Skip to main content

Apolipoprotein A1

Order Code CH116
Turnaround Time 24 hours
Test Includes

Apolipoprotein A1

Specimen Requirements
Specimen Source
Transport Container
(Specimen Container)

SST (Tiger Top)
Lithium Heparin/ Sodium Heparin/ EDTA

Preferred Specimens
Minimum Volume (uL)
.5 mL
Collection Instructions
(Transport Temperature)
Specimen Stability
Temperature Period
Room temperature 3 days
Refrigerated 7 days
Frozen 3 months
Test Details
Clinical Significance

Lipids that are synthesized in the intestine or liver need to be transported to tissues and organs for their varied metabolic functions. Given the hydrophobic nature of the neutral fats, triglycerides, and cholesterol esters, lipid transport and delivery via plasma would not be possible without some form of hydrophilic adaptation. Lipids are transported by means of a series of micellar structures known as lipoproteins that consist of an outer monolayer of protein (apolipoprotein), polar lipids, and an inner core of neutral lipids. Apolipoprotein A-I (ApoA-I) is synthesized in both the liver and intestine, while ApoA-II synthesis appears to occur only in the liver. ApoA-I and ApoA-II are the major apolipoproteins found in HDL, with small amounts found in chylomicrons. Approximately 50% of HDL mass is protein, with ApoA-I and ApoA-II constituting approximately 90% of the lipoprotein fraction. The ratio of A-I to A-II is roughly 3:1. On average, ApoA-I levels are higher in women than in men, whereas ApoA-II levels are similar. Lipoprotein particles that contain only ApoA-I appear to stimulate cholesterol efflux (movement of cholesterol from extrahepatic tissues to the liver for disposal). ApoA-I also has a role in the activation of LCAT (lecithin-cholesterol acyltransferase). Measurement of ApoA-I is useful in predicting patients with high risk of coronary artery disease (CAD). Levels of ApoA-I are inversely correlated with the risk of premature CAD. The relative proportion of ApoB, a major component of VLDL and LDL, to ApoA is effective in differentiating individuals with or without ischemic heart disease. An increased ApoB/ApoA ratio at a young age is potentially a marker for CAD. Elevated ApoA-I levels are seen in familial hyper-α-lipoproteinemia and weight reduction. Decreased levels are associated with various forms of familial and non-familial hypo-α-lipoproteinemia, Tangier disease, premature CAD, hypertriglyceridemia, uncontrolled diabetes, hepatocellular disorders, cholestasis, nephrotic syndrome, and chronic renal failure.

Reference Ranges

>115 mg/dL

>125 mg/dL