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Cardiovascular Medicine > Lipids Metabolism > Flashcards

Lipids Metabolism Flashcards

1
Q

biological functions of lipids

A
  1. principal source of stored energy
  2. major structural elements of biological membranes e..g, phospholipids, glycolipids and cholestrol
  3. play important roles in metabolism: enzyme cofactors, electron carriers, emulsifying agents in the digestive tracts
  4. intra and inter signalling event: precursors of steroid hormones
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2
Q

are triglycerides hydrophobic or hydrophilic?

A

hydrophobic

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3
Q

what is beta oxidation

A

oxidative process that releases free energy from breaking down fatty acid chains to CO2 and H2O.

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4
Q

the process of beta oxidation

A

Palmitoyl CoA–(acyl dehydrogenase)/FAD-FADH2–> Enoyl CoA–(enoyl CoA hydratase)/H2O—> b-hydroxyacyl-CoA—(b-hydroxyacyl-dehydrogenase)/NAD+-NADH–>b-ketoacyl-CoA—(b-ketothiolase)–> Acetyl Coa and 14C CoA

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5
Q

how many NADH, FADH2 and Acetyl CoA does beta oxidation yeild?

A

1 NADH, 1 FADH2, 1 Acetyl CoA

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6
Q

how many ATP does one NADH yield

A

3 ATP

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7
Q

how many ATP does one FADH2 yield

A

2 ATP

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8
Q

how many ATP does one Acetyl CoA yield

A

12 ATP

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9
Q

how many ATP does palmitoyl CoA yield

A

131-2=129 ATP (2 used for the beta oxidation process)

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10
Q

how does glucagon regulate lipid metabolism

A

triglycerides are broken down to glycerol and fatty acid chains by hormone sensitive lipase.
When blood glucose levels drop, the pancreas produces glucagon which triggers further release of lipase and increases the breakdown of stored triglycerides into glycerol and fatty acids which can be used to produce energy

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11
Q

where does the addition of CoA to fatty acid happen and what enzyme??

A

once inside the target cell where the fatty acid can be metabolised- which is any cell with mitochondria, but mostly liver cells.
Fatty Acid —(fatty acyl CoA synthetase)/ATP-ADP—> Fatty acyl CoA

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12
Q

why is the carnitine shuttle system used

A

Acetyl CoA cannot cross the mitochondrial membrane and the fatty acid CoA needs to access the mitochondrial matrix to be able to be metabolised. Therefore the carnitine shuttle system is used.

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13
Q

explain the carnitine shuttle system

A

Fatty-acyl CoA + Carinitine Acyltransferase 1 (CAT1) -> Fatty acylCAT + CoA—-(crosses the mitochondrial membrane)—-> CAT2 reverses the process to remake Fatty acyl CoA + CAT1. CAT1 then travels back across the mitochondrial membrane to repeat the process.

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14
Q

what can inhibit the action of CAT1

A

malonyl CoA

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15
Q

what is the rate limiting step of beta oxidation

A

carnitine shuttle

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16
Q

what mutations causes the SIDS?

A

sudden infant death syndrome- disorders of beta oxidation
most common mutation- one of the acyl CoA dehydrogenase enzyme catalysing the first step of oxidation of beta oxidation of a fatty acyl-CoA.
there are other mutations that can cause SIDS, but this is the most common

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17
Q

where does fatty acid synthesis occur?

A

adipocytes and liver

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18
Q

how does glucose get converted to acetyl CoA

A

increase of glucose levels encourages the pancreas to produce insulin and allow cells to take in and process a lot more glucose. in glycolysis, glucose breaks down to 2pyruvate molecules releasing ATP, and further more, the pyruvate molecule in the mitochondria gets converted to Acetyl CoA by the enzyme pyruvate dehydrogenase.

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19
Q

citric acid cycle

A

Acetyl CoA and Oxaloacetate —-> Citrate —–> electron carriers that can be used in the electron transport chain.

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20
Q

what cycle enables the acetyl CoA to be moved from the mitochondria to the cytoplasm

A

citrate malate cycle

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21
Q

action of pyruvate caroxylase

A

increase in acetyl CoA conc in mitochondria can increase activity of pyruvate carboxylase that can further catalyse the conversion of pyruvate to oxaloacetate which is used in the Citric Cycle

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22
Q

the citrate malate cycle

A

citrate leaves the mitochondria to the cytoplasm and by the action of citrate lyase breaks down to oxaloacetate and acetyl CoA.
the oxaloacetate then by the action of malic enzyme breaks down to pyruvate (NADP+-> NADPH) which can travel across the membrane from the cytoplasm to mitochondria

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23
Q

what two conditions ensure fatty acid synthesis

A
  1. acetyl CoA in cytoplasm 2. presence of NADPH
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24
Q

what is the rate limiting step of fatty acid synthesis (explain the process)

A

acetyl CoA in the presence of Acetyl CoA carboxylase and HCO3- converts to Malonyl-CoA (3C)

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25
Q

how is Acetyl-CoA carboxylase regulated?

