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Metabolism and Biochem > Lipids > Flashcards

Lipids Flashcards

1
Q

Do plant sources of lipids contain cholesterol?

A

No

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2
Q

Lipids all contain a (hydrophilic/hydrophobic group) making them water (soluble/insoluble)

A

Hydrophobic → Water insoluble

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3
Q

What are 3 functions of lipids?

A

1) Energy store
2) Structural function
3) Signalling molecule

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4
Q

FA are carboxylic acids with long ____________ chains and can be _________ or__________- depending on the presence of C=C. They are categorized based on __________.

A

Long aliphatic chain
can be saturated or unsaturated (have C=C)

Categorised based on length

Very long chain FA (VLCFA): 22 C or more
Long chain FA (LCFA): 14-20 C (most common)
Medium chain FA (MCFA): 8-12 C
Short chain FA (SCFA): 4-6 C

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5
Q

Most FAs have (even/odd) number of carbons.

A

Even

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6
Q

Naturally occurring unsaturated FAs have primarily (cis/trans) C=C.

A

Cis

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7
Q

A saturated FA has a (straight/bent) chain, therefore allowing for (maximal/reduced) surface area for intermolecular interactions, granting them a (higher/lower) m/b.p.t.

A

Saturated: usually animal sources
- Straight → Max SA for FOA → higher m/b.p.t.

(Unsaturated: usually plant sources
- Bent → ↓SA for SOA → ↓m/b.p.t.)

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8
Q

How are cis unsaturated FAs different from trans?

A

1) Cis: Hydrocarbons chains same side as double bond
Trans: opposite

2) Cis: Naturally occurring
Trans: Hydrogenation (↓prone to rancidity → ↑shelf life)

3) Trans: ↑LDL ↓HDL → ↑atherosclerosis risk

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9
Q

How are TG/TAGs digested?

A

By lipases (mainly pancreatic)
Triacylglycerol → Monoacylglycerol + 2 FA

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10
Q

How are cholesterol esters digested?

A

By Pancreatic esterase
Cholesterol ester → Cholesterol + FA

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11
Q

How are phospholipids digested?

A

By pancreatic phospholipase A2
Phospholipid → Lysophospholipid + FA

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12
Q

Lipids are firstly digested by _____________ which are most active in the stomach (low pH). They are then mostly digested in the _________, mediated by _______________, forming micelles and ______________ to be absorbed into enterocytes.

A

1st digested by lingual and gastric lipase (both most active in stomach)

Mostly digested in small intestine, mediated by:
i) Bile salts → emulsify to form micelles

ii) Pancreatic enzymes (lipase, esterase, phospholipase A2)

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13
Q

Bile salts are amphipathic molecules synthesised in the _______ and stored in the __________, where is can be released into the intestines to emulsify (i) ________ and (ii) ________, forming micelles to increase the surface area of lipid droplets for enhanced interaction with enzymes.

A

Synthesised in liver, stored in gall bladder

Emulsify (i) lipids and (ii) lipid-soluble vitamins

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14
Q

Lipases in intestinal lumen requires ______________ to aid in lipid digestion as __________________.

A

Colipase
- anchor pancreatic lipase to lipid-aqueous interface of micelles
- remove inhibitory effect of bile salts on lipase

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15
Q

What are 2 hormones that regulate lipids digestion in the intestines?

A

1) CCK
- ↑ CCK → ↑gall bladder + pancreatic secretion

2) Secretin
- ↑ secretin → ↑HCO3- from ductal cells → ↑pH for optimal enzyme digestion

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16
Q

How does an irreversible inhibitor of lipases eg. Orlistat help in obesity control?

A

↓digestion of TGs → excreted in feces rather than metabolised

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17
Q

Which vitamins should be supplemented in a px taking irreversible lipase inhibitors (eg. Orlistat)?

A

ADEK
- ↓digestion → ↑excretion of TGs in feces along with fat-soluble vitamins
→ need to supplement to compensate for ↓absorption

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18
Q

What are 3 causes of steatorrhea?

