lipoprotein
Lipid dalam Tubuh
Asam lemak
Trigliserida
Kolesterol
Fosfolipid
Glikolipid
Prostaglandin
Lipid ditransportasikan melalui aliran darah dalam bentuk
lipoprotein
Struktur Lipid
Peranan Biologis Lipid
sumber energi
komponen membran sel dan berbagai struktur sel
menstabilkan membran sel dan memungkinkan terjadinya transport
transmembran
prekursor untuk sintesa hormon.
Absorpsi Lipid
Trigliserida dan kolesterol dari makanan dalam usus dikemas sebagai kilomikron diangkut sal. limfe
darahlipoprotein lipase dalam jaringan lemak menghidrolisis trigliserida asam lemak dan kilomikron
remnantrigliserida/energy dlm jar. Lemak/otot
Kilomikron remnant dibersihkan oleh hati dalam sirkulasikolesterol bebas sintesis berbagai struktur, disimpan
dalam hati/dieksresikan ke empedu (sebagai kolesterol/asam empedu)/lipoprotein endogen (
Kolesterol dapat juga dari asetat dipengaruhi oleh HMG co A reduktase jika kolesterol endogen kurang
Dengan bantuan enzim, trigliserida monogliserida, digliserida dan asam lemak bebas, kolesterol
ester kolesterol bebas, fosfolipid turunan liso-nya
Monogliserida, digliserida, asam lemak bebas, kolesterol diemulsi garam empedu diserap dalam
mikrovili usus
Asam lemak 10 C diserap masuk ke sirkulasi darah berikatan dengan plasma menuju ke hati
Dalam sel mukosa usus, asam lemak rantai panjang diubah menjadi bentuk esternya yaitu
trigliserida dan ester kolesterol dimasukan ke dalam inti kilomikron untuk ditransportasikan dalam
darah
90-95% trigliserida dari makanan terserap
50% kolesterol yang terserap
Reseptor lipoprotein
Reseptor LDL
reseptor ini mengenali apo E dan B-100, memediasi pengikatan
lipoprotein di sel, uptake dan degradasi LDL, VLDL, IDL, berperan
menjaga kesimbangan kesetimbangan kolesterol sistemik dan
selular
Reseptor Remnant
reseptor ini mengenali apo E dan merupakan reseptor utama untuk
pembersihan sisa kilomikron dan beta-VLDL dari sirkulasi darah
Reseptor Scavenger
terdapat di permukaan makrofag dan sel otot,memediasi
pengambilan modifikasi LDL
Hormon yang Berpengaruh
Diabetics often have low HDL-C levels with elevated LDL-C and
triglyceride levels.
The National Cholesterol Education Program (NCEP) committee states
that diabetics with elevated cholesterol develop plaque formation in
their blood vessels leading to narrowing of the vessel lumen.
In type 2 diabetics who exhibit elevated triglyceride levels the
cholesterol level needs to be less than 200 mg/dL and the LDL-C level
needs to be maintained at 100 mg/dL or less low risk for plaque
formation in the blood vessels.
Because type 2 diabetics cannot move glucose from the bloodstream
into the tissues for metabolism as efficiently as the nondiabetic person,
they convert the excess glucose into fatty acid chains (in the liver) and
make more triglycerides.
HDL (good) cholesterol levels and triglyceride levels
cardiovascular problems
National Cholesterol Education
Program
The NCEP provides guidelines for evaluation of lipid panel results in
regard to risk factors for cardiovascular problems.
HDL (good) cholesterol protects against heart disease, so for HDL,
higher numbers are better.
HDL-C level less than 40 mg/dL is considered abnormally low and a
major risk factor (HDL levels of 60 mg/dL or more help to lower risk for
heart disease)
High amounts of triglycerides can also raise risk of heart disease.
Individuals with triglyceride levels that are borderline high (150 to 199
mg/dL) or high (200 mg/dL or more) may need treatment.
Type 2 diabetics often exhibit elevated cholesterol, triglycerides, and
LDL-C with low HDL-C.
Decreasing the LDL-C level is necessary to decrease the risk of
cardiovascular disease in the type 2 diabetic.
Glucose, total cholesterol, triglycerides, and hs-CRP These results
indicate medication changes may be needed to better control her
glucose levels.
hypertriglyceridemia, as may be common with type 2 diabetes.
inadequate or poorly functioning insulin leads to more triglyceride
formation in the liver VLDL cholesterol (VLDL-C), total cholesterol , HDL-
C, which means less removal of LDL-C. LDL-C deposits as plaque in the
blood vessels, narrowing and decreasing blood flow to all tissues and
especially to coronary arteries may lead to atherosclerosis, or hardening
and obstruction of her coronary blood vessels, and possibly lead to heart
attacks.
more utilization of triglycerides by the tissues for energy. Increased
demand leads to more triglyceride mobility from the liver to the tissues.
Pembentukan Fatty Streak
Lesi Arterosklerosis Lanjut
Plak Tidak Stabil
Primary and Secondary
Hyperlipoproteinemia
Elevations of LDLs and HDLs can rarely result from inborn errors of metabolism such as
enzyme or apoprotein deficiencies or, more commonly, from secondary causes or
underlying diseases (diabetes mellitus, blood pressure medication, and certain
estrogen hormone replacement therapies)
nephrotic syndrome, chronic renal failure, hepatic disorders including biliary
obstruction, other acute and transient stressrelated conditions, and medications such
as corticosteroids total cholesterol, LDL, and triglyceride
Hypertriglyceridemia can result from enzyme deficiency or from abnormal forms of
VLDL.
One fairly common condition of triglyceride excess is familial hypertriglyceridemia
(FHTG). In FHTG, the particle size but not the amount of VLDL is usually large
One notable cause of primary hypertriglyceridemia is deficiency in lipoprotein lipase
activity (enzyme is found in peripheral cells and the liver) dietary fats are not
properly metabolized, and circulating levels of chylomicrons cause lipemic serum
even in a fasting state and serum triglyceride levels that are well in excess of 500
mg/dL. These patients are also prone to acute pancreatitis and skin and eye
disorders.
Apoproteins
Interference :
Remove sample from red cells after blood clots or plasma has been spun
down.
The peroxidase assay can be susceptible to increases in uric acid, ascorbic
acid, bilirubin, hemoglobin, or other reducing substances. Samples should
have only the normal amount of these substances present.
The Specimen :
Nonhemolyzed serum or plasma, free from clots.
The patient need not be fasting if this is the only lipid test requested. However, if total cholesterol is
requested as part of a lipid panel, the patient must be fasting for 10 to 12 hours.
LDL CHOLESTEROL