A

hormones and allosteric

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26
Q

explain the hormonal regulation of Acetyl-CoA

A

insulin can decrease the activity, glucagon can increase the activity

27
Q

explain the allosteric regulation of acetyl-CoA

A

citrate can increase the action and fatty acids can decrease the action

28
Q

explain the fatty acid synthesis process

A
  1. acetyl CoA converts to malonyl CoA
  2. Acetyl CoA breaks down to CoA and Acetate in the presence of Acetyl-CoA ACP transcyclase
  3. Acetate binds to the ACP end and spontaneously transfers to the Cys end
  4. Malonyl-CoA breaks down to Malonate and CoA in the presence of malonyl-CoA ACP transcyclase and attaches to the ACP end
  5. Malonate in the presence of 3-Ketoacyl ACP synthase breaks down into CO2 and Acetate. (the breakdown to CO2 produces NADPH-> NADP+)
  6. Acetate + Acetate –(NADPH–> NADP+)–>4C molecule on the Cys end.
    Step 4 repeats until a 16C palmitoyl CoA molecule forms.
29
Q

the yield from the formation of one 16C palmitoyl-CoA

A

8 Acetyl-CoA, 14 NADPH

30
Q

where is palmitoyl stored after formation

A

liver as triglycerides until the need to break down to ATP

31
Q

what is cholesterol synthesised from

A

Acetyl-CoA

32
Q

what form is cholesterol eliminated as

A

bile acids

33
Q

what enzyme catalyses the formation of cholesterol esters and where

A

Acyl-CoA cholesterol acyltransferase in the liver

34
Q

function of LCAT

A

lethicin Cholesterol Acyltransferase makes cholesterol ester enter the blood stream to trap cholesterol inside lipoproteins for transport

35
Q

what is cholesterol a precursor to

A

VitD, steroids, bile acids

36
Q

why is there an emphasis on recycling cholesterol

A

it is a large complex molecule and there is a high energy cost of production. therefore, cells can absorb cholesterol from diets and there is a emphasis on recycling e.g., bile acids.

37
Q

cholestrol molecule is a. hydrophobic b. hydrophilic c. amphipathic

A

c. amphipathic

38
Q

bile acids is a. hydrophobic b. hydrophilic c. amphipathic

A

a. hydrophilic

39
Q

route of bile acids in the body

A

produced from cholesterol in the liver and excreted into the gall bladder for release into the small intestine, but bile acids can be reabsorbed by the gut and recycled.

40
Q

the name for pathway/cycle to form cholestrol

A

mevalonate pathway

41
Q

explain the mevalonate pathway

A
  1. 2 x acetyl CoA forms acetoacetyl-CoA in the presence of Acetyl-CoA Acyl- transferase (ACAT)
  2. acetoacyl-CoA + HMG-CoA synthase forms HMG CoA + CoA
  3. HMG-CoA to mevalonate in the presence of HMG-CoA reductase (releases CoA-SH and H2O)
  4. Mevalonate in the presence of ATP and mevalonate-5-kinase forms mevalonate-5-phosphate
  5. mevalonate-5-phosphate in the presence of phosphome valonate kinase and ATP forms mevalonate pyrophosphate
  6. mevalonate pyrophosphate in the presence of mevalonate pyrophosphate decarboxylase forms isopentenyl pyrophosphate x 3
  7. isopentenyl pyrophosphate in the presence of geranyl transferase forms 2 x farnesyl pyrophosphate (15C)
  8. farnesyl pyrophosphate (15C) in the presence of squalene synthase forms squalene (last linear precursor to cholesterol)
  9. cyclisation of squalene in the presence of oxidosqualene cyclase to form lanosterol
  10. lanosterol –> 7-dehydrocholestrol –> cholestrol
42
Q

what is the rate limiting step of the mevalonate pathway

A

HMG-CoA to mevalonate in the presence of HMG-CoA reductase

43
Q

reasons for why lipids need to be transported

A
  1. bring dietary lipids to cells for energy production or storage
  2. more lipids from storage in adipose tissue for use in energy production
  3. provide lipids from the diet to cells for synthesising cell membranes
  4. carry cholesterol from peripheral tissues to the liver for excretion
  5. short-chain fatty acids are transported bound to blood proteins like albumin
44
Q

lipoproteins are a. hydrophobic b. hydrophilic c. amphipathic

A

trick question- they can be composed of all three

45
Q

apolipoproteins

A

specific carrier proteins combine with lipids to form several classes of plasma lipoproteins

