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Metabolism-Alaa > Lipid transport > Flashcards

Lipid transport Flashcards

1
Q

Describe how lipids are transported in the blood (percentages)

A

~ 2% of lipids (mostly fatty acids) carried bound to ALBUMIN but this has a limited capacity (~ 3 mmol/L)

~ 98% of lipids are carried as lipoprotein particles consisting of phospholipid, cholesterol, cholesterol esters, proteins & TAG

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2
Q

what r some various classes of lipids?

A
  • TAG
  • FFA
  • Cholesterol/ cholesterol esters
  • phospholipids
  • Vit A K E D
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3
Q

above______mmol/L of cholesterol is a risk of CVS

A

5.0

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4
Q

Explain how hyperlipoproteinaemia may be treated?

A

FIRST APPROACH

**diet and lifestyle should be .

aim is to reduce cholesterol levels,increase finer intake if no response then.. give em

DRUGS

**STATINS>>

1) reduces synthesis of cholestrol in liver by inhibiting enzyme HMG-CoA reductase.
2) increases the expression of lipoprotein lipase

***BILE SALT SEQUESTRANTS

• Bind bile salts in GI tract. Forces liver to produce more bile acids using more cholesterol e.g. Colestipol

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5
Q

what r cholesterol esters, what forms them?

A

cholestrol w/ FFA

via Lecithin Cholesterol Acyltransferase (LCAT) or Acyl-coenzyme A: cholesterol acyltransferase

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6
Q

describe structure of phospholipids

A

Choline>polar head

Phosphate

Glycerol

Fatty acid>hydrophobic tail

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7
Q

what is a micelle?

A

single layer phospholipid monolayer

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8
Q

**cholesterol made in the liver is secreted as BILE SALTS

A

ok

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9
Q

describe structure of a lipoprotein

A
  • phospholipid monolayer w/ apolipoproteins either on the surface or integral.
  • a cargo inside consisting of various lipid classes the wish to transport.
  • transport insoluble lipids to the BS*
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10
Q

Name the five distinct classes of lipoproteins according to their DENSITY

A
  • Chylomicrons
  • VLDL (Very Low Density Lipoproteins)
  • IDL (Intermediate Density Lipoproteins)
  • LDL (Low Density Lipoproteins
  • HDL (High Density Lipoproteins)

(keep hawraa for last ;p)

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11
Q

How many classes of apoplipoproteins r there?

A

6 major classes (A,B,C,D,E &; H)

-Peripheral Apolipoproteins (e.g. apoC, ApoE)

(u can “see” themm)

-Integral Apolipoproteins (e.g. apoA, ApoB)

(apple ben (ya3ny pen))

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12
Q

which class of lipoproteins mostly carry C.esters? Fat?

A

Fat>> chylomicron, VLDL

Cholestrol esters>> IDL,LDL,HDL

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13
Q

what is the largest lipoprotein?

A

chylomicrons

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14
Q

**the density of the lipoprotein is depended on the amount of proteins on their surface.

A

ex: HDL, is the smallest but has the highest density hence its name.

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15
Q

if u take a sample of blood from a person who just had a cheeseburger, how will his blood appear?

A

creamy appearance, bc of the fatty chylomicrons present inside.

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16
Q

Chylomicrons are normally only present in blood______after a meal

A

4 – 6 h

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17
Q

what r the roles of the apoliporotein? (apple is my colleague)

A

Have two roles:

Structural: Packaging water insoluble lipid

Functional: (co-lig) Co-factor for enzymes Ligands for cell surface receptors

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18
Q

function of LDL, how to they enter tissues?

A

transport cholesterol from liver to peripheral tissues. cell express LDL receptor and take it up LDL via receptor mediated endocytosis.

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19
Q

why is LDL more susceptible to oxidative damage?

A

it has a longer half-life in comparison with the others bc the liver cannot clear it efficiently bc LDL does not have Apo C or E & (Liver LDL-Receptor has a high affinity for apoE)

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20
Q

explain how high LDL can lead to atherosclerosis

A

macrophages will recognise it and engulf it, these macrophages then transform into FOAM cells and accumalate in intimate of blood vessel walls forming a FATTY STREAK. which can then become an atherosclerotic plaque. this plaque grows and enroaches on the lumen of the artery.>>this can rupture or cause angina>>and trigger thrombosis (clot) by activating platelets and clotting cascades>>STROKE & MI

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21
Q

what is hypercholesterolaemia? what r some clinical signs?

