

How does water solubility change with fatty acid chain length?

What implications does this have on absorption of lipolytic products?

A

Inversely proportional.

Shorter fatty acids will be able to diffuse through the unstirred water layer more easily, so are absorbed more readily.

54
Q

Why are fatty acids protonated at the enterocyte surface?

A

Due to the low pH created by the Na-H exchange at the brush border.

55
Q

List 3 ways by which fatty acids can enter the enterocyte.

A

1 - Diffusion.

2 - Incorporation into the cell membrane.

3 - Novel evidence that there is an active carrier mediated process.

56
Q

After entry of lipolytic products into the enterocyte, where are the remaining bile salts absorbed?

Where are the bile salts redirected to? What is this circulation of bile salts called?

A

At the terminal ileum and colon.

They are redirected to the liver in the portal blood AKA enterohepatic circulation.

57
Q

Once in the enterocyte, which molecules are immediately converted back to triglycerides, phospholipids and esters of cholesterol in the SER?

A

1 - Long chain fatty acids,

2 - Monoglycerides,

3 - Phospholipids,

4 - Cholesterol.

58
Q

What is an apoprotein?

A

The protein portion of a complex consisting of a protein molecule joined to a nonprotein protein molecule such as a lipid -> lipoprotein.

59
Q

Where in the enterocyte do fat droplets form?

A

In the SER.

60
Q

Where are apoproteins synthesised?

A

In the RER.

61
Q

Where are apoproteins transferred to after being synthesised?

Why are they transferred there?

A

Transferred from the RER to the SER.

To become associated with lipid droplets to form lipoproteins.

62
Q

Which molecules pass through the enterocytes’ basolateral membranes to enter capillaries directly from the apical membrane (without re-esterification)?

A

Glycerol, short and medium chain fatty acids.

63
Q

Give 2 examples of products of association of apoproteins (from the RER) with lipid droplets (at the SER).

A

Nascent chylomicrons and VLDLs (very low density lipoproteins).

64
Q

Where are nascent chylomicrons and VLDLs glycosylated?

A

At (the cis face of) the golgi apparatus.

*Golgi apparatus: cis face -> golgi stack -> trans face.

65
Q

What happens to nascent chylomicrons and VLDLs after they are glycosylated?

A

They are transported in transport vesicles to the basolateral membrane.

They then fuse with the basolateral membrane and are released into lymphatic capillaries.

66
Q

What is the fate of a long chain fatty acid that enters an enterocyte?

A

It is re-esterified in the SER in conjunction with apoproteins.

It is then glycosylated at the golgi apparatus and released into lymphatic capillaries as a chylomicron or as a VLDL.

67
Q

Give 2 examples of substrates that can be used to re-esterify long chain fatty acids to form triglycerides in the SER.

Describe the pathway taken by one of these substrates to form a triglyceride.

A

1 - Glycerol-3-phosphate.

2 - 2-MG:

  • 2-Monoglyceride (2-MG) accepts a FA chain from FA-CoA.
  • This produces diacylglycerol and CoA.
  • Diacylglycerol accepts another FA chain from another FA-CoA.
  • This produces triglyceride and CoA.
68
Q

What are the 3 reasons for long chain fatty acids binding to fatty acid binding proteins in the enterocyte?

A

1 - Prevents leakage back out of the enterocyte.

2 - Prevents lipid toxicity.

3 - Ensures transfer of fatty acids to the SER.

69
Q

Why are glycerol, short and medium chain fatty acids suitable fat substitutes for patients with fat malabsorption?

A

Because they are transported unmodified directly into blood capillaries through the enterocyte.

70
Q

What happens to chylomicrons after they are exported from the enterocyte?

A
  • They find their way to the endothelial surface, where they encounter lipoprotein lipase.
  • Lipoprotein lipase hydrolyses the triglyceride components of the chylomicrons.
  • The products are fatty acids and glycerol, leaving behind remnant chylomicrons.
71
Q

List 3 lipoproteins, excluding chylomicrons.

A

1 - VLDLs.

2 - LDLs.

3 - HDLs.

72
Q

What is the function of HDLs?

A

HDLs scavenge cholesterol and return it to the liver (protective function).

73
Q

What is steatorrhoea?

A

The excretion of abnormal quantities of fat with the faeces owing to reduced absorption of fat by the intestine.

74
Q

What is Orlistat?

How does it work?

A
  • A medicinal treatment for obesity.

- An inhibitor of lipase.

75
Q

8 points to summarise this deck:

A

1 - Importance of fat and b-oxidation.

2 - Fat soluble vitamins.

3 - Essential fatty acids.

4 - Digestion.

5 - Action of emulsification, fat droplet formation, lipase action and bile acids.

6 - Absorption and processing into triglycerides and incorporation in chylomicrons.

7 - Fate of chylomicrons.

8 - Obesity.

DIG (20 decks)

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