Evaluation of: Calabresi L, Baldassarre D, Castelnuovo S et al.: Functional lecithin:cholesterol acyltransferase is not required for efficient atheroprotection in humans. Circulation 120, 628-635 (2009). Lecithin:cholesterol acyltransferase (LCAT) is an HDL-associated enzyme responsible for esterifying free cholesterol to cholesteryl ester within the plasma compartment. Mutations in the LCAT gene can cause LCAT deficiency, a very rare metabolic disorder associated with two hypoalphalipoproteinemia syndromes; familial LCAT deficiency, characterized by complete lack of enzyme activity, and fish-eye disease, with a partially defective enzyme. As LCAT deficiency causes hypoalphalipoproteinemia, carriers should be at increased risk of coronary artery disease because of defective reverse cholesterol transport; however, owing to the relatively small number of cases available, this hypothesis has not been confirmed. Calabresi et al. take advantage of the availability of 13 LCAT-deficient families to investigate the extent of carotid preclinical atherosclerosis in these patients.
Lecithin:cholesterol acyltransferase and vascular disease / G.D. Norata, A.L. Catapano. - In: CLINICAL LIPIDOLOGY. - ISSN 1758-4299. - 5:1(2010), pp. 13-15. [10.2217/clp.09.77]
Lecithin:cholesterol acyltransferase and vascular disease
G.D. Norata
;A.L. CatapanoUltimo
2010
Abstract
Evaluation of: Calabresi L, Baldassarre D, Castelnuovo S et al.: Functional lecithin:cholesterol acyltransferase is not required for efficient atheroprotection in humans. Circulation 120, 628-635 (2009). Lecithin:cholesterol acyltransferase (LCAT) is an HDL-associated enzyme responsible for esterifying free cholesterol to cholesteryl ester within the plasma compartment. Mutations in the LCAT gene can cause LCAT deficiency, a very rare metabolic disorder associated with two hypoalphalipoproteinemia syndromes; familial LCAT deficiency, characterized by complete lack of enzyme activity, and fish-eye disease, with a partially defective enzyme. As LCAT deficiency causes hypoalphalipoproteinemia, carriers should be at increased risk of coronary artery disease because of defective reverse cholesterol transport; however, owing to the relatively small number of cases available, this hypothesis has not been confirmed. Calabresi et al. take advantage of the availability of 13 LCAT-deficient families to investigate the extent of carotid preclinical atherosclerosis in these patients.File | Dimensione | Formato | |
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