Lecithin phospholipids also called
phosphatidylcholine
Lecithin is any of a
group of phospholipids found in egg yolks and the plasma membrane of plant and
animal cells, used as an emulsifier in a wide range of commercial products,
including foods, cosmetics, paints, and plastics; also called
phosphatidylcholine.
When researchers use the term “lecithin,” they are referring to a purified
substance called phosphatidyl choline (PC) that belongs to a special category of
fat-soluble substances called phospholipids.
Phospholipids are essential components of cell membranes. Supplements labeled
as “lecithin” usually contain 10–20% PC. Relatively pure PC supplements are
generally labeled as “phosphatidylcholine.”
Department of Endocrinology, University Medical Center
Groningen, P.O. Box 30001, 9700 RB Groningen, The Netherlands. STUDY:
CONTEXT: Lecithin:cholesterol acyltransferase (LCAT), which
esterifies free cholesterol to cholesteryl esters, is required for normal plasma
lipoprotein structure and is instrumental in high density lipoprotein (HDL)
remodeling, but the relationship of variation in plasma LCAT activity with
subclinical atherosclerosis is unclear. OBJECTIVES: The aim of the study was to
determine the effect of the metabolic syndrome (MetS) on plasma LCAT activity
and its relationship with carotid artery intima media thickness (IMT). SETTING:
The study was conducted at the vascular laboratory of a university medical
center. METHODS: In 74 subjects with MetS and 90 subjects without MetS (National
Cholesterol Education Program Adult Treatment Panel III criteria), mean carotid
artery IMT, plasma lipids, LCAT activity (exogenous substrate method),
high-sensitive C-reactive protein, and homeostasis model assessment insulin
resistance (HOMA(ir)) were documented. RESULTS: IMT was greater (P = 0.01) and
plasma LCAT activity was higher (P < 0.001) in subjects with MetS compared to
subjects without MetS. Similar increases in IMT and LCAT were found in MetS
subjects without type 2 diabetes mellitus. Multiple linear regression analysis
demonstrated that plasma LCAT activity was independently and positively related
to HOMA(ir), plasma triglycerides, non-HDL cholesterol, and HDL cholesterol (all
P < 0.001). After adjustment for age and sex, IMT was positively associated with
LCAT activity (P < 0.01), independently of the presence of MetS (or
alternatively of plasma lipids), HOMA(ir), and high-sensitive C-reactive
protein. CONCLUSIONS: Plasma LCAT activity is elevated in MetS and may be a
marker of subclinical atherosclerosis. Our findings do not support the
contention that strategies to elevate LCAT more than this study provides are
necessarily beneficial for cardioprotection.