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3) Metabolism and Human Nutrition > Textbook and Required Readings (Midterm) > Flashcards

Textbook and Required Readings (Midterm) Flashcards

1
Q

What are the three principal lipid components of bile?

A

Bile salts, pancreatic lipase, and sterols

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2
Q

What is bile?

A

The emulsifying fluid produced by the liver

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3
Q

Which fatty acids are resistant to hydrolysis by lipase?

A

FAs linked at the sn-2 position of MGs, PLs, and CEs

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4
Q

Under what form is cholesterol present in bile?

A

Unesterified form

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5
Q

How does phospholipase differ from pancreatic lipase?

A

Phospholipase cleaves FAs at the sn-2 position of PLs

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6
Q

Where is biliary cholesterol absorbed?

A

At a site more proximal than diet-derived cholesterol within the small intestine

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7
Q

What is the function of ABCG5 and ABCG8? Where are they found?

A

CH efflux proteins on the apical surface of the intestinal enterocyte

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8
Q

What do mutations in ABCG5 and ABCG8 cause?

A
  • Phytosterolemia

- Hyperabsorption of plant sterols and premature atherosclerosis

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9
Q

What explains the low absorption efficiency of phytosterols?

A

1) Apical ABCG5 and ABCG8 transporters possess high affinity for phytosterols and preferentially excrete them back into the intestinal lumen
2) Inadequate esterification of phytosterols as ACAT dependent esterification of CH exceeds that of B-sitosterol

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10
Q

What are the functions of apolipoproteins?

A
  • Increase particle solubility

- Increase recognition by enzymes and receptors located at the outer surface of lipoproteins

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11
Q

What are the hydrophilic components in lipoproteins?

A

Phospholipid polar head groups and cholesterol hydroxyl groups

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12
Q

What forms the core of lipoprotein molecules?

A

Hydrophobic cholesterol esters and triglycerides

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13
Q

What does the exogenous transport system transfer?

A

Transfers lipids of intestinal origin to peripheral and hepatic tissues

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14
Q

What is the relation between MTP and Apo-B?

A

MTP transfers lipids onto nascent Apo-B particles to create chylomicrons

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15
Q

What kind of lipids do not require chylomicron incorporation?

A

FAs less than 14 carbons in length undergo direct internal transport via the portal circulation (direct delivery to the liver)

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16
Q

What do chylomicron TG-depleted remnant particles take up? Where are they taken?

A
  • Take up CE from HDLs

- Rapidly taken up by the liver

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17
Q

What is the function of ABCA1?

A

Mediate the efflux of cellular cholesterol and phospholipids to lipid-poor HDL

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18
Q

Where is Apo E synthesized? Where is it present?

A
  • In the liver

- On all forms of lipoproteins

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19
Q

Why is Apo E important?

A

In the hepatic clearance of TG-depleted chylomicron remnants

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20
Q

Where is LDL cleared from the plasma?

A
  • Liver
  • Adipocytes
  • Smooth muscle cells
  • Fibroblasts
  • All contain the LDLR
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21
Q

As HDL becomes enriched with CE, ______ and ______ are picked up from other proteins to form spherical HDL.

A

Apo-C-II and Apo-C-III

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22
Q

What does CETP exchange?

A
  • CE from HDL2 to VLDL and CM

- TG from VLDL and CM to HDL2

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23
Q

As a result of CETP’s action, what does HDL2 convert to?

A

Reconverts to HDL3

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24
Q

What is the consequence of manipulating ER calcium?

A
  • Causes the re-distribution of a portion of intracellular UC to a pool that is NOT available to the SCAP-SREBP complex
  • Not directly accessible to the components of the cholesterol-sensing mechanism
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25
Q

What is the consequence of a reduction in ER luminal calcium?

A
  • Increased abundance of nSREBP

- Increase in LDLR, FASN, HMGR

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26
Q

What kind of nuclear receptors are steroid receptors?

A

Homodimers

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27
Q

What kind of nuclear receptors are RXR receptors?

A

Heterodimer

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28
Q

How do co-regulators influence transcription?

A

Through chromatin remodeling with histone modifications

29
Q

What is the consequence of increased function of LXR?

A

Decreases cholesterol from the GI tract

30
Q

What are the two properties of the LDL receptor?

A
  • Allows large amounts of cholesterol to be delivered to the body
  • Keeps concentration of LDL in the blood low enough to avoid buildup (plaques)
31
Q

What is the second messenger responsible for suppressing HMGR activity?

A

Cholesterol generated from LDL within the lysosome

32
Q

What lipoproteins does LDLR bind?