A

↓ Lipid digestion/absorption:
1) Bile salt deficiency
2) Pancreatic insufficiency
3) Disease affecting Small intestine → ↓abs

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19
Q

What is Steatorrhea?

A

Excessive fats in stools (fatty, floating)

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20
Q

How does fat-soluble vitamin deficiency present?

A

A: ↓retinol → ↓vision, immune f(x)

D: ↓Ca and ↓PO4 Abs → Osteomalacia

E: antioxidant → ↓oxidative stress

K: ↓coagulation factors, 2,7,9,10 deficiency → coagulopathy

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21
Q

How are (i) short/medium chain FAs (ii) micelles (iii) Bile salts absorbed into enterocytes?

A

i) Short/medium chain FAs → soluble, direct Abs

ii) Micelles → interact w cell membrane → lipid soluble contents diffuse into cell

iii) Bile salts → resorbed @ terminal ileum

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22
Q

How are absorbed lipids transported into circulation?

A

1) Conversion of digested lipids back into original form
- 2-Monoacylglycerols (2-MGs) + FAs → triacylglycerols (TAGs)
- Cholesterol + FAs → cholesterol esters
- Lysophospholipids + FA → Phospholipids

2) Formation of nascent chylomicrons
- need ApoB-48 (produced by enterocytes)

3) Exocytosis of nascent chylomicron into lymphatics

4) Lymphatics → blood circulation

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23
Q

What are lipoproteins?

A

Spherical macromolecule
Core: Lipids
Coat: monolayer of phospholipid
- have apolipoprotein associated

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24
Q

How are nascent chylomicrons converted into mature chylomicrons?

A

HDLs transfer (i) ApoE and (ii) ApoCII to nascent chylomicron → mature

(formed 1-3hrs after meal, cleared >8hrs)

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25
Q

Why can’t nascent chylomicrons just enter blood system directly?

A

Too large to pass through fenestrations in blood capillaries but can fit through larger pores in lymphatic capillaries

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26
Q

How do mature chylomicrons transport dietary TGs to muscles and adipose tissue?

A

1) ApoCII (from HDLs) → cofactor for lipoprotein lipase (on capillary walls of muscles and adipose tissue, stimulated by insulin)

2) Lipase → (TG → FAs + Glycerol)

3) FAs taken up by muscle and adipose tissues
- muscle → oxidised → ATP
- adipose → TG → storage

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27
Q

What happens to (i) glycerol and (ii) chylomicron remnants after mature chylomicron is acted on by lipoprotein lipase?

A

(i) Glycerol (passive) uptake by hepatocytes via Aquaporin-9

ii) Mature chylomicron loses ApoCII
→ Chylomicron remnants (have ApoB-48 and ApoE)
→ taken up by liver via ApoE receptor
→ degraded by lysosomal enzymes

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28
Q

What is the pathogenesis of hyperchylomicronemia?

A

Genetic deficiency of (i) lipoprotein lipase (LPL) or (ii) ApoCII
→ ↓hydrolysis of TG in mature chylomicrons
→ HyperTG
→ Xanthomas on knees, butt, arms (build up of foam cells)

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29
Q

What should be the dietary recommendation for px with hyperchylomicronemia?

A

Low fat diet
(↓chylomicron synthesis)

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30
Q

De novo lipogenesis is the synthesis of FAs from __________ precursors.

A

Non-lipid (eg. carbohydrates)

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31
Q

How does glucose contribute to de novo FA synthesis in the liver?

A

1) Glucose → pyruvate (glycolysis in cytosol)

2) Pyruvate → Acetyl CoA (PDH) + Oxaloacetate (Pyruvate carboxylase)
- in mitochondria

3) Acetyl CoA → Citrate (Citrate synthase)

4) Citrate transported to cytosol

5) Citrate → Acetyl CoA + Oxaloacetate (ATP citrate lyase)

6) Acetyl CoA → DNL

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32
Q

What is the committed/rate limiting step of DNL?

