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metab > lipids > Flashcards

lipids Flashcards

1
Q

what are the functions of lipids?

A
  1. energy store
  2. structural function (e.g. cell membranes)
  3. important signalling molecules
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2
Q

what are the essential FA in the body? (2)

A
  1. omega-3/a-linolenic acid (ALA) (required for DHA synthesis)
  2. omega-6/linolenic acid (LA) (required for AA synthesis)
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3
Q

what are fatty acids?

A

carboxylic acids w long aliphatic chains (saturated/unsaturated)

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4
Q

what are saturated fatty acids?

A
  • “anoic”
  • single bond in aliphatic chain, straight hydrocarbon chain
  • allows close packing of molecules→ maximise SA for intermolecular interactions→ higher mp/bp
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5
Q

what are unsaturated fatty acids?

A
  • “enoic”
  • > =1 double bond in aliphatic chain, bent hydrocarbon chain
  • kinked→ disrupts packing among molecules→ decrease SA for intermolecular interactions→ lower mp/bp
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6
Q

what are cis forms of unsaturated fatty acids?

A
  • naturally occurring
  • hydrocarbon chains are on the same side as the double bond
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7
Q

what are trans forms of unsaturated fatty acids?

A
  • mostly generated through hydrogenation in food industry
  • large consumption of trans fat→ increase low-density lipoprotein, decrease HDL→ increase atherosclerosis risk
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8
Q

what are triacylglycerol/triglycerides (TAG/TGs)?

A

glycerol backbone + 3 fatty acids (variable length, saturated/unsaturated)

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9
Q

where are TAGs/TGs synthesized? (2)

A
  1. liver: exports to extra hepatic organs
  2. adipose tissue: stored during fed state
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10
Q

how are components of TAGs/TGs synthesized?

A

glycerol
liver: direct glycerol uptake (fr CM) or fr DHAP (fr diet: glucose→ DHAP→ glycerol-3-phosphate)
adipose tissue: fr DHAP

fatty acids (x3)
liver: de novo synthesis fr glucose
adipose tissue: uptake (dietary and hepatic)

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11
Q

what is the composition of dietary lipids?

A

10%: cholesterol, cholesterol esters, phospholipids, fatty acids
90%: TAG

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12
Q

how are TGs/cholesterol esters/phospholipids digested?

A

TG: ingual/gastric/pancreatic lipase (TG→ glycerol + 2FA)
cholesterol ester: pancreatic esterase (CE→ cholesterol + FAs)
phospholipids: pancreatic phospholipase A2 (phospholipid→ lysophospholipid + FA)

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13
Q

what is the function of colipase?

A
  • secreted into intestinal lumen w pancreatic enzymes
  • counters displacement of lipase by bile salts at micelles→ anchors lipase @ lipid-aq interface→ increase activity of pancreatic lipase
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14
Q

what is the MOA of a drug that targets lipases for obesity control? + what supplement

A

orlistat
- irreversible inhibitor of gastric & pancreatic lipases→ decrease digestion/absorption of TGs→ excrete undigested TGs in feces
- also decreases fat soluble vitamin absorption→ needs vit ADEK supplements

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15
Q

what are the hormones released by the small intestine for lipid digestion? (2)

A
  1. CCK: stimulate bile salt + pancreatic lipase/colipase secretion
  2. secretin: stimulate HCO3- release from pancreas→ neutralise acidic chyme from stomach→ provides optimal pH for pancreatic digestive enzymes to work
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16
Q

what happens to lipids after absorption into small intestine? (3)

A
  1. reform initial lipids:
    - monoacylglycerol + 2FAs→ TAG
    - cholesterol + FA → cholesterol ester
    - lysophospholipid + FA→ phospholipid
  2. formation of nascent chylomicron
    - TAG, cholesterol esters, phospholipid + fat soluble vitamins→ form nascent chylomicron
    - ApoB-48 (produced by enterocytes) required for proper assembly of chylomicron
  3. export into lymphatic system
    - chylomicron transport out of enterocyte to lymphatics via exocytosis
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17
Q

what is the structure of lipoproteins eg chylomicrons?

