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Biochemistry > Lipid Metabolism > Flashcards

Lipid Metabolism Flashcards

1
Q

Steps of lipid absorption

A
  1. Minor digestion in mouth and stomach (lingual lipase)
  2. Major digestion in duodenum (pancreatic lipase)
  3. Micelle formation by bile
  4. Passive absorption into intestinal epithelial cells
  5. Reesterification with FFA
  6. Addition of apoproteins to form chylomicrons
  7. Export to lymphatics
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2
Q

Abnormalities in lipid absorption

A
  1. Defective digestion: steatorrhea, more than 6g of unsplit fat in faeces per day. Due to chronic illnesses of pancreas.
  2. Defective absorption: split fat in faeces. Due to coeliac diseases, sprue, crohn’s disease, surgical removal of intestine, obstruction of bile duct.
  3. Chluria: abnormal connection between urinary tract and lymphatic drainage system. Milky urine. Seen in filariasis
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3
Q

Site and precursor for synthesis of TAG

A

ER of liver cells and adipose tissue

Fatty acid, Glycerol

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4
Q

Site and product of TAG degradation

A

Liver

Glycerol, 3 FFA

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5
Q

CoA contains (beta oxidation)

A

Pantothenic acid

Beta mercapto ethanolamine (has SH group to form thioester bond in acyl CoA)

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6
Q

Activation of fatty acids for beta oxidation

A
  • in cytosol
  • forms acyl CoA
  • uses ATP (to AMP)
  • thiokinase/acyl CoA synthetase
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7
Q

Role of carnitine

A
  1. Beta hydroxy gamma trimethyl ammonium butyrate
  2. Synthesised from lysine, methionine
  3. In liver and kidney
    - beta oxidation is mitochondrial
    - long chain fatty acyl CoA cannot pass through inner mitochondrial membrane
    - carnitine helps in transport
    - CAT-1 forms acyl carnitine
    - translocase protein carries this across membrane
    - CAT-2 transfers back acyl group
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8
Q

Intermediates of beta oxidation

A 
Acyl CoA
Transenoyl CoA
B hydroxyacyl CoA
B ketoacyl CoA
Acyl CoA + Acetyl CoA
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9
Q

Energetics of beta oxidation

A

1 cycle gives 1 FADH2 (1.5) and 1 NADH+H+(2.5)
1 acetyl CoA = 10

Palmitic acid has 16 C i.e., 8 Acetyl CoA, 7 cycles
80 + 28 - 2
106

(2 for initial activation)

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10
Q

Regulation of beta oxidation

A
  1. Availability of FFA
  2. Indirectly by insulin: glucagon ratio
  3. CAT-1 (-) Malonyl CoA
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11
Q

Fate of propionyl CoA

A

Propionyl CoA (carboxylase)
D methyl Malonyl CoA (racemase)
L methyl Malonyl CoA (mutase)
Succinyl CoA

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12
Q

Alpha oxidation

A
  • 1 C removed at a time
  • In brain, ER
  • No activation of fatty acid needed
  • Hydroxylation occurs at alpha C
  • Then oxidised to keto acid which gets decarboxylated
  • Does not generate energy
  • Used for FA with methyl grp at beta C which blocks beta oxidation ex: phytanic acid
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13
Q

Omega oxidation

A
  • in microsomes
  • hydroxylase enzymes
  • uses NADPH, cytochrome P450
  • produces dicarboxylic acids
  • used when beta oxidation is defective
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14
Q

De novo synthesis of fatty acids site and precursor

A

Liver, adipose, brain, kidney, mammary glands
Cytoplasm
Acetyl CoA

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15
Q

Transport of Acetyl CoA for de novo synthesis of fatty acids

A
  • Acetyl CoA is formed in mitochondria
  • inner membrane of mitochondria is not permeable to it
  • converted into citrate
  • transported by TCA transporter
  • citrate split into OAA and Acetyl CoA in cytoplasm using ATP citrate lyase
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16
Q

Components of fatty acid synthase complex

A

Only functions as dimer

  1. Ketoacyl synthase
  2. Acetyl transacylase
  3. Malonyl transacylase
  4. Dehydratase
  5. Enoyl reductase
  6. Ketoacyl reductase
  7. ACP
  8. Thioesterase
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17
Q

Advantages of multi enzyme complex in de novo synthesis of fatty acids

A
  1. Intermediates can react easily with active sites
  2. One gene codes of all enzymes, so equimolar concs.
  3. Efficiency enhanced
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18
Q