A

Acetyl CoA → Malonyl CoA
- via Acetyl CoA Carboxylase

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33
Q

How is ACC in DNL regulated?

A

1) Allosteric
+: Citrate
-: LCFA CoA (-ve feedback)

2) Hormonal
+: Insulin
-: Glucagon and epinephrine

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34
Q

Fatty acid synthase is a multi-enzyme complex that converts Acetyl-CoA and Malonyl CoA into FA in the ________ of cells and its expression is induced by ____________ hormone.

A

Cytoplasm
Insulin

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35
Q

For TAG synthesis in the liver, where do (i) FAs and (ii) Glycerol come from?

A

FAs: DNL (from glucose)

Glycerol: Direct glycerol uptake (Mature chylomicrons) or DHAP (from glucose)

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36
Q

For TAG synthesis in the adipose tissue, where do (i) FAs and (ii) Glycerol come from?

A

FA: Uptake (dietary and hepatic)

Glycerol: From DHAP (from glucose)

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37
Q

How does the fate of TAG synthesised in the liver differ from that in the adipose tissue?

A

TAG in liver exported to other extra-hepatic organs.

TAG in adipose tissue stored during fed state.

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38
Q

How are VLDLs formed?

A

1) Synthesised (FA of TGs from DNL) and secreted from hepatocytes with ApoB100 as nascent VLDL

2) Nascent VLDL acquire ApoE and ApoCII from HDL → mature VLDL

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39
Q

What is the primary function of VLDL?

A

To delivery hepatic TAG to other tissues

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40
Q

What happens to VLDL after TG delivery?

A

Loss of TG and ApoCII (during TG delivery)
→ IDL
a) return to liver via ApoE receptor

b) remain in circulation and deliver more TG → LDL (via HTGL)

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41
Q

What are 3 key dysregulated biochemical features in hepatocytes?

A

1) ↑FA synthesis → ↑TG
2) Rate of TG synthesis&raquo_space; VLDL synthesis → TG accumulation
3) Impaired VLDL secretion

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42
Q

How are TAG stores in adipose tissue after feeding?

A

After feed → ↑glucose → ↑insulin

a) ↑glucose uptake → glycolysis → DHAP → G-3-P for TAG synthesis

b) ↑Lipoprotein lipase exp. → ↑FA from VLDL/chylomicrons → Fatty acyl CoA for TAG synthesis

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43
Q

Describe how lipolysis is induced in adipocytes under fasting conditions.

A

Fasting → ↓glucose → ↑glucagon
→ HSL (hormone sensitive lipase)
→ (TG → FAs + Glycerol)

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44
Q

How are FAs transported in the blood?

A

As a FA-albumin complex (no need lipoprotein)

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45
Q

How are FAs transported into the mitochondria?

A

1) FA → FACoA in cytosol

2) FACoA + Carnitine → CPT1 transporter → into mitochondrial intermembrane space

3) FA-carnitine → CPT2 → FACoA into mitochondria + Carnitine back into cytoplasm

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46
Q

What is the rate limiting step for oxidation of fatty acids in the mitochondria?

A

Carnitine-mediated entry of FA into mitochondria

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47
Q

CPT 1 which is responsible of the transport of ___________ into the mitochondrial intermembrane space is inhibited by _______________.

A

CPT 1: FA transport (with Carnitine)
Inhibited by Malonyl CoA

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48
Q

How is FA ß-oxidation regulated after a heavy meal?

A

Heavy meal → ↑Glucose + ↑insulin

↑glucose → ↑Substrate for ACC
↑ Insulin → ↑ACC activity

→ ↑Malonyl CoA →inhibit CPT1
→ ↓transport of FA into the mitochondria for ß-oxidation

v.v. for ↓glucose and ↑glucagon

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49
Q

In FA ß-oxidation, ______ produces ___________ where it enters the TCA cycle or used for ketogenesis. This process produces ___________ and ____________.

A

Fatty acyl CoA → Acetyl CoA (until fatty acyl chain has no more Cs)

Produces NADH and FADH

50
Q

Ketogenesis only occurs in the ________ under ______________ conditions in healthy individuals.