A

outer layer
- single layer phospholipid: phosphate group face out; hydrophobic FA chains face inward
- embedded apolipoproteins: essential in structure, metabolism & function of lipoprotein particles

core (lipids)
- TAG, cholesterol esters

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18
Q

how do nascent CM get converted to mature CM?

A
  • movement from lymph nodes (nascent) into blood (mature)
  • HDLs in blood transfer apolipoproteins ApoE and ApoCII to nascent chylomicrons→ mature
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19
Q

what are the apoproteins on mature vs nascent chylomicrons?

A

nascent: ApoB48
mature: ApoCII, ApoE, ApoB48

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20
Q

what happens to mature chylomicrons in the blood? (4)

A
  1. ApoCII (LPL cofactor) activates LPL at capillary walls of muscles/adipose tissues (LPL synthesized & secreted by insulin)
    LPL: TG→ FAs + glycerol
  2. FA get taken up by muscles (→ATP) and adipose tissues (→TG for storage), glycogen by liver (lipogenesis)
  3. chylomicron remnants are taken up by liver (by ApoE)
  4. chylomicron remnants→ [lysosomal enzymes]→ FAs, glycerol, AA, cholesterol→ used by hepatocytes
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21
Q

nascent CM vs mature CM vs CM remnants? (2)

A
  1. apolipoproteins:
    nascent: ApoB48
    mature: ApoB48, ApoE, ApoCII
    remnants: ApoB48, ApoE
  2. CM remnant has low TG! (broken down to FA & glycerol by LPL)
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22
Q

what is hyperchylomicronemia?

A
  • LPL or ApoCII deficiency→ impair TG hydrolysis in mature CM→ high lvl of CM→ severe hypertriglyceridemia→ xanthomas (lipid buildup under skin due to foam cells)
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23
Q

what are the main differences between chylomicron and VLDL? (2)

A
  1. apolipoproteins: ApoB48 (CM) vs ApoB100 (VLDL)
  2. TG content: dietary (CM) vs hepatic (VLDL)
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24
Q

what are the similarities between CM and VLDL (2)

A
  1. apolipoproteins: ApoCII and ApoE
  2. function: both deliver TG to extrahepatic tissues
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25
Q

how are fatty acids synthesised?

A
  • from glucose→ glycolysis→ TCA cycle→ citrate→ [ATP citrate lyase]→ acetyl CoA→→→ LCFA-CoA
  • in hepatocytes cytoplasm
26
Q

what is the rate limiting enzyme of FA synthesis?

A

acetyl-coa carboxylase

27
Q

how does FA synthesis get regulated after a meal?

A

insulin (hormone)→ upregulate Acetyl-CoA carboxylase→ upregulate FA synthesis

28
Q

how does FA synthesis get regulated during fasting/exercise?

A

glucagon/epinephrine→ inhibit acetyl-coa carboxylase→ downregulate FA synthesis→ glucose conserved for energy production

29
Q

how is FA synthesis allosterically regulated? (2)

A

citrate: upregulate
LCFA-CoA: downregulate (pdt inhibition)

30
Q

what is steatosis + pathophysiology? (3)

A

accumulation of TG in hepatocyte vacuoles (fatty liver)
- AFLD, NAFLD

  1. increase FA synthesis→ increase TG synthesis
  2. TG synthesis rate> VLDL synthesis rate→ little TG exportation fr liver→ accumulates
  3. impaired VLDL secretion
31
Q

what is the function of VLDL?

A

to deliver hepatic TAG to extra-hepatic tissues (FA of TAG in VLDL are synthesized by hepatocytes via de novo lipogenesis)

32
Q

how is VLDL formed?

A

synthesized in the liver→ secreted to blood as nascent VLDL (contains ApoB100)→ acquire ApoE & ApoCII fr HDL→ mature VLDL

33
Q

how does mature VLDL progress to IDL?

