SummaryBackgroundSerum small dense LDL-cholesterol (sdLDL-C) value is suggested to bean important risk factor for atherosclerosis. Since sdLDL-C changes may be related to PCSK9 and SREBP-2 functions, the aim of this study was to investigate correlations between sdLDL-C, circulating PCSK9, SREBP-2 expression and some lipid parameters in serum and butty coat fraction of healthy subjects.MethodsOne hundred and twenty-four subjects were randomly included in the study. The lipid profile was measured using routine laboratory methods. The serum sdLDL-C level was calculated by a heparin-related precipitation technique. The cellular LDL-C/protein and cholesterol/protein values were measured