A

high levels of cholesterol in the blood, Cholesterol depositions in various areas of body

  • Xanthelasma - Yellow patches on eyelids
  • Tendon Xanthoma - Nodules on tendon
  • Corneal arcus - obvious white circle around eye.

Common in older people but if present in young could be a sign of hypercholesterolaemia

22
Q

what is Hyperlipoproteinaemias? what causes it? How many classes r there?

A

Raised plasma level of one or more lipoprotein classes.

or

any condition, in which after 12 hrs of fast, plasma cholesterol/TAG is raised

Caused by either:

  1. Over-production
  2. Under-removal

Defects in:

  • Enzymes
  • Receptors
  • Apoproteins
23
Q

what is familial Hypercholeserolaemia?

A

type 2a Hyperlipoproteinaemia. there is absence or deficiency of functional LDL RECEPTORS. causing elevated levels of LDL and cholesterol in plasma.

“u did not give my family the receipt for that fatty avocado”

24
Q

why and how r Hyperlipoproteinaemias classified?

A

bc each have different causes & respond to different treatments and have a different risk in coronary heart Disease.

25
Q

what r the actions of bile salt sequestrants? eX: cholestyramine

A

lower plasma cholesterol by increasing its disposal from the body. they act by binding to bile salts in the GI tract and prevent them from being reabsorbed into the hepatic portal circulation.

26
Q

Explain why individuals with a defect in the enzyme lecithin- cholesterol acyltransferase produce unstable lipoproteins of abnormal structure. What are the clinical consequences of this defect?

A

LCAT, is responsible for forming the lipoprotein particle AND maintaining its structure. **it converts Cholesterol (a surface lipid) into cholesterol ester ( a CORE Lipid) DEFICIENCY in this enzyme leads to UNSTABLE lipoproteins w/ abnormal structure and fails in transporting lipid. this will cause LIPID deposits, and ATHEROSCLEROSIS

27
Q

Describe metabolism of VLDL where is it made? what it responsible for?

A

in liver and responsible in transporting TAG to tissues. binds to LPL on endothelail cells of cappillaries on muscles and adipose tissue, to release TAG in muscles>>released FFA used for energy in adipose>> they remake TAG again and stored as fat.

28
Q

Describe metabolism of IDL and LDL where is it made?

A

IN BLOOD as VLDL is being depleted (about 30%) some detach from the LPL receptor and go back to liver.. OR some VLDL r converted to IDL, which is retaken up by liver or rebind to LPL. when 10% is depleted, IDL then becomes an LDL! SO BASICALLY LALLS VLDL>>IDL>>LDL (Vgaygay comes first)

29
Q

how do LDL enter cells?

A

by receptor mediated endocytosis! those cells that want cholestrol will express LDL recepters on their surface, so LDL can bind and get in, fuse with lysosomes and cholesterol and FF r released.

30
Q

what is responsible for the presence of LDL receptor on cells?

A

its controlled by the concentration of cholesterol in a cell.

31
Q

Describe metabolism of HDL where is it made? function?

A

made in liver & intestines. liver makes these nascent (empty) HDL which will ggein its journey in picking up any excess cholesterol from tissues. in the peripheral tissues, ABCA1 (abbas) will load cholesterol in HDL( hoor), cholestrol is then broken down into cholestrol esters by LCAT. once they’re loaded up, they carry on with their journey in the BS & on their way, some transfer may occur on the way with other lipoproteins Ex: swapping can happen btw HDL and LDL (exchanging Cholesterol esters with TAG) via CETP (cholesterol exchange transfer protein) HDL is either taken up by cells that need cholesterol or taken back to liver where it is needed to bake bile salts used in DIGESTION.

32
Q

what does ABCA 1 do?

A

a protein within cells that will help load the HDL with cholesterol.

33
Q

what is function of LCAT?

A

LCAT, is responsible for forming the lipoprotein particle AND maintaining its structure. **it converts Cholesterol (a surface lipid) into cholesterol ester ( a CORE Lipid) .

34
Q

which cells require HDL the most? by which receptor r they taken up?

A

the steroidegenic cells, (those that make steroid hormones) they obviously need cholesterol to make steroid hormones via scavenger receptor (SR-B1)

35
Q

Cholesterol test

A

Total Cholesterol (TC) Ideally 5 mmol/L or less • Non HDL-Cholesterol (total cholesterol minus HDL-cholesterol) Ideally 4mmol/L or less • LDL-Cholesterol (LDL-C) Ideally 3 mmol/L or less • HDL-Cholesterol (HDL-C) Ideally over 1mmol/L (men) and over 1.2mmol/L (women). • Total cholesterol:HDL-C ratio Ratio above 6 considered high risk - the lower the ratio the better. • Triglyceride (TG) Ideally < 2mmol/L in fasted saample

36
Q

function of HDL

A

transport excess cholestrol from cells to liver, to make bile salts used in digestion OR transports cholesterol to those cells that need ziyada.

37
Q

difference btw dyslipoproteinemia and Hyperlipoproteinemia

A

dyslipoproteinemia>> any defect in the METABOLISM of the lipoprotein. Hyperlipoproteinemia>>raised in levels of one or more plasma lipoproteins.

38
Q

which 2 ezmymes is the major control site in the pathway of gluconeogenesis?

A

PEPCK &amp; fructose 1,6 biphosphotase

39
Q

where does FFA synthesis occur? what about oxidation?

A

FFA synthesis occurs on the cytoplasm oxudation occurs in mitochondra

40
Q

which lipoprotein particle contains the greatest amount of cholesterol and cholesterol esters?

A

LDL

41
Q

which lipoprotein particle facilitates reverse cholesterol transport?

A

HDL

42
Q

which enzyme is inhibited by statin drugs?

A

HMG-CoA reductase

43
Q

Explain why individuals with a defect in the enzyme lecithin-cholesterol acyltransferase LCAT produce unstable lipoproteins of abnormal structure. What are the clinical consequences of this defect?

A

All mature lipoproteins found in normal human plasma are spherical particles that consist of a surface coat and a hydrophobic core. Lipoproteins particles are only stable if they maintain their spherical shape and this is dependent on the ratio of core to surface lipids. As the lipid from the hydrophobic core is removed and taken up by tissues the lipoprotein particles becincome UNSTABLE as the ratio of surface to core lipids INCreases. Stability can be restored if some of the surface lipid is converted to core lipid. This is achieved by the enzyme LCAT LCAT>> which is important both in the 1) formation of lipoprotein particles and in maintaining their structure. 2) The enzyme converts cholesterol (a surface lipid) to CE (a core lipid) using fatty acid derived from lecithin (phophatidylcholine).

44
Q

What classes of lipoprotein r present in the serum from a fasting blood sample taken from a normal individual and what are their functions?

A

VLDL (Transport of triacylglycerol synthesised in liver to tissues) LDL (Transport of cholesterol from liver to tissues HDL (transport of excess cholesterol from cells to liver for disposal) IDL would also be acceptable ❌❌❌ but NOT chylomicrons as this is a fasting sample❌❌❌

45
Q

List 2 signs or symptoms of the very high blood cholesterol that you might expect to find in a patient w/ hypercholestremia?

A

~Corneal Arcus ~Xanthelasma ~tendom xanthoma ~increased risk in getting atheresclerotic plaques

46
Q

Outline two pathways by which tissues can obtain the cholesterol they need.

A

1) Direct synthesis of cholesterol from acetyl CoA within tissues. (…from HMG-CoA would also be acceptable) 2) Cells can also obtain cholesterol synthesised in the liver via receptor mediated endocytosis of LDL particles

47
Q

Give ecample of a statin?

A

Atorvastatin!

48
Q

alaa look at table on types of hyper lipoproteinemia

A

ok

49
Q

Functions of cholestrol

A
50
Q

Mechanism of actions of statins, give an example of a statin

A

Metabolism-Alaa (23 decks)

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