A

ApoCII on mature VLDL activates LPL at capillary wall of muscles/adipose
LPL converts TG→ FA + glycerol
FA: taken up by muscles (→ATP) and adipose tissues (→ TG for storage)
glycerol: taken up by liver

VLDL→ IDL (less TG→ increase density)

34
Q

compare nascent/mature VLDL to IDL to LDL (3)

A
  1. apolipoproteins:
    nascent VLDL: ApoB100
    mature VLDL: ApoB100, ApoE, ApoCII
    IDL: ApoB100, ApoE
    LDL: ApoB100
  2. TG levels:
    nascent/mature VLDL: same
    IDL: low TG (broken down to FA & glycerol by LPL)
    LDL: no TG (removed by HTGL)
  3. cholesterol/cholesterol esters (all contain same amt :)
35
Q

what happens to IDL? (2)

A
  1. forms LDL:
    - transfers ApoE to HDL
    - removes TG by hepatic triacylclycerol lipase (HTGL)
  2. binds to APoER on hepatocytes→ endocytosis→ degraded
36
Q

what happens to LDL? (2)

A
  1. ApoB100 binds to LDLR on hepatocytes→ endocytosis→ degraded
  2. taken up by extra-hepatic tissues via ApoB100 binding to LDLR→ delivers cholesterol/CE
37
Q

how is LDL uptake by extra-hepatic tissue regulated?

A

sufficient cholesterol→ downregulation of LDLR→ decrease LDL/cholesterol uptake

38
Q

what can go wrong with LDL uptake by extra-hepatic tissues?

A

e.g. lack of LDLR on liver: LDL can get oxidised in blood circulation→ taken up by scavenger receptors on macrophages→ foam cells→ atherosclerosis

39
Q

what is the function of HDL? (2)

A
  1. transfers ApoCII and ApoE to nascent chylomicrons and nascent VLDLs→ mature :)
  2. reverses transport of C/CE fr extrahepatic tissue to liver

nascent HDL is synthesised in liver/small intestines

40
Q

how does HDL directly reverse C/CE transport? (3)

A
  1. HDL take up C fr extrahepatic tissues, convert to CE
  2. lipid-rich HDL (HDL2) bind to SR-B1R on liver→ release C/CE, TG removed by HTGL
  3. lipid poor HDL (HDL3) released, continue picking up more C from extrahepatic tissues
41
Q

how does HDL indirectly reverse C/CE transport? (3)

A
  1. HDL exchange CE for TG with VLDL via CETP (cholesterol ester transfer protein)
  2. loss of TG converts VLDL→IDL→ LDL
  3. IDL and LDL can transport CE back to liver via ApoER and LDLR-mediated endocytosis respectively
42
Q

what is the difference in the transfer of cholesterol from HDL to liver vs LDL/VLDL?

A
  • direct HDL transfer DOES NOT require endocytosis of whole lipoprotein
  • indirect IDL/ LDL transfer require endocytosis of whole lipoprotein
43
Q

how are FAs stored in adipose tissue?

A
  • stored as TG (glycerol + FA)
    FA: insulin stimulates LPL synthesis/secretion→ ApoCII (VLDL, CM) activate LPL→ FA taken up by adipose tissues, glycerol taken up by liver
    glycerol: insulin activates glycolysis of glucose→ DHAP→ G3P (TG backbone)
44
Q

how is lipolysis regulated during fasting state?

A

glucagon→ activates HSL (hormone sensitive lipase)→ converts TG to FAs + glycerol→ FAs transported as FA-albumin in blood to liver and muscles, glycerol transported to liver

45
Q

why is long chain FA a good energy source? (2)

A
  1. oxidation produces fatty acyl-CoA that allows further rounds of oxidation→ produce more acetyl CoA
  2. oxidation of fatty acyl-CoA also produces FADH2 and NADH→ ETC→ ATP production
46
Q

how is FA oxidation and lipogenesis regulated after feeding?