46
Q

why determines the function of a specific apolipoprotein

A

-point of synthesis -lipid composition -apolipoprotein content

47
Q

chylomicron

A

largest (50-200nm), least dense
exogenous lipid transport
key lipoproteins: ApoE, ApoC-II
84-89% TG, 1-3% cholesterol, 3-5% cholesterol esters

48
Q

VLDL

A

28-70nm, endogenous lipid transport
key lipoproteins: ApoE, ApoC-II
50-65% TG, 5-10% cholesterol, 10-15% cholestrol esters

49
Q

LDL

A

20-25nm, endogenous lipid transport
key lipoprotein: ApoB-100
7-10% TG, 7-10% cholesterol. 34-40% cholesterol esters

50
Q

HDL

A

High density lipoproteins 8-11nm
Reverse transport
key lipoproteins: ApoE
3-5%TG, 3-4% cholesterol, 12% cholesterol esters

51
Q

which lipoproteins use ApoE

A

Chylomicron, VLDL, HDL

52
Q

which lipoproteins use ApoC-II

A

chylomicron, VLDL

53
Q

which lipoproteins use ApoE

A

HDL

54
Q

2 major steps in the digestion of dietary TGs

A
  1. TGs need to be emulsified by bile acids

2. TGs are hydrolysed by the enzyme pancreatic triacylglycerol lipase

55
Q

process of breaking down fat globules by lipase

A

bile sale break down fat globules into smaller globules and free fatty acids+ monoglycerides and lipase (from SI, saliva and pancrease) attaches to these smaller globules and further breaks them into free fatty acids+ monoglycerides which assembles as mixed micelles which have a hydrophobic interior and hydrophilic exterior

56
Q

the route of the mixed micelles after processing by lipase into the intestinal mucosa

A
  1. the bile salts leave the micelles leaving behind free fatty acids and monoglycerides that can travel into the intestinal wall (enterocytes) where they assemble as triglycerides.
  2. chylomicron then carries the triglycerides to the lacteal (lymph node) and via the thoracic duct, releases the triglycerides into the blood stream, bypassing the portal system.
  3. the triglycerides (as fatty acids and TGs) is released into peripheral tissues such as muscles for energy and adipose tissues for storage
  4. the chylomicron then shrinks and then taken in by endocytosis by the liver after release. the liver recognises the remnants by the ApoE content
57
Q

define endogenous tranport

A

transport of lipids from the liver to the adipose tissue or muscle tissue as VLDL lipoproteins

58
Q

explain endogenous tranport

A

ApoC-II activates tissue bound lipoprotein lipases which releases fatty acids. Triacylglyceride depleted remnants of CDLs from IDLs which on further loss of triacylglycerides becomes LDLs. These cholesterol/cholesterol ester rich lipoproteins are taken up by endocytosis within extrahepatic tissues by binding of the ApoB-100 apolipoprotein to the LDL receptors on the cell surface of the liver and extrahepatic tissues

59
Q

Reverse transport definition

A

returning cholesterol from the extrahepatic tissues to the liver

60
Q

reverse transport explain

A

endogenous cholesterol and cholesterol esters are transported from the extrahepatic tissues back to the liver via HDL. these do not enter the liver by endocytosis but rather by attachment to scavenger receptors SR-B1 on the cell surface that media transfer of cholesterol into the cell.

61
Q

Regulation of intracellular cholesterol (short-term)

A

cellular cholesterol levels are controlled by regulating LDL-cholesterol uptake and biosynthesis
short-term: regulation achieved by modifying HMG-CoA reductase activity: controls biosynthesis of cholesterol.

62
Q

Regulation of intracellular cholesterol (long-term)

A

Regulation achieved by modifying numbers of molecules involved in maintaining cellular cholesterol levels
HMG-CoA and LDL Receptors
transcription and protein production increase under low cholesterol levels, repressed under high levels.
protein degradation of HMG-CoA and LDL receptors reduce numbers under high cholesterol levels.

63
Q

regulation of LDL uptake by cells

A

mediated by LDL receptors on cell surface binding to ApoB-100–> LDL receptors separated from LDL and recycled back to cell surface —> Endosome fuses with lysosome: lytic enzymes degrade ApoB-100, releasing amino acids, fatty acids, cholesterol and cholesterol esters

Cardiovascular Medicine (6 decks)

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