Sorted By Test Name - Mayo Medical Laboratories

LCATD
83253
C, Buchet JP, Leroyer A, et al: Renal and neurologic effects of cadmium, lead, mercury, and arsenic in
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Health Perspect 2006;114:584-590 3. Pascal DC, Ting BG, Morrow JC, et al: Trace metals in urine of
United States residents: reference range concentrations. Environ Res 1998;76(1):53-59
Lecithin Cholesterol Acyltransferase Deficiency Profile
Clinical Information: Lecithin cholesterol acyltransferase (LCAT), a glycoprotein with an apparent
molecular weight of 67 kD, is the enzyme responsible for synthesizing the majority of cholesteryl esters in
serum. It acts by transferring fatty acid from phosphatidylcholine to the 3-hydroxyl group of cholesterol.
In serum, LCAT protein is bound to high-density lipoproteins (HDL) and it esterifies cholesterol
primarily in this class of lipoproteins. The major structural protein of HDL, apolipoprotein AI (apo AI), is
believed to be the principal activator of LCAT. There is evidence that serum LCAT also may act directly
on lower-density lipoproteins. It is believed that LCAT regulates the transport of cholesterol between
extravascular pools. In the theoretical pathway, known as reverse cholesterol transport, cholesterol is
moved from peripheral tissues to the liver for catabolism. The esterification of cholesterol by LCAT in
serum serves to maintain a chemical concentration gradient for unesterified cholesterol between
peripheral cells and the serum. Plasma lysophosphatidylcholine (LPC) is 1 of the products of LCAT and
as such, LPC concentration is diminished in patients with LCAT deficiency.
Useful For: Detection of lecithin cholesterol acyltransferase deficiency
Interpretation: Norum-Gjone disease is a severe form of lecithin cholesterol acyltransferase (LCAT)
deficiency characterized by: -Diminished serum levels of cholesterol ester (