A
  • Apo B-100

- Apo E

33
Q

Where is the largest amount of LDL receptors found?

A

In the liver

34
Q

What converts IDL to LDL?

A

TG hydrolysis and the departure of Apo E (Apo B-100 is remaining)

35
Q

What are the two reasons that explain why a deficiency in the LDLR causes LDL to accumulate?

A
  • Overproduction

- Delayed removal

36
Q

What are the four human genetic disorders that cause hypercholesterolemia?

A
  • FH
  • Autosomal recessive hypercholesterolemia
  • Sitosterolemia
  • Familial defective Apo B
37
Q

How is FH related to SREBP?

A
  • Mutations in the sterol-sensing region of SCAP blocks sterol regulation in SREBP processing
  • Activates SRE responsive genes (HMGCR, LDLR) if it senses low cholesterol (as it is in FH)
38
Q

How does LXR increase fatty acid synthesis?

A

By inducing SREBP-1c

39
Q

Which SREBP is implicated in glucose metabolism?

40
Q

How does vitamin A regulate the expression of specific target genes?

A

Through its binding to nuclear RARs and RXRs

41
Q

Mutations in which genes are linked to sitosterolemia?

A

ABCG5 and ABCG8 in intestinal enterocytes

42
Q

Where is Apo E synthesized?

A

In the liver

43
Q

What does HDL exchange with chylomicrons in circulation?

A
  • HDL exchanges Apo E and Apo C

- CM exchange Apo A-I and Apo A-IV

44
Q

What does CETP convert?

A

HDL2 to HDL3

45
Q

Genes account for approximately 2% of the total human DNA sequence, what makes up the rest?

A

Non-coding DNA, which serves structural and/or regulatory or no known roles

46
Q

Which kind of polymorphism is heritable? Why?

A
  • SNPs

- Because they are present in the germ line

47
Q

What are SNPs?

A

Nucleotide base pair differences in the primary sequence of DNA

48
Q

Differentiate synonymous and non-synonymous SNPs.

A
  • Synonymous are silent

- Non-synonymous result in AA replacement

49
Q

What is the consequence of CETP deficiency?

A

Causes high plasma levels of HDL

50
Q

What is the consequence of Tangier disease? What is it caused by?

A
  • Nearly total absence of HDL

- Molecular lesion in ABCA1 gene

51
Q

What are the consequences of abetalipoproteinemia?

A
  • Failure to thrive, vitamin deficiencies (particularly E)

- Low plasma levels of CM, VLDLs, and LDLs

52
Q

Which genetic disorders cause elevated LDL?

A
  • FH
  • PCSK9
  • Familial defective Apo B
  • Autosomal recessive hypercholesterolemia
53
Q

Which genetic disorders cause elevated HDL?

A
  • CETP deficiency

- Hepatic lipase deficiency

54
Q

Which genetic disorders cause low HDL?

A
  • Tangier disease
  • LCAT deficiency
  • Apolipoprotein A-1 deficiency
55
Q

Which genetic disorders cause low TG or cholesterol?

A

Abetalipoproteinemia

56
Q

What is FH treated with?

A

Combination of statin and ezetimibe

57
Q

What is phytosterolemia treated with?

58
Q

What is the function of MTP?

A
  • Allows for the combining of Apo B-48 with TG for the secretion of CM particles in the intestine
  • Allows for the combining of Apo B-100 for secretion of VLDL in the liver
59
Q

Which apolipoproteins are not present in abetalipoproteinemia? Which ones are?

A
  • No Apo-B particles are present

- Only HDLs

60
Q

Is bacteroidetes good or bad?

A
  • Good: comprise >98% of normal gut microbiota with firmicutes
  • Bacteria
61
Q

Is lactobacillus good or bad?

A
  • Good, used in the food industry (probiotic)

- Firmicutes

62
Q

is C. difficile good or bad?

A
  • Bad

- Firmicutes

63
Q

Is bifidobacteria good or bad?

A
  • Good

- Actinobacteria

64
Q

Is streptomyces hygroscopicus good or bad?

A
  • Good

- Actinobacteria

65
Q

Is H. pylori good or bad?

A
  • Bad

- Proteobacteria

66
Q

Is methanobrevibacter smithii good or bad?

A
  • Associated with obesity

- Necessary, but may be bad in large quantities

67
Q

Is pichia anomala good or bad?

A
  • Good

- Eukarya

68
Q

Is a bacteriophage good or bad?

A
  • Good

- Viruses that attack bacteria (phage therapy)

3) Metabolism and Human Nutrition (17 decks)

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