A

Mitochondria of hepatocytes
under fasting conditions

51
Q

Which of the ketone bodies are important energy sources for extrahepatic tissues during periods of fasting?

A

1) Acetoacetate
2) ß-hydroxybutyrate

52
Q

During periods of fast, what are the hormonal mechanism that supply high levels of acetyl CoA for ketogenesis?

A

Fasting:
a) ↑glucagon → HSL → ↑Lipolysis → FA-albumin → from adipocytes to liver

b) ↑glucagon + ↓insulin → inhibit ACC → ↓inhibition of CPT 1 → ↑ß-oxidation of FA

Both ↑Acetyl CoA

53
Q

True or false:
Ketogenic amino acids are the main source of ketone bodies.

A

False
FAs are main source

54
Q

Of the ketone bodies, ________ is volatile and can be smelt in the breath and is the least amount of the 3 ketone bodies.

A

Acetone (nail polish, sweet/fruity smell)

55
Q

Does the liver carry out ketolysis?

A

No, no exp. of 3-ketoacyl-CoA transferase required for catabolism of ketone bodies

56
Q

Why do px with Type 1 DM exhibit ketoacidosis?

A

Type 1 DM → destruction of ß-cells of pancreas
→ ↓insulin but ↑glucagon
→ ↑lipolysis (via HSL) + ↑ß-oxidation (↓inhibition of CPT via ↑inhibition of ACC)
→ rate of ketogenesis&raquo_space; ketolysis
→ ketoacidosis (acidic and soluble)
→ ketonuria

57
Q

What is a ketogenic diet?

A

High fat diet (4:1 by weight) of lipid:carbohydrate

58
Q

What are 2 clinical applications of ketogenic diets?

A

1) ↓freq. of epileptic seizures in children

2) treat children w pyruvate dehydrogenase deficiency → fuel by brain in place of TCA

59
Q

What are 2 functions of cholesterol?

A

1) Maintain cellular membrane and fluidity

2) Precursor for biosynthesis
(eg. bile acids, vit. D, steroid hormones)

60
Q

What is the hepatic cholesterol pool and what are 3 cholesterol sources?

A

Liver

From:
1) Dietary (Chylomicron remnants
2) De novo synthesis
3) Extrahepatic tissues (reverse cholesterol transport by HDL)

61
Q

What are 3 fates of cholesterol in the liver?

A

1) VLDL synthesis
2) Conversion into bile salts/acids
3) Secreted as free cholesterol in the bile

62
Q

What is the moa of Ezetimibe (inhibitor of intestinal sterol absorption)?

A

Inhibit NPC1L1 transport (responsible for transporting cholesterol from intestinal lumen to enterocytes)

Usually Rx w Statins

63
Q

Cholesterol and its derivates have a characteristic ______ (3 6C and 1 5C ring structure). If its has a _________ linked to it, it is known as a cholesterol ester.

A

Steroid nucleus

+ Fatty acid → Cholesterol ester

64
Q

Where does stage 1 (Mevalonate synthesis) of cholesterol synthesis occur?

A

Cytoplasm and ER

65
Q

Where are (i) HMG-CoA synthase and (ii) HMG-CoA reductase found in cells?

A

(i) HMG-CoA synthase: cytosolic

(ii) HMG-CoA reductase: ER membrane

66
Q

What is the comitted step and rate limiting step of cholesterol synthesis?

A

HMG-CoA → Mevalonate
- via HMG-CoA reductase

67
Q

How is cholesterol synthesis physiologically regulated?

A

At HMG-CoA by allosteric covalent modification

Low energy → ↑glucagon + ↑AMP
- AMPK activated by (i) AMP (ii) Glucagon
→ P HMG-CoA reductase → inactive
→ ↓cholesterol synthesis

High energy → ↑insulin
- Activate phosphatase
→ de-P HMG-CoA reductase → active
→ ↑cholesterol synthesis

68
Q

What is the moa of statins?

