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MBOD Week 13 > Lipoprotein Metabolism (end of cholesterol) > Flashcards

Lipoprotein Metabolism (end of cholesterol) Flashcards

1
Q

What cholesterol importer is located on enterocytes in the ileum and to a lesser extent in the colon and kidney?

A

ASBT

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2
Q

What cholesterol exporter is located on enterocytes in the ileum and to a lesser extent in the colon and kidney?

A

OST-alpha/beta

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3
Q

What is phase I bile composition?

A

-Bile is a micellular liquid

Composition:

  • Bile Salts: Moderate amount (40-90%)
  • Cholesterol: Low ( 85%)
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4
Q

What is the precursor for all steroid hormones?

A

Cholesterol

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5
Q

Where are glucocorticoids made (be specific)?

A
  • Adrenal Cortex (zona fasciculata and zona reticularis)

* Cortisol = glucocorticoid

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6
Q

Where are mineralcorticoids made (be specific)?

A
  • Adrenal Cortex (zona glomerulosa)

* Aldosterone = mineralcorticoid

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7
Q

Where are sex hormones made (be specific)?

A
  • Made in testis and ovary

* Androgens and estrogens = sex hormones

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8
Q

When is cortisol released?

  • regulation
  • effects
A
  • Released in response to stress
  • MOST POTENT glucocorticoid

effects:

  • Gluconeogenesis, and glycogen synthesis stimulated
  • Protein Catabolism
  • ANTI-inflammatory
  • Inhibits leukocyte migration
  • Na+ retention (swelling)
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9
Q

What result does cortisol have on an infection?

A

Infection may persist because it prevents leukocyte migration

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10
Q

What disease state might result from cortisol stimulating gluconeogenesis and glycogen synthesis?

A

Diabetes

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11
Q

Estradiol

  • Where is it produced?
  • What does it do?
A
  • Produced in ovarian granulosa cells
  • Has an affect on bone turnover
  • This is why post menopausal women are more susceptable to osteoporosis
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12
Q

What is the precursor for estrodiol?

A

Testosterone

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13
Q

What disease results from a 21-hydroxylase deficiency?

A

Congenital Adrenal Hyperplasia

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14
Q

What causes the ambiguous genitalia in patients with Congenital Adrenal Hyperplasia?

A

21-hydroxylase Deficiency leads to build up of 17-hydroxyprogesterone that is converted to testosterone

  • This masculinizes female infants
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15
Q

Why is microgenitalia not the biggest issue for patients with Congenital Adrenal Hyperplasia?

A
  • Along with not being able to make estrodiol they also don’t make CORTISOL and ALDOSTERONE
  • No aldosterone means you pee all your Na+ (and thus H2O) out and get dehydrated
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16
Q

What needs to happen for Vitamin D to get activated?

- name of activated species

A

1 C-25 hydroxylation in the liver

2 Hydroxylations

Final METABOLICALLY ACTIVE product = 1,25-dihydroxycholecalciferol

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17
Q

What the sources of Vitamin D?

- biggest contributor

A

MAJORITY made by Malpighian layer of the epidermis by SUNlight

Small amounts also come from the diet

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18
Q

What does the active form of Vit D. (1,25-dihydroxycholecaliferol) do?
(3 things)

A
  • Stimulates expression of genes involved in intestinal absorption of calcium
  • Recruits stem cells to make osteoclasts that mobilize Calcium form bone
  • MAJOR EFFECT is to get correct Ca2+ and phosphate balance
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19
Q

Where is Vitamin D synthesis most highly regulated?

A
  • Renal Hydroxylation by 1 alpha-hydroxylation

liver hydroxylation is only loosely regulated

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20
Q

What are the regulators of 1 alpha-hydroxylase in the kidney?

A

(+) PTH (induced by low Ca2+ in blood)
(+) Hypocalcemia
(+) Hypophosphatemia

(-) Fibroblast Growth Factor 23 from osteocytes

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21
Q

What does vitamin D deficiency lead to in adults and in children?
- causes

A

Children - Rickets
Adults - Osteomalacia

Causes:

  • no sunlight
  • Liver or Kidney Disease
  • Genetic defects of Vit D receptor
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22
Q

Why would liver or kidney disease cause osteomalacia?

A
  • You can’t complete one of the two hydroxylation steps needed to get to the active form
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23
Q

What is Rachitic Rosary?

A
  • swelling of costochondral junctions resulting from rickets
24
Q

What is the cause of biliary rickets?

A
  • Lack of bile production
  • Vit D. is fat solubule so it can’t be absorbed without bile
  • Lack of vitamin D = bad
25
Q

What is the purpose of lipoproteins?

A
  • They provide a thermodynamically stable particle to transport lipid through the bloodsteam
26
Q

What type of Lipoproteins are made by the liver?

A
  • VLDLs
  • LDL (from VLDL)
  • HDL
27
Q

What type of lipoprotein is important in reverse cholesterol transport?