Rate limiting enzyme of de novo synthesis of fatty acids

A

Acetyl CoA carboxylase
Converts acetyl CoA to Malonyl CoA
(+) Citrate
(-) palmitoyl CoA

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19
Q

Intermediates of de novo synthesis of fatty acids

A 
Acetyl enzyme
Acetyl (acyl) Malonyl enzyme
Beta ketoacyl ACP (NADPH)
Beta hydroxyacyl ACP
Transenoyl ACP (NADPH)
Acyl ACP
Acyl enzyme
FAS + Palmitate
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20
Q

Sources of NADPH in de novo synthesis of fatty acids

A

HMP shunt
Malic enzyme
Malate + NADP+ = Pyruvate + CO2 + NADPH+H+

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21
Q

Ketogenesis site

A

Liver mitochondria

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22
Q

Structure of cholesterol

A
  1. Cyclopentanoperhydrophenanthrene ring
  2. 27 C atoms in total
  3. Hydroxyl group at 3rd position
  4. Double bond b/w C5-C6
  5. 8 C side chain attached to 17th C
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23
Q

Major sites of cholesterol synthesis

A
  1. Liver
  2. Adrenal cortex
  3. Testes
  4. Ovary
  5. Intestine
    Partly in ER, partly in cytoplasm
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24
Q

C atoms of cholesterol come from

A

Acetyl CoA

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25
Q

ATP citrate lyase reaction

A

Citrate + ATP + CoA + H2O

OAA + acetyl CoA + ADP + Pi

Provides acetyl CoA for cholesterol and fatty acid synthesis

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26
Q

Fate of HMG CoA in mitochondria and cytosol

A

Mitochondria - ketogenesis

Cytosol - cholesterol synthesis

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27
Q

Intermediates of cholesterol synthesis

A 
Acetyl CoA
Acetoacetyl CoA
HMG CoA
Mevalonate
Mevalonate 5 P
Mevalonate 5 pyroP
3phospho 5pyrophospho mevalonate
Isopentyl pyroP
Geranyl pyroP
Farnesyl pyroP
Squalene
Squalene epoxide
Lanosterol
Zymosterol
Desmosterol
Cholesterol
28
Q

Regulation of cholesterol synthesis

A
  1. HMG CoA reductase regulation at transcription
    (+) Dephosphorylation
    (-) phosphorylation
    (+) Insulin, thyroxine
    (-) cortisol, glucagon
  2. Statins are competitive inhibitors of HMG CoA reductase
29
Q

Enzymes of cholesterol synthesis

A 
Thiolase
Synthase
Reductase
Kinase
Kinase
Kinase
Decarboxylase
Isomerase
Transferase
Synthase
Epoxidase
Cyclase
Isomerase
Reductase
30
Q

Role of liver in cholesterol metabolism

A
  1. Synthesizes cholesterol
  2. Removes cholesterol from lipoprotein remnants
  3. Excrete cholesterol through bile
  4. Converts cholesterol to bile acids
31
Q

Apoprotein of chylomicrons

A

B48, A, C, E

32
Q

Apoprotein of VLDL

A

B100, C, E

33
Q

Apoprotein of LDL

A

B100

34
Q

Apoprotein of HDL

A

A, C, D, E

35
Q

As density of Lp increases, diameter and lipid conc.

A

Decreases

36
Q

Function of chylomicrons

A

TAG from gut to muscle and adipose tissue

37
Q

Function of VLDL

A

TAG from liver to muscle and adipose tissue

38
Q

Function of LDL

A

Cholesterol from liver to peripheral tissues

39
Q

Function of HDL

A

Cholesterol from peripheral tissues to liver

40
Q

Function of Apo A1

A

In HDL

  1. Activates LCAT
  2. Ligand for HDL receptor
  3. Anti atherogenic
41
Q

Function of Apo A2

A

In HDL

  1. Inhibits LCAT
  2. Stimulates lipase
42
Q

Function of apo B 100

A

In LDL, VLDL

1. Binds LDL receptor

43
Q

Function of apo C

A

In chylo, VLDL

  1. Activation of LCAT
  2. Anti atherogenic
44
Q

Function of apoE

A

In LDL, VLDL, Chylo

  1. Arginine rich
  2. Ligand for hepatic uptake
45
Q

Lp(a)

A
  • associated with MI
  • attached to B 100 by disulphide bond
  • risky when conc. >30mg/dl
  • higher in Indians than Western
  • homologous to plasminogen
  • interferes with plasminogen activation
  • impairs fibrinolysis
  • leads to intravascular thrombosis and MI
46
Q