A

Structural analogs of HMG-CoA → CI of HMG-CoA reductase
→ ↓mevalonate synthesis (rate limiting)
→ ↓ de novo cholesterol synthesis
→ ↓hepatic cholesterol pool
→ ↑exp. of LDL receptors on hepatocytes
→ ↑LDL uptake via receptor-mediated endocytosis
→ ↓risk of atherosclerosis

69
Q

How is cholesterol catabolised?

A

Sike, it doesn’t.

70
Q

How do cholesterol synthesis and ketogenesis not compete for HMG-CoA in hepatocytes?

A

Cellular compartmentalisation
1) Cytosol
- cholesterol synthesis

2) Mitochondria
- ketogenesis

71
Q

How are primary bile acid synthesised?

A

Cholesterol → Cholic acid or Cenodeoxycholic acid
- via 7α-hydroxylase

72
Q

How is primary bile acid production regulated?

A

Feedback inhibition
- primary bile acids → ↓exp. of 7α-hydroxylase

73
Q

How are primary bile salts formed?

A

Primary bile acid conjugated w taurine or glycine → primary bile salts

74
Q

Why do bile acids need to be conjugated to taurine or glycine?

A

To have a lower pKa
→ ↑deprotonated (conjugate base) form
→ ↑solubility
→ better emulsifiers

75
Q

What is the difference between a bile salt and a bile acid?

A

Bile acid: protonated form of acid (eg. R-COOH)
Bile salt: salt of conjugate base (eg. R-COO-)

76
Q

After digestion, most primary bile salts are actively reabsorbed at the ileum. What happens to the rest?

A

Intestinal bacteria convert some to secondary bile acids (by deconjugated and dehydroxylation)

→ 2° bile acids passively absorbed at colon

77
Q

How are bile acids recycles?

A

Enterohepatic circulation:
- Liver produce bile salts → gall bladder → intestines

a) 1° actively reabsorbed at ileum
b) 2° (deconjugated and dehydroxylated by intestinal bacterial) passively reabsorbed at colon

→ both return to portal circulation
(only <5% excreted in feces)

78
Q

What is the moa of bile salt resins eg. cholesyramine?

A

Bile acid sequestrants:
- binds to bile salts in intestines to form insoluble complex → excreted in feces
→ ↓recycling of bile acids
→ induce ↑cholesterol synthesis in liver

↓hepatic cholesterol pool
→ ↑exp. of LDL receptors on hepatocytes
→ ↑LDL uptake via receptor-mediated endocytosis
→ ↓risk of atherosclerosis

79
Q

How is Vitamin D synthesised?

A

1a) 7-dehydrocholesterol→ UV exposure in skin → Vit. D3
or
1b) dietary Vit. D2/3 → Vit. D3

2) Transported to liver
Vit. D3 → 25-(OH)D3

3) 25-(OH)D3 → Active calcitrol/Vit. D3 in kidney

80
Q

How does calcitrol (active vit. D3) aid in calcium absorption from the intestine?

A

Steroid hormone → diffuse into cell
→ bind to Vit. D receptor in cytoplasm
→ transported to nucleus
→ ↑exp. of genes for Vit. D action
→ ↑Ca transporters in intestine

81
Q

What is the common precursor for all steroid hormones?

A

Cholesterol

82
Q

What are 3 organ sites of steroid hormone synthesis?

A

1) Adrenal cortex
2) Testes
3) Ovarian follicle

83
Q

Where is Lipoprotein Lipase located?

A

Capillary walls of muscles and adipose tissue

84
Q

What is the function of ApoCII?

A

Cofactor of LPL → lipolysis

85
Q

What are 2 fates of LDL?

A

1) Returned to liver via LDL receptors (ApoB100-LDL receptor)

2) Delivers cholesterols to extrahepatic tissues

86
Q

What is the difference between Chylomicrons and VLDL?

