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Tissues > T11-12 Lipid Digestion and Absorption > Flashcards

T11-12 Lipid Digestion and Absorption Flashcards

1
Q

A single alcohol functional group can form how many hydrogen bonds?

A

2

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2
Q

An un-ionized carboxyl group forms how many hydrogen bonds?

A

3

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3
Q

Is glucose hydrophobic or hydrophilic?

A

hydrophilic, because of its many -OH groups

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4
Q

Which three classes of molecules are considered to be amphipathic?

A

fatty acids; phospholipids; cholesterol

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5
Q

Which two classes of molecules are considered to be hydrophobic?

A

triglycerides; cholesteryl esters

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6
Q

Describe the solubility of fatty acids in water.

A

low, but finite, solubility in water

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7
Q

How are fatty acids transported in blood? (2)

A

transported as part of a triglyceride (glycerol backbone + 3 fatty acids); or attached to albumin

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8
Q

Describe the solubility of cholesterol in water.

A

no solubility in water — it exists at the aqueous/lipid interface

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9
Q

Do most fatty acids have an even or odd number of carbons?

A

most have an even number of carbons

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10
Q

List the four major groupings of fatty acids and the associated criteria.

A

short chain (<6 carbons)

medium chain (6-12 carbons)

long chain (13-21 carbons)

very long chain (>20 carbons)

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11
Q

Differentiate between saturated, monounsaturated, and polyunsaturated fatty acids.

A

saturated = 0 double bonds

monounsaturated = 1 double

polyunsaturated = more than 1 double bond

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12
Q

What are the most common long-chain fatty acids in the human diet?

A

stearic acid (C18:0)

oleic acid (C18:1)

linoleic acid (C18:2), both double bonds in cis configuation

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13
Q

Why are free fatty acids dangerous? What is a consequence of this property?

A

they are soaps/detergents that can destroy biological membranes

therefore, FFAs have to be stored as triacylglycerol

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14
Q

Which molecule is the major energy source for all eukaryotes?

A

triacylglycerol

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15
Q

Describe the hydrophilicity/hydrophobicity of triacylglycerol.

A

Triacylglycerol is very hydrophobic

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16
Q

In adipose tissue, how are triacylglycerols stored?

A

stored into one large lipid droplet

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17
Q

How much triglyceride is consumed by the typical American each day?

A

50-100 grams per day, with 50% from plants and 50% from animals

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18
Q

Describe the relationship between fatty acid saturation and phase of matter.

A

more saturation (i.e. more C-H bonds and fewer C=C double bonds) means the fat will be more solid at room temperature

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19
Q

Why are plant fats more liquid and animal fats more solid at room temperature?

A

plant fats = higher proportion of 18:1 and 18:2 unsaturated fatty acids

animal fats = higher 16:0, 18:0 saturated fatty acids

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20
Q

What is an exception to the general trend that plant fats are liquid at room temperature?

A

tropical plant fats (coconut oil or palm oil) have larger proportions of saturated long-chain fatty acids, so they are more solid at room temperature

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21
Q

What are the major dietary plant sterols? (2)

A

sitosterol

campesterol

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22
Q
A
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23
Q

Describe the cholesterol content of meat.

A

1.4 mg cholesterol per gram

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24
Q

Describe the cholesterol content of egg yolks.

A

250 mg (surprisingly high)

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25
Q

On average, how much cholesterol and plant sterol do humans eat per day?

A

300 mg cholesterol

200 mg plant sterol

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26
Q

Describe how well (i.e. the extent) dietary triacylglycerides, dietary cholesterol, and dietary plant sterols are absorbed in humans.

A

intestine absorbs:

100% of dietary triacylglycerols (remember, fat is energy)

50% of dietary cholesterol

<5% of dietary plant sterols

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27
Q

Lipid absorption occurs in what organ?

A

small intestine (composed of smaller duodenum + longer jejunum and ileum)

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28
Q

What is the precursor to bile acids?

A

cholesterol

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29
Q

Describe how cholesterol is converted to a bile acid, and the consequences of this conversion.

A

27-carbon cholesterol (hydrophobic) has 3 carbons removed and additional hydroxyl groups added on one surface to create a hydrophilic 24-carbon bile acid

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30
Q

What are the three biliary lipids that pass through the bile duct?

A

bile acids

cholesterol

phospholipids

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31
Q

Describe the pathway of biliary lipids synthesized in the liver.

A

liver → bile canaliculi → common bile duct → pancreas → duodenum

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32
Q

Cholesterol is either synthesized in the liver or synthesized de novo in peripheral tissue. How is cholesterol synthesized in peripheral tissue sent to the liver?

A

reverse cholesterol transport pathway

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33
Q

Where is cholesterol esterase synthesized?

A

acinar cells of pancreas

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34
Q

Bile acids, cholesterol, and phospholipids drain through bile canaliculi, through the common bile duct, and toward the pancreas. Once in the pancreas, what substances are added to this mixture? (2)

A

digestive enzymes (pancreatic lipase + co-lipase)

cholesterol esterase

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35
Q

Through which structure do pancreatic enzymes enter the common bile duct?

