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
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.
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

LOW DENSITY LIPOPROTEIN
STRUCTURE :
SURFACE (AMPHIPATHIC)
CORE (HYDROPHOBIC)
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