Primary bile acids

A

Cholic acid

Chenodeoxycholic acid

47
Q

Conjugated bile acids

A

Glycocholic
Taurocholic
Glycochenodeoxycholic
Taurochenodeoxycholic

48
Q

Secondary bile acids

A

Deoxycholic

Lithocholic

49
Q

Digestion of medium chain fatty acids

A
  • pancreatic lipase and bile salts not needed
  • MCT specific lipase catalyses complete hydrolysis into glycerol and FA
  • Free MCFA diffuse into portal circulation
  • oxidised by peripheral cells
50
Q

Examples of very long chain fatty acids

A 
Eicosapentaenoic acid
Decosahexanoic acid (DHA)
51
Q

Decosahexanoic acid

A
  • synthesised in liver
  • from linoleic acid
  • needed for development of brain and retina
  • low levels associated with retinitis pigmentosa
  • accumulates in brain before birth and 12 wks after
  • needed for rotational mvmt of rhodopsin for photoactivation
52
Q

Digestion of VLCFA

A
  • partly oxidised in peroxisomes
  • unlike beta oxidation, electrons from FADH2 are directly donated to O2 to give H2O2
  • this is one mechanism to kill bacteria by neutrophils
  • H2O2 detoxified by catalase
53
Q

Beta oxidation of MUFA

A
  • same until double bond is reached
  • in palmitoleic acid, db is cis
  • converted into trans by isomerase
  • continues with 2, 3, 4 steps of b oxidation
  • FAD dependent dehydrogenation not needed
  • 1.5 ATP less per db
54
Q

Examples of PUFA

A

Linoleic acid 18
Linolenic acid 18
Arachidonic acid 20

55
Q

Significance of PUFA

A
  1. In vegetable oils
  2. Nutritionally essential. Essential FA
  3. Prostaglandins, thrombaxane, leukotrienes from arachidonic
  4. Integral part of mitochondrial membranes
  5. Components of cell membranes
  6. Cannot be closely packed. Inc. fluidity of membrane
  7. Can undergo peroxidation easily. Cells with PUFA liable to ROS damage
  8. DHA needed for retina and brain
56
Q

Desaturation of FA

A
  • MUFA can be synthesised from saturated FA using desaturase
  • NADH, O2, cytochrome b5 needed
  • PUFA can be formed from MUFA
  • db can be added only b/w existing bond and carboxyl end
  • hence, linoleic cannot be from oleic
  • linoleic can be converted into arachidonic
57
Q

Essential fatty acids

A

Linoleic

Linolenic

58
Q

Gamma linolenic acid

A
  • Omega 6 family
  • from linoleic
  • desaturated to arachidonic
  • prevents CVS diseases
  • dilates blood vessels
  • lowers BP
  • prevents atherosclerosis
  • inhibits tumor growth and cancer spread
59
Q

Synthesis of prostaglandins

A
  • not stored as such
  • precursors of PG stored in membranes as phospholipids
  • AA release by action of phospholipase A2 on phospholipids
  • synthesis needs PG H synthase containing cyclooxygenase and peroxidase
  • PGG2, PGH2 formed as intermediates
60
Q

Regulation of PG synthesis

A 
1. Phospholipase
\+ Epinephrine, thrombine, angiotensin ii
- steroids
2. Cyclooxygenase
\+ Catecholamines
- aspirin, NSAIDs
3. Cyclooxygenase is a suicide enzyme
4. PGs are quickly inactivated by 15-hydroxy-PG-dehydrogenase
61
Q

Effects of PG on CVS

A
  • PGI2 synthesised by vascular endothelium
  • vasodilation
  • inhibit platelet aggregation
  • TXA2 causes vasoconstriction and platelet aggregation
62
Q

Effects of PG on ovaries

A
  • PGF2 used for MTP, inducing labour, arresting postpatum haemorrhage
  • involved in LH induced ovulation
63
Q

Effects of PG on respiratory tract

A

PGF - bronchoconstrictor

PGE - bronchodilator - relieves bronchospasm

64
Q

Effects of PG on immunity

A

PGE2, PGD2 - produce inflammation by Inc. capillary permeability
PGE2 - reduces T, B cell function

65
Q

Effects of PG on GIT

A

Inhibit gastric secretion
Inc. Intestinal motility
Used to treat acid peptic disease

66
Q

Effects of PG on metabolism

A

Inc. Lipolysis
Inc. Ca+2 mobilisation from bone
Inc. glycogen synthesis

Biochemistry (18 decks)

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