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Biochemistry > Block 3 Lipid Absorption & Transport > Flashcards

Block 3 Lipid Absorption & Transport Flashcards

1
Q

What are the major dietary lipids?

A

TGs, C, CE (chol esters), PL, FFA

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2
Q

Where does metabolism of dietary lipids happen?

A

Proteolytic digestion in small int lumen
Absorption into enterocytes
Re-synthesis of major lipid classes in enterocytes
Transport in lymph, blood
Utilization by peripheral tissues & storage by adipose tissue

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3
Q

What kind of degradation happens in stomach, duodenum, and jejunum?

A

St: lingual & gastric lipases (infants)
Duo: Emulsification (chemical by bile salts, mechanical by peristalsis)
Jej: Proteolysis (panc enzymes)

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4
Q

How do TG, PL, CE, and FA change from mouth to stomach to small intestine?

A

Highly hydrophobic to stomach (TG limited and <C12, FA limited); in SI, hydrophilic mixed micelles

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5
Q

What form do TG, PL, CE, and FA take in the small intestine?

A

TG: 2-MAG + FA
PL: glycerylphosphorylbase
CE: cholesterol + FA
FA: FA

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6
Q

What are bile salts?

A

Amphipathic molecules that increase SA/V ratio for interaction with lipases

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7
Q

What are lipases?

A

Carboxylesterases acting on long chain acylglycerols, act at lipid/water interface

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8
Q

What lipases act on exogenous and endogenous lipids?

A

Exo: pancreatic (& lingual, stomach, mucosal, some phospholipase)
Endo: lipoprotein, hepatic, hormone-sensitive (& some phospholipase)

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9
Q

How are TAGs degraded by pancreatic lipase?

A

Removes FA of all chains lengths at C1,3. Colipase reduces surface tension to stabilize. Product: MAGs & FAs stabilized by bile salts.

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10
Q

How are cholesteryl esters degraded by esterase?

A

Hydrolyzed by pancreatic cholesteryl ester hydrolase (cholesterol esterase) –> free chol and FA

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11
Q

How are phospholipids degraded by phospholipase?

A

PLA2 from pancreas activated in int lumen by trypsin. Removes FA at C2 -> lysoPL. Lyso-PLase removes FA at C1 -> glycerylphosphorylbase for excretion or degradation/absorption

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12
Q

Where is the main site of absorption of mixed micelles? What happens to bile salts?

A

Brush border membrane of enterocytes; BS remains in gut, extensively reabsorbed in ileum (95%)

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13
Q

Where are micelles of short and medium chain FFA absorbed?

A

They don’t need micelles for absorption

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14
Q

What is DGAT?

A

Diglycerol acyltransferase converts passively diffused 2 FA + monoglyceride -> TG

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15
Q

How is cholesterol absorbed in enterocyte?

A

Taken up by NPC1L1-R, pumped out of cell by ABCG5/G8. *Same transporters for non-chol plant sterols

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16
Q

What’s the difference in absorption of chol and non-chol sterols & why?

A

Chol: 50-60% absorbed
Non: 1-5% absorbed
ABCG5/G8 transporter more efficient with non-chol sterols

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17
Q

What happens to the cholesterol that isn’t pumped back out through ABCG5/G8?

A

Esterified by acyl-coenzyme cholesterol acyl-transferase (ACAT) into cholesteryl esters

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18
Q

What are the major approaches to reduce cholesterol absorption?

A

Increase dietary intake plant sterols (stanols/phytosterols, Benecol) or antagonize NPC1L1 transporter (Ezetimibe/Zetia)

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19
Q

What is lipid malabsorption?

A

Loss of lipids (including lipo-soluble vitamins & essential FAs); steatorrhea; perhaps reduced bile acids synthesis, secretion deficit of panc enzymes, defective enterocytes

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20
Q

How are TG and CE resynthesized in the enterocyte?

A

Acyltransferases specific to chol and TG; use activated LCFFA for esterification (act by fatty acyl CoA synthetase/thiokinase)

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21
Q

How are SCFA and MCFA secreted from intestinal cells? Cholesterol, FFA, acyglycerols, & partly hydrolyzed PLs?

A

SC/MC: bind to albumin, secreted into portal circulation, transported to liver
Other lipids: chylomicrons -> lymph

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22
Q

What is a lipoprotein?

A

Macromolecular complex of different lipids and apolipoproteins; surface Apo & PLs, intermediate free chol, core of TG and CE

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23
Q

What is transported by chylomicrons, VLDL, LDL, and HDL?

A

Ch: exogenous TG
VLDL: endogenous TG
LDL: endo chol (liver to peripheral tissues)
HDL: endo chol (per to liver)

24
Q

How does size, density, and lipid/protein ratio change among the 4 classes of LPs?

A

Chylos are biggest, least dense, with highest L/P ratio. HDLs are smallest, densest, and lowest L/P ratio.

25
Q

How does affinity for LPL, density, and atherogenicity ratio differ among the 4 classes of LDL?

A

LDL 1 is least dense, with highest affinity for LPL and least atherogenicity. LDL 4 is the opposite.

26
Q

What are the functions of apolipoproteins?

A

Bind and emulsify lipids, ligands for Apo receptors involved in lipid uptake (ApoE,B), cofactors for enzymes involved in lipoprotein metabolism (Apo A-1, C-2)

27
Q

What are the following apolipoproteins associated with and what are their functions: B48, B100, C2, C3, E, A1?

A

B48: chyl for assembly, exocytosis chylos
B100: VLDL, IDL, LDL to bind LDL-R
C2: chyl, VLDL, IDL, HDL to activate LPL
C3: chyl, VLDL, IDL, HDL to inhibit LPL
E: chyl, remnant, VLDL, IDL, HDL to bind LDL-R
A1: HDL to activate LCAT

28
Q

Where are chylomicrons assembled? What happens with a lack of ApoB48?