A

pancreatic duct

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36
Q

Describe the triacylglycerol-hydrolyzing properties of pancreatic lipase and co-lipase.

A

pancreatic lipase and co-lipase hydrolyze C1 and C3 ester linkages, resulting in 2 free fatty acids + 1 2-monoacylglycerol

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37
Q

How do mixed micelles form?

A

bile acids + emulsified fats + free fatty acids + 2-monoacylglycerol = mixed micelle

38
Q

Beyond the four “core” substances that make up a mixed micelle, what three other substances can be incorporated into mixed micelles?

A

unesterified cholesterol

plant sterols

fat soluble vitamins (ADEK)

39
Q

What is the function of pancreatic cholesterol esterase in the context of intraluminal digestion?

A

pancreatic cholesterol esterase converts cholesterol esters → free cholesterol + fatty acids, which are incorporated into mixed micelles

40
Q

What structure must the lipid components of mixed micelles cross in order to reach the enterocytes of the duodenum and jejunum?

A

must cross apical membrane (i.e. luminal surface)

41
Q

What is NPC1L1 and what is its function?

A

transmembrane sterol transporter that transports unesterified cholesterol + plant sterols into enterocytes via apical membrane

42
Q

What is ABCG5/ABCG8 and what is its function?

A

sterol transporter on apical membrane that pumps out plant sterols and some cholesterols, thereby limiting amount of sterols absorbed

43
Q

Why is cholesterol re-esterified once it enters an enterocyte?

A

because free cholesterol is toxic to enterocytes/most absorptive cells

44
Q

What enzyme carries out the re-esterification of cholesterol in enterocytes? Describe the location and properties of this enzyme.

A

acetyl-CoA acetyltransferase (ACAT)

located in ER

attaches long-chain FA to 3-β-OH group of sterol

45
Q

What drives plant sterols to leave enterocytes via ABCG5/ABCG8? In other words, what physical property doesn’t keep them in the cell?

A

ACAT’s preferred substrate is unesterified cholesterol instead of plant sterols

46
Q

Draw out a diagram showing the esterification of cholesterol and plant sterols in enterocytes by ACAT.

A
47
Q

What is the fate of the free fatty acids and 2-monoacylglycerol that enter enterocytes?

A

FFA + 2-MAG are re-esterified to form triglycerides, because free fatty acids are detergents and therefore toxic

48
Q

What are the two possible pathways for the re-esterification of FFAs and 2-MAGs into TGs?

A

monoacylglycerol pathway

glycerol-3-phosphate pathway

49
Q

Describe the monoacylglycerol pathway of FFA/2-MAG re-esterification in enterocytes.

A

2-MAG + fatty acid-CoA → [MG acyltransferase] → 1,2 diacylglycerol (DAG)

a second fatty acid-CoA is added → [DG acyltransferase] → TG

50
Q

Describe the glycerol-3-phosphate pathway of FFA/2-MAG re-esterification in enterocytes.

A

3-glycerophosphate (derived from glucose) backbone + fatty acid-CoA → 1,2-diacylglycerol phosphate → [PA hydrolase] → 1,2 diacylglycerol → [DG acyltransferase] → TG

51
Q

What is the composition of lipid droplets in enterocytes?

A

contain 100% of TG

50% of cholesterol

small fraction of plant sterols

52
Q

Describe how ApoB-48 is synthesized.

A

ApoB mRNA transcribed in nucleus → transported to cytoplasm → cytosine deaminase changes CAA to UAA stop codon at 48% mark → ApoB-48 forms

53
Q

Describe the relationship between the LDL receptor binding domain and ApoB-48.

A

LDL receptor binding domain is in the C-terminal half of ApoB-100 and therefore not included in ApoB-48.

54
Q

(T/F) Cytosine deaminase is synthesized in the liver.

A

False. Cytosine deaminase is not synthesized in the liver, meaning that only ApoB-100 is formed in the liver.

55
Q

Where does initial chylomicron synthesis occur?

A

in the ER of enterocytes

[lecture slides say ER + Golgi]

56
Q

Describe how the chylomicron forms in the ER of enterocytes (specifically, what is added to make the chylomicron). (3)

A

ApoB-48 forms

re-esterified TGs + re-esterified CEs + phospholipids join

fat soluble vitamins (ADEK) + ApoAI join

57
Q

The initial chylomicron assembly process is dependent on what protein?

A

microsomal TG transfer protein (MTTP)

58
Q

What is the function of microsomal TG transfer protein (MTTP)?

A

transfers TG to ApoB to form TG-rich particles

59
Q

Following the formation of the nascent CM in the ER of the enterocyte, what happens?

A

CM goes through ER → Golgi complex → enterocyte basolateral membrane → lacteal (lymphatic vessel)

60
Q

The secretion of newly-formed CMs out of the enterocyte basolateral membrane requires what protein?