A

1) Apolipoproteins
Chylomicron: ApoB48, ApoCII, ApoE
VLDL: ApoB100, ApoCII, ApoE

2) TAG content
Chylomicron: Dietary
VLDL: Hepatic

3) Function
Chylomicron: Deliver dietary TG
VLDL: Deliver hepatic TG

4) Fate of remnants
Chylomicron: Chylomicron remnants → liver
VLDL: IDL → liver/IDL → liver

87
Q

What are 2 fates of IDL?

A

1) TG hydrolysed by HTGL + Transfer ApoE to HDL→ LDL

2) Taken up into liver via ApoE receptor (receptor-mediated endocytosis)

HTGL = Hepatic TG lipase (hepatic lipase)

88
Q

What are the function of 3 apolipoproteins?

A

B100 → LDL receptor (Liver and peripheral cells)

ApoE → ApoE receptors (Liver only)

ApoCII → LPL coenzyme

89
Q

In the pathogenesis of atherosclerosis, LDL can be ________ and taken u[p by scavenger receptors of ____________ leading to the formation of _______________.

A

Oxidised → Macrophages → Foam cells

90
Q

Describe the role of LDL in atherosclerosis.

A

1) ↑LDL levels → can be retained/trapped at damages site of endothelium → oxidised LDL

2) Endothelial cells exposed to oxidised LDL → cytokines → accumulation of monocytes

3) Monocytes → macrophages → internalise oxidised LDL, cholesterol esters, cholesterol → foam cells

4) Foam cells accumulate → plaque → thicken and harden arterial wall (atherosclerosis)

5) Smooth muscle cells of artery replicate and migrate → firm cap covering plaque

Plaque can rupture → release of cytokines and thrombogenic agents → AMI or ischaemic stroke

91
Q

Which 2 lipoproteins contain the higher % of TGs?

A

Chylomicrons and VLDLs

92
Q

Which lipoproteins contain the highest % of cholesterol/cholesterol esters?

A

LDL

93
Q

What is the process of direct reverse cholesterol transport by HDL?

A

1) Nascent HDL synthesis by liver and small intestine

2) HDL take up cholesterol from cell membrane of extrahepatic tissues and convert C to CE

3) Lipid-rich HDLs (HDL2) bind to SR-B1 on liver → release C/CE, TG is removed by HTGL

4) Resultant lipid-poor HDL (HDL3) released → pick up more C/CE from extra hepatic tissues

94
Q

What is the process of indirect reverse cholesterol transport by HDL?

A

1) HDL exchange CE for TG with VLDL via CETP (CE transfer protein)

2) Loss of TG → (VLDL → IDL → LDL)

3) IDL (via ApoE) and LDL (via LDL receptor/B100) transport CE back to liver

95
Q

What is the difference between direct and indirect reverse cholesterol transport by HDLs?

A

Direct: HDLs transfer C/CE/TG directly to liver via SR-B1 (C/CE) or HTGL (TG)

Indirect: HDLs exchange C/CE w TG with VLDL (via CETP) → transport back to liver in IDL (via ApoE) or LDL (LDL-receptor/B100 mediated endocytosis)

96
Q

How does the transfer of lipids to the liver differ between (i) HDL and (ii) Chylomicron remnants, IDL, LDL?

A

i) HDL does not require endocytosis of whole lipoprotein

ii) Chylomicrons, IDL, LDL undergo receptor-mediated endocytosis

97
Q

How are cholesterol/lipids measured for clinically (4)?

A

Fasting (overnight/10-14hr) blood sample:
1) TAG
2) Total cholesterol (HDL, LDL, VLDL)
3) LDL-cholesterol
4) HDL-cholesterol

98
Q

Which of the lipoproteins are not routinely measured?

A

IDL and Chylomicrons

99
Q

What is familial hypercholesterolemia?

A

Genetic mutation in LDL receptor gene (homo/heterozygous)
→ ↑LDL and LDL-cholesterol in blood

→ premature CHD, AMI, atherosclerosis
→ Xanthomas

100
Q

What is the pathogenesis of familial hypercholesterolemia that leads to ↑LDL and LDL-cholesterol?

