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Lipoproteins: Synthesis, Transport and Metabolism

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Lipoproteins: Synthesis, Transport and Metabolism
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-Today: Lipoproteins



-Friday: Quiz, b-oxidation and some paper discussion



-Monday: Dr. Neile Edens Guest Lecture

-Read McGary review before lecture

Transport of Fat: Lipoproteins



I. Chylomicrons

II. Triglyceride storage in adipose

III. VLDL, LDL, IDL, HDL

IV. Reverse Cholesterol Transport

V. Medical implications

VI. Nutritional regulation of lipoproteins







Stipanuk 351-364

Overview

• Transport dietary lipids from intestine to liver

(exogenous)



• Transport lipids from liver to peripheral tissues

(endogenous)



• Lipoproteins

– Core of TG and CE

– Surface of phospholipids and some cholesterol

– Apolipoproteins (regulators of LP metabolism)

– CM, VLDL, IDL, LDL, HDL





• Clinical importance for disease

Liver

Dietary TG

CE Apo B48



cholesterol

Apo B48

CII

FFA FFA-FABP TG

TG/CE

micelle

E

CIII



chylomicron

ER/golgi





enterocyte









Plasma

Chylomicron Assembly



-assembled in enterocyte golgi/ER



-Apolipoprotein (Apo) B organizes assembly

-B48



- Requires phospholipids



-2 forms of apo B

-B100, large- liver

-B48, smaller – intestine



- Picks up apo C and apo E in plasma



- TG composition closely resembles dietary intake

I. Synthesis of apoB



II. ApoB associates with

lipids



PDI (protein disulfide isomerase)

and MTP (microsomal TG transfer

protein) aid in LP folding and TG

addition



No MTP = No LP release

(a-betalipoproteinemia)



III. Lipoprotein release



IV. If not enough TG associates with

lipoprotein a protease removes apoB

and prevents its secretion



V. If lipoprotein is not properly formed

protease also can remove apoB and

prevent lipoprotein secretion

Major Lipoproteins Apolipoproteins Density (g/mL)



Apo B-48: chylomicrons C-II, C-III, E 1.21

alpha-HDL A-II 1.063-1.21









Density inversely proportional to lipid content

Type Association Function



B48 Chylomicron Lacks LDL recpt

binding domain



B100 VLDL,IDL,LDL Binds LDL recpt.



C-II Chyl. VLDL, IDL, HDL Activates LPL



C-III Chyl. VLDL, IDL, HDL Inhibits LPL



E Chyl. Remnant, VLDL, IDL Binds LDL recpt

HDL



A-1 HDL LCAT activator

(lecithin:cholesterol

acyltransferase)

Plasma

TG

B48 FFA

Oxidation

CII

muscle

TG/CE Lipoprotein

CIII Lipase



chylomicron





Lipoprotein B48 CII

FFA Lipase

TG/CE

CIII

FFA E

Chylomicron remnant

G3P liver





Triglyceride

adipose

storage

Fat accumulation in adipose: High I/G (Fed)

Capillary endothelium

(+)

B48 insulin

CII

LPL LPL deficiency?

TG/CE

CIII





chylomicron FFA Glucose

glut4

(+) Insulin

regulated

glucose

CoA transport

G3P

Fatty acyl CoA







Triglycerides

adipose

Fat accumulation in adipose: Low I/G (ketogenic)

Capillary endothelium

(-)

B48 insulin

CII

LPL

TG/CE FFA-albumin (oxidation)

CIII





chylomicron FFA Glucose



(-) Insulin

glut4 regulated

glucose

CoA transport

G3P

Fatty acyl CoA







Triglycerides

adipose

Regulation of Lipoprotein Lipase





Fed state - LPL synthesis (adipocytes)





Fasted/ -

LPL synthesis (muscle)

exercise

state

Dietary factors affecting Chylomicron and Chylomicron remnant clearance







-elevated postprandial lipoproteins and cardiovascular disease



-Diets rich in PUFA can reduce postprandial TG response

-compared to diets rich in SFA

-Increased LPL activity = Increased TG clearance from CM

-Preferential hydrolysis of PUFA-containing CM

-Increased clearance of CMr

-Human data are less convincing than animal studies



-Omega 3 CE)

• Regulated by SREBP

monitors free cholesterol

Free cholesterol = LDL receptors, chol. synthesis

ACAT

Plasma

Dietary Carbohydrate

LIVER







glucose pyruvate Acetyl CoA





Acetyl CoA

mitochondria

cholesterol

(exogenous) TG

Cholesterol

(endogenous)

B100



CE/TG VLDL

FFA FFA TG









VLDL

From liver Cholesterol.