A

increase glucose→→→ citrate→ acetyl CoA→ [ACC]→→ malonyl CoA→ FA synthase→ increase lipogenesis

malonyl CoA is negative allosteric modulator of CPT1→ inhibits FA oxidation

47
Q

what are ketone bodies? (3)

A
  1. acetoacetate
  2. B-hydroxybutyrate
    impt energy fuel for extrahepatic tissues
  3. acetone
48
Q

where are ketone bodies produced/ketogenesis?

A

produced in the mitochondria of hepatocytes

49
Q

what is the purpose of ketogenesis?

A

to produce ketones thats can be broken down (ketolysis) under fasting conditions to generate acetyl CoA→ TCA cycle→ ATP generation

50
Q

how does ketogenesis occur? (2)

A

fasting→ glucagon!!
1. glucagon inhibits ACC (FA synthesis)→ no malonyl CoA→ increased B-oxidation (FA breakdown)→ generates acetyl CoA
2. glucagon upregulates HSL→ converts TG to FA & glycerol (lipolysis)→ FA-albumin travels into liver→ catabolysed to acetyl CoA

acetyl CoA enters ketogenesis pathway in the liver

51
Q

where does ketolysis occur?

A

mitochondria of extrahepatic tissue (liver don’t have 3-ketoacyl-CoA transferase needed for ketolysis)

52
Q

how does ketolysis occur?

A

ketone bodies move into extrahepatic tissues→ undergo ketolysis→ generates acetyl CoA→ TCA cycle→ ATP generation :)

53
Q

how does type 1 DM cause ketoacidosis?

A

type 1 DM→ low insulin, high glucagon→ stimulates HSL (lipolysis)→ increase FA→ increase B-oxidation in liver→ increase acetyl CoA→ increase ketogenesis→ ketogenesis»ketolysis→ ketoacidosis→ ketonuria

54
Q

what is the function of cholesterol?

A
  1. maintains cell membrane rigidity & fluidity
  2. precursor for key molecules synthesis e.g. bile acids, vit D, steroids
55
Q

what are the sources of the hepatic cholesterol pool? (3)

A

cholesterol is stored in liver
1. dietary cholesterol (chylomicron remnants)
2. de novo synthesis in the liver
3. cholesterol from extrahepatic tissues (reverse cholesterol transport by HDL)

56
Q

what happens to the cholesterol in the hepatic cholesterol pool? (3)

A
  1. transported in VLDL/IDL/LDL
  2. converted to bile acids/salt
  3. small amount excreted in bile
57
Q

where does cholesterol synthesis take place?

A
  • occurs in the liver (cytoplasm & ER)
  • all carbons are derived from acetyl CoA
58
Q

what is the rate limiting step of cholesterol synthesis?

A

HMG-CoA reductase

59
Q

how is cholesterol synthesis regulated by hormones? (2)

A

anabolic process→ should only be activated if nutrients are readily available (not when limiting)

insulin:
- upregulate chol synthesis
- activates phosphatase→ dephosphorylate (activate) HMG-CoA reductase

glucagon:
- inhibit chol synthesis
- activate protein kinase→ phosphorylate/deactivate HMG-CoA reductase

60
Q

how is cholesterol synthesis allosterically regulated? (2)

A

AMP (low ATP): activates AMP-activated protein kinase→ phosphorylates/deactivates HMG-CoA reductase
phosphatase: dephosphorylates/activates HMG-CoA reductase

61
Q

how is cholesterol used in the synthesis of bile acids?

A

cholesterol→ [7a-hydroxylase]→→ primary bile acid→ feedback inhibition

62
Q

how is cholesterol used in the synthesis of vit D3?

A

7-dehydrocholesterol (immediate precursor of cholesterol)→ [uv light]→ cholecalciferol (Vit D3, fr diet)→→ calcitrol (active vit D3)

metab (11 decks)

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