A

HDLs

28
Q

What types of lipoproteins are made by the intestines?

A
  • Chylomicrons

- Small amounts of VLDL and HDL

29
Q

Why are Apo proteins need in lipoproteins?

A
  • Assembly
  • Assembly
  • Secretion
  • Interaction with the appropriate enzymes
30
Q

Why do lipoproteins get worse for you as you progress from Chylomicron toward LDL?

A
  • The cholesterol is becoming more concentrated in the particle
31
Q

If Lipoproteins get worse for you as they get small, then why are HDLs good for you?

A
  • Because they participate in reverse cholesterol transport
32
Q

What 3 pathways exist for lipoproteins?

A
  1. Exogenous Pathway (Chylomicrons)
  2. Endogenous Pathways (VLDL)
  3. Reverse Cholesterol Transport back to liver (HDL)
33
Q

Where are lipoproteins produced?

A

Liver and Small Intestine

34
Q

What is the only apoliprotein that stays with the lipoprotein throughout its lifetime?

A

Apo B

35
Q

What are the 2 types of Apo B?

  • structural difference
  • functional difference
A
  • ApoB-100 and ApoB-48 (from same mRNA transcript)

ApoB-100

  • VLDL packaging
  • LDL RECEPTOR BINDING DOMAIN

Apo-48

  • Chylomicron Packaging
  • NO LDL RECEPTOR
36
Q

Apo A-1

  • Produced where?
  • associated lipoprotein type?
  • What does it do?
A
  • Produced in liver and small
  • apolipoprotein of plasma HDL
  • Its a co-factor for LCAT
37
Q

What is LCAT and what does it do?

A
  • Lecithin Cholesterol Transferase (LCAT)

- Esterfies Fatty acid from LECITHIN onto free cholesterol to make HDL

38
Q

How does ApoB mRNA editing happen?

A
  • ApoB 100 and 48 are synthesized from the same gene
  • ApoB 48 has a stop codon in the middle inserted by a single basepair change that shortens the protein (excludes LDL binding domain)
39
Q

What is APOBEC-1?

A
  • ApoB editing complex
40
Q

How does APOBEC-1 work?

A
  1. Binds the ApoB gene at MOORING SEQUENCE

2. Mooring sequence lines it up to change a single residue resulting in ApoB 48 and not 100

41
Q

Apo A-IV

  • Location
  • associated lipoprotein
A

“Jack of all Trades”
- Produced by intestine

  • Secreted with Chylomicrons
42
Q

What does Apo A-IV do?

A
  • Activate LCAT
  • Facilitate Reverse Cholesterol transport
  • Lipid ANTIOXIDANT
  • SATIETY INDICATOR
  • Prevent atherosclerosis
  • Allow packaging of absorbed lipids into CHYLOMICRONS
43
Q

When is the packaging of absorbed lipids into chylomicrons most important?
- What protein helps in this packaging?

A
  • In neonates its important to getting more fat into breast milk
  • ApoA-IV
44
Q

Apo C-II

  • associated lipoprotein
  • job
A
  • VLDL, HDL, chylomicrons

- activates LPL

45
Q

what links LPL to capillaries in muscle and adipose tissue?

A
  • Heparan Sulfate Proteoglycans
46
Q

What activates LPL?

A

Apo CII

47
Q

What does LPL do?

A
  • Hydrolyzes triglyceride in VLDL and chylomicrons to liberate free fatty acids for OXIDATION (muscle) or STORAGE (fat)
48
Q

Does does Hepatic Lipase (HL) do?

A
  • helps absorb remnants of chylomicrons into liver
49
Q

What is Lecithin:Cholesterol Acyltransferase (LCAT)?

A
  • Catalyzes transfer of fatty acid from LECITHIN (phosphatidylcholine) to free cholesterol in HDL

AKA ESTERIFIES IT

50
Q

What process does LCAT play an important role in?

A
  • Reverse Cholesterol Transport back to the liver
51
Q

What is the rate limiting enzyme in cholesterol synthesis?

A

HMG-CoA reductase

52
Q

What does ACAT do?

A
  • conversion of free cholesterol to cholesterol ester in cells for STORAGE

**Note: similar function as LCAT except LCAT works in reverse cholesterol transport

53
Q

What type of receptor recognizes apoB-100 and apoE?

A

LDL Receptor

54
Q

What plays a role in uptake of remnant lipoproteins?

  • hepatic
  • cellular
A
  • LDL receptor-related protein in hepatocytes

- LDL receptor in cells

55
Q

What is the difference between LDL receptors and LDL receptor-related protein (LRP?)

A
  • LDL receptor takes up LDL
56
Q

What does Scavenger Receptor-BI (SR-BI) job?

A
  • Mediates hepatic uptake of cholesteryl ester from HDL in reverse cholesteol Transport

MBOD Week 13 (7 decks)

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