12/2/2008

0,1 ml.
standard
5 ml. LB

0,1 ml.
serum
5 ml. LB

TARUH DALAM ES SELAMA 5 MENIT

KOCOK +

DIAMKAN SELAMA 30 MENIT

BACA DENGAN SPEKTROFOTOMETER

KADAR KOLESTEROL = RU/RS x 250 mg%
SERUM

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CHOLESTEROL
SOURCE
TRANSPORT
USE

Intestinal cholesterol absorption is an important origin of circulating

LDL-C. Although dietary cholesterol does contribute, the majority
(2/3 to 3/4) of cholesterol delivered to the intestine is derived from
biliary cholesterol excretion. Intestinal cholesterol undergoes micellar
adaptation by bile acids and is then absorbed into the intestinal cells.
The ensuing free cholesterol may subsequently be "pumped" back
into the intestine through adenosine triphosphate binding cassette
(ABC) transporters ABCG5 and ABCG8. Alternatively, intestinal free
cholesterol may be esterified through acyl-coenzyme A:cholesterol
acyltransferase (ACAT), and then packaged into chylomicrons (CMs) in
the intestinal epithelial cell by microsomal triglyceride transfer
protein (MTP). As CMs leave the intestine, their cholesterol is
transported through the lymphatic system to the liver.

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Hyperlipoproteinemia type II a (Familial

hypercholesterolemia )
Elevated serum cholesterol, most notably the LDL fraction (VLDL
and triglycerides are typically normal)
on lipoprotein electrophoresis (rarely done), a hyperlipoproteinemia type II
pattern is recognized

Premature cardiovascular disease, such as:

Angina pectoris, leading to PTCA or CABG

Myocardial infarction
Transient ischemic attacks (TIA's)
Cerebrovascular incidents/Strokes
Peripheral artery disease (PAOD)

A family history of premature atherosclerosis

Physical signs (not always present):
Tendon xanthomas (thickening of tendons due to accumulation of
macrophages filled with cholesterol).
Xanthelasma palpabrum (yellowish patches above the eyelids)
Arcus senilis cornea, whitish discoloration of the iris

Hyperlipoproteinemia type II a
(Familial hypercholesterolemia )
There are four major classes of FH:
Class I: LDL receptor (LDL-R) is not synthesized at all
Class II: LDL-R is not properly transported from the
Endoplasmic Reticulum to the Golgi Apparatus for
expression on the cell surface
Class III: LDL-R does not properly bind LDL on the cell surface
(this may be caused by a defect in either Apolipoprotei B100
(R3500Q) or in LDL-R)
Class IV: LDL-R bound to LDL does not properly cluster in
Clathrin-coated pits for Receptor-mediated endocytosis

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LOW DENSITY LIPOPROTEIN

STRUCTURE :
SURFACE (AMPHIPATHIC)
CORE (HYDROPHOBIC)

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METABOLISM of LIPOPROTEIN

This slide depicts sterol absorption and lipoprotein

synthesis and remodeling. Dietary cholesterol (free
cholesterol [C]) and plant sterols (non cholesterol
sterols [NC]) are transported into the intestinal
enterocyte through an NPC1L1-mediated pathway.
C and NC are effluxed back into the gut lumen by
apical ABCG5 and ABCG8 transporters. Cholesterol
is effluxed from the enterocyte by the basolateral
ABCA1 transporter and is etherified (CE) for
incorporation into chylomicrons (CM). CM
remnants generated by lipoprotein lipase (LPL)
hydrolysis are cleared by the hepatic LDL receptor
(LDL-R). Lipoprotein cholesterol is re-esterified and
repackaged with de novo-synthesized triglycerides
(TG) into VLDL, which is remodeled through the
actions of LPL and CETP.

C=free cholesterol (dietary cholesterol)

NC=non cholesterol sterols (plant sterols)
NPC1L1=Niemann-Pick C1 Like 1
ABCG5=ATP-binding cassette transporter G5
ABCG8=ATP-binding cassette transporter G8
ABCA1=ATP-binding cassette transporter A1
CE=cholesterol ester
LDL=low-density lipoprotein
VLDL=very low-density lipoprotein
LPL=lipoprotein lipase
CETP=cholesteryl ester transfer protein

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