A

Genetic mutation in LDL receptor gene
→ cannot effectively induce normal LDL uptake into organs and tissues
→ accumulation of LDL in circulation
→ ↑ LDL-cholesterol in the blood

101
Q

What is the moa of Fibrates?

A

Active transcription factor (PPAR-α) → ↑exp. of genes for lipid catabolism (eg. LPL, CPT1)

a) → ↑ FA catabolism
→ ↓liver TG by ↑ß-oxidation
→ ↓VLDL secretion
→ ↓LDL production from

b) ↑apolipoproteins of HDL and HDL synthesis

102
Q

What is the difference between glycerophospholipids and sphingolipids?

A

Glycerophospholipids: Glycerol backbone

Sphingolipids: Spingosine backbone

103
Q

What are 2 functions of phospholipids?

A

1) Structural (eg. lipoproteins, cell/mitochondrial membrane)

2) Cell signaling (eg. phosphatidylinositol)

104
Q

What is the key phospholipid in myelin sheath?

A

Sphingomyelin

105
Q

How are phospholipids catabolised?

A

By phospholipases
→ cleave into fatty acids, polar head group, etc.
(occur at cellular membranes)

106
Q

What are 3 types of eicosanoids?

A

1) Prostaglandins
2) Thromboxanes
3) Leukotrienes

107
Q

Eicosanoids are most frequently derived from ___________________ and acts as _____________ hormones.

A

Derived from arachidonic acid

Para/autocrine hormones

108
Q

How are eicosanoids synthesised?

A

Stimuli (eg. inflammation, mitogenic)
→ activation and translocation of phospholipase A2 from cytosol to cell membrane

→ Membrane phospholipids containing arachidonic acid → cleaved by phospholipase A2

Arachidonic acid then used to synthesise eicosanoids

109
Q

Where does arachidonic acid come from?

A

Synthesised from linoleic acid (essential fatty acid)

110
Q

What are essential fatty acids?

A

FAs not synthesised by body but needed for health and must be obtained from diet.

(LCFAs with double bonds at ω-3 or ω-6 carbon → cannot be synthesised by humans)

111
Q

Linoleic acid and α-linolenic acids are _________ fatty acids that are polyunsaturated. They are required for the synthesis of important fatty acids such as AA and DHA.

A

Essential

112
Q

True or false.
EPA and DHA can be synthesised from ALA but is still recommended to be consumed in the diet due to their low conversion efficiency.

A

True

113
Q

Arachidonic acid is synthesised from which essential fatty acid?

A

Linoleic acid (ω-6)

114
Q

Docosahexaenoic acid (DHA) is synthesised from which essential fatty acid?

A

α-Linolenic acid (ω-3)

115
Q

What are 4 actions of prostaglandins?

A

1) vasodilation
2) ↓platelet aggregation
3) Inflammation
4) ↑ Pain
5) Gastric mucosal barrier

116
Q

What are 2 actions of thromboxanes?

A

1) ↑Platelet aggregation
2) Vasoconstriction

117
Q

What is the action of leukotrienes?

A

Contraction of lung muscles
(Overproduction → inflammation in allergic rhinitis and asthma)

118
Q

Why is aspirin (Acetylsalicylate) an irreversible COX inhibitor?

A

It acts by transferring an acetyl group to the serine residue on the active site of COX

119
Q

Why does COX1 inhibition cause stomach ulcers?

A

COX1 (constitutively expressed in the gastric mucosa) → PGE2 (promotes gastric mucosal barrier)

Inhibition of COX 1 → ↓PGE2 synthesis → ↓cytoprotective effects

120
Q

Why do COX2 selective inhibitors reduce the risk of stomach ulcers?

A

COX2 not expressed in the stomach

121
Q

Why have some COX2 selective NSAIDs been withdrawn from clinical use?

A

Use was a/w heart attacks
- ↓PGI2 synthesis in endothelium → vasodilation and ↓platelet aggregation

Metabolism and Biochem (8 decks)

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