A

Lipids in SER, proteins in RER. Assembly in Golgi; secreted in lymph by exocytosis; B48 deficit -> TG accumulation in intestinal cells (congenital abetalipoproteinemia)

29
Q

What is MTP (microsomal transfer protein)?

A

Involved in lipid then TG transfer to ApoB48 and maturation of chylos. Also involved in lipidation of ApoB100 and assembling VLDL in liver.

30
Q

How do chylomicrons mature?

A

While circulating in blood and lymph, they acquire ApoC2 and ApoE from HDLs

31
Q

What do ApoC2 and ApoE do?

A

C2: assists degradation of TG by lipoprotein lipase
E: recognized by receptors in liver and help remove partially digested chylos from bloodstream

32
Q

What enzyme is responsible for TG hydrolysis in capillaries?

A

Lipoprotein lipase

33
Q

Where is Lp lipase synthesized, and how is it transported?

A

Synth in adipose, muscle (cardiac), lactating mammary glands; transported on surface of capillary endothelium anchored via heparin sulfate PGs

34
Q

How do apoC2 and C3 affect Lp lipase? ApoE?

A

C2 required for activity, C3 inhibits activity; ApoE assists clearance of chylomicron remnants (lack -> familial type 3 hyperlipoproteinemia)

35
Q

What are the products of lipoprotein lipase activity?

A

Releases 3 FA from TG. Glycerol -> Gly-3-P in liver, FA -> adipose/mm, chylo -> remnants

36
Q

How are mm and adipose LPL different?

A

Isoenzymes; mm (cardiac): low Km, unaltered in fed state, increased/unaltered in fasted/exercise
Adipose: high Km, increased in fed state (insulin), no effect in fasted state

37
Q

What are the major steps of TG synthesis? Where are they stored?

A

Generation of glycerol backbone from glucose, activation FFA, synthesis of TG; adipocyte and hepatocyte

38
Q

What enzyme is missing in adipose that is present in liver? How is Gly3P made then?

A 
Glycerol kinase (gly -> Gly3P)
Glucose -> DHAP + NADH -> Gly-3P
39
Q

How is Gly-3P modified to make TAG?

A

Gly3P + 2 FACoA -> phosphatidic acid - Pi -> DAG + FACoA -> TAG

40
Q

How does fat accumulation differ in fed and post-absorptive states?

A

In fed state, insulin upregulates adipose LPL on cap endo & GLUT-4. Post-ab: low insulin = lower LPL, downregulated GLUT-4. Most FA bound to albumin for B-ox

41
Q

How are VLDL TGs synthesized?

A

In liver, glycerol kinase converts glycerol to Gly3P; glucose -> DHAP -> Gly-3P -> PA (Gly3P PAT & Acyl-3P AT) -> TG (Pase & DGAT)

42
Q

What enzymes are important for final step of CE and TG synthesis in liver?

A

CE: ACAT
TG: DGAT

43
Q

What is MTTP?

A

Microsomal TG transfer protein in liver ER lumen helps assemble VLDL & transfer lipids to ApoB100 while being translocated into ER during translation

44
Q

How does VLDL change as it is secreted from liver and cleared from circulation?

A

Released with ApoB100 and ApoA1, + C2 and E from HDL, exchanges lipids with HDL (cat by CETP). ⅔ cleared by liver, ⅓ hydrolyzed by LPL (becomes IDL)

45
Q

What stimulates VLDL synthesis by the liver?

A

Excessive consumption calories, alcohol, carbs; high concentration FFA reaching liver

46
Q

What do LDLs do, and how are they made?

A

Major delivery route for cholesterol (endocytosis by LDL-R) & major plasma chol carrier (high chol & CE) & atherogenic LP, formed by sequential hydrolysis VLDL by LPL, contains only ApoB100

47
Q

Where is HDL produced? ApoA1 and A2?

A

HDL: liver & intestine (coalescence of individual PL-Apo complexes)
A1: liver & intestine
A2: liver only

48
Q

What are the major potential targets for atherosclerosis therapies?

A

HDL-assc apo: ApoA1 & E
HDL-modifying plasma enzymes & transfer proteins: LCAT, CETP, LPL, hepatic lipase
Cellular/cell-surface proteins influencing HDL metabolism: ABCA1, ABCG1, SR-B1

49
Q

What is the function of HDL?

A

Major cholesterol carrier from peripheral tissues back to liver

50
Q

What are lipid poor ApoA1 (pre-HDL), nascent (pre-beta) HDL, and mature (alpha) HDL?

A

Lipid poor: smallest HDL with little PL, no chol
Nascent: produced after free chol acquired from per tissues
Alpha: following chol esterification by LCAT & exchange of CE for TG with VLDL, LDL (by CETP), can acquire more free chol from per tissues

51
Q

What is CETP?

A

Exchanges CE from HDL for TG from VLDL/LDL (ApoB-containing)

52
Q

What is hepatic lipase?

A

Hydrolyzes TG to convert HDL2 to HDL3 (CE enriched, smaller), which can be cleared by the kidney

53
Q

What are desirable LDL/HDL ratio and cholesterol levels in mg/dl?

A

Low LDL/HDL protective against coronary heart disease, Total/HDL >4.5 risk factor
Desired: total chol 60

54
Q

What lipid levels indicate diabetic dyslipidemia?

A

High TG, LDL & low HDL

55
Q

What are the goal ApoB levels for highest-risk and high-risk patients with CMR and lipoprotein abnormalities?

A

Highest: ApoB <80

Biochemistry (17 decks)

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