A

Sar1b

61
Q

Following secretion out of the enterocyte’s basolateral membrane, what further modifications are made to CMs?

A

CM interacts with HDL and acquires ApoCII and ApoE

62
Q

Describe the weight composition of CMs.

A

over 90% of weight is made up of TGs

63
Q

What is the functional purpose of cholesterol/phospholipids/apolipoproteins on the surface of CMs?

A

help to solubilize the particle

64
Q

Lacteals in the lymphatic system eventually lead to what structure?

A

leads to thoracic duct

65
Q

The thoracic duct empties into

A

venous circulation, therefore bypassing the liver

66
Q

Differentiate between sugars/amino acids and lipids in terms of how they are metabolized and transported throughout the body. (2)

A

sugars/amino acids absorbed from intestine into blood capillaries and delivered directly to liver via portal vein

lipids transported to systemic venous circulation via lacteal/thoracic duct, allowing lipids to bypass liver and be directly delivered to peripheral tissue

67
Q

What is postprandial hyperlipidemia?

A

phenomenon of opalescent plasma resulting from large CMs refracting light

68
Q

As CMs circulate throughout the body, what enzyme do they encounter?

A

lipoprotein lipase (LPL)

69
Q

Where is lipoprotein lipase synthesized?

A

adipocytes

myocytes

cardiomyocytes

70
Q

Write out/describe the pathway/mechanism of lipoprotein lipase action.

A

LPL released into interstitial space → binds to GPIHBP1 on subendothelial surface of capillaries → GPIHBP1 escorst LPL to vascular surface by crossing endothelial cell → ApoCII on circulating particle interacts with LPL to promote hydrolysis of TGs in CM core

71
Q

What happens to fatty acids liberated by the action of lipoprotein lipase interacting with ApoCII on circulating CMs?

A

free fatty acids either cross the endothelium into the adipocyte/myocyte/cardiomyocyte OR become bound to albumin and are transported back to the liver

72
Q

What happens to free fatty acids liberated by lipoprotein lipase action that cross the endothelium and enter the adipocyte/myocyote/cardiomyocyte?

A

if entering adipocytes → re-esterified to TG and stored

if endering myocytes/cardiomyocytes → oxidized

73
Q

Describe the process of intravascular metabolism of CMs to CM remnants.

A

once 75% of TG is removed from CM core, ApoCII and ApoAI transferred back to HDL

ApoE becomes exposed on surface of CM remnant

74
Q

Describe how CM remnants are cleared by the liver.

A

exposed ApoE binds to LDL receptor on surface of hepatocytes

CM remnant-LDL receptor complex uptaken into cell via receptor-mediated endocytosis

75
Q

What are the possible fates of dietary lipids once CM remnants have been cleared by the liver?

A

oxidized

re-esterified by ACAT and stored in lipid droplets

re-esterified by ACAT and packaged into TG-rich lipoproteins (called VLDLs)

76
Q

At what point is lipid absorption in the body considered “complete?”

A

after VLDL formation and VLDL transport of lipids + fat soluble vitamins from liver to peripheral tissue

77
Q

Which tissue/organ is primarily responsible for clearing CM remnants?

A

liver

78
Q

What are the three major nutrients of humans?

A

sugars

protein

lipids

79
Q

What is the most dense component of the human diet?

A

fat is the most dense, in terms of kcal/mol

80
Q

Describe the effect of fatty acid “bending” on membrane fluidity.

A

bending → can’t pack as closely → more fluid

81
Q

What is the primary structural difference between animal sterols and plant sterols?

A

the difference is in the side chains

82
Q

In what structure do mixed micelles form?

A

duodenum

83
Q

(T/F) Cholesterol in the diet is essential.

A

False. Cells can produce cholesterol endogenously.

84
Q

(T/F) Triacylglycerol in the diet is essential.

A

True. Triacylglycerols are the primarily fuel/energy source.

85
Q

Describe the relationship between ApoB-48, ApoB-100, enterocytes, and hepatocytes.

A

The ApoB protein is expressed in both enterocytes and hepatocytes. However, in enterocytes, cytosine deaminase introduces a premature stop codon that results in 48% of the protein being expressed.

In short: ApoB-100 found in hepatocytes; ApoB-48 found in enterocytes

86
Q

Mutatins in the Sar1b protein would result in what clinical presentations? (3)

A

skinniness

no appetite

indigestion

87
Q

(T/F) ApoB never leaves the chylomicron.

A

True. Unlike ApoCII and ApoAI, it never leaves the chylomicron.

88
Q

Why are chylomicrons transported to circulation using the lympathic system instead of the normal portal circulation system?

A

this is in order to bypass the liver and go directly to other tissues

89
Q

What would be the complaints of a patient in whom ApoB is mutated/defective? (3)

A

gas/bloating

lack of appetite

failure to thrive

90
Q

What would be the complaints of a patient with a defective MTTP enzyme?

A

same complaints as someone without functional ApoB — only difference is in the inheritance pattern

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