In bile LIVER

Endogenous cholesterol

B100 E



CII

CE/TG





VLDL B100 E

LDL receptor

CE/TG



IDL E





B100

LPL TG CE



FFA LDL Extrahepatic tissue





muscle adipose LDL receptor

HDL and Reverse Cholesterol

Transport

Lipid poor AI are the

Liver and small intestine smallest HDLs (liver and SI)



Discoidal HDL are produced

Lipid poor AI by the action of LCAT

(pre HDL) (esterify cholesterol)



spherical Spheroidal HDLs are

produced by the further action

Cholesterol of LCAT and CETP (tranfer

cholesterol to LP for TG)

LCAT

LCAT HDLs pick up apoproteins from

CETP

other LP



Discoidal HDL

HDL picks up free cholesterol from Extrahepatic tissue/cells

peripheral tissues and converts it into

cholesterol esters

Cholesterol esters

LCAT acat

Free cholesterol





Cholesterol and lecithin (phospholipid)

Extracellular space

LCAT

AI HDL Discoidal HDL



AI

1

HDL/Cholesterol

To liver 2 CETP

3

Cholesterol to IDL,

Adrenal, gonadal LDL and VLDL

PLASMA

CETP exchanges cholesterol esters in HDLs for triglycerides in VLDLs and

chylomicrons.





VLDL

CE



CETP

FFA

LPL TG





Liver IDL TG

(LDL receptor) HDL

CETP

CE





LPL

FFA TG

CETP

Liver

CE

(LDL receptor)

LDL

Extrahepatic tissue/cells



1. LCAT deficiency?

2. CETP deficiency? CE

3. apo AI deficiency? ACAT

FC





Cholesterol and lecithin (phospholipid)

Extracellular space

LCAT

Pre b HDL Discoidal HDL





AI

1

HDL/Cholesterol

To liver 2 CETP

3

Cholesterol to IDL,

Adrenal, gonadal LDL and VLDL

PLASMA

Reverse cholesterol transport: HDLs return cholesterol to liver





LCAT

FC

Free Discoidal HDL CE Spherical HDL

cholesterol







TG

Peripheral tissue AI HDL

CETP







IDL CE VLDL CE VLDL TG









liver

Bile acids/Free cholesterol

LDL





Dietary fat Bile salts Endogenous

Cholesterol

extrahepatic

small Exogenous tissue

intestine cholesterol





HDL

chylomicrons

chylomicrons reminants

VLDL



IDL









capillaries



Lipoprotein Lipase Lipoprotein Lipase

FFA FFA

Adipose, muscle

Dietary Regulation of Lipoprotein

Synthesis

Chylomicron Synthesis VLDL Synthesis (Liver)









Chylomicron VLDL (+)

High CARB FA/TG

Insulin



(+)

Acetyl CoA

Dietary Fat



Intestinal Epithelium

(+)

Glucose

Atherogenic Particles



Apolipoprotein B

MEASUREMENTS:

Non-HDL-C









VLDL VLDLR IDL LDL Small,

dense

LDL

TG-rich lipoproteins



Thanks to Lipids Online: http://www.lipidsonline.org/

Hypertriglyceridemia and CHD Risk:

Associated Abnormalities



 Accumulation of chylomicron remnants

 Accumulation of VLDL remnants

 Generation of small, dense LDL-C

 Association with low HDL-C

 Increased coagulability

-  plasminogen activator inhibitor (PAI-1)

-  factor VIIc

- Activation of prothrombin to thrombin

Relationship between HDL/LDL and heart disease:

One Theory



Monocyte (white blood cell)

Cholesterol to liver



LDL

vascular endothelium



(+)

differentiate Oxidized LDL

Arterial intima



Macrophage



LDL (+) (-) HDL









Foam cells (fatty streak)

Alcohol Increases HDL-C Level

• Alcohol increases HDL-C level in a dose-dependent

manner.

• Half bottle of wine per day (39 g alcohol) for 6 weeks

significantly increased mean HDL-C level by 7 mg/dL

in 12 healthy subjects.1

– Wine intake did not significantly affect Total-C,

Total-TG, or LDL-C.1

• One beer per day (13.5 g alcohol) for 6 weeks

significantly increased mean HDL-C level by 2 mg/dL

in 20 healthy subjects.2

– Beer intake did not significantly affect LDL-C,

VLDL-C, TG, or apolipoproteins.



1. Thornton J et al. Lancet 1983;ii:819–822

2. McConnell MV et al. Am J Cardiol 1997;80:1226–1228

Postprandial Changes in Plasma

Lipid Metabolism

Fat storage via LPL

Transfer of cholesterol from cells into plasma

reverse transport of cholesterol from peripheral tissue to liver



Exchange of cholesterol for VLDL TG in HDL (CETP)



LCAT activity = esterification of free cholesterol (HDL)







These postprandial changes are beneficial in maintaining

whole body homeostatsis of glycerides and cholesterol

Cholesterol levels are regulated

• 1. Synthesis : HMG CoA reductase

• 2. LCAT/ACAT : Free cholesterol

• 3. LDL receptor levels

• 4. Reverse cholesterol transport

• 5. Dr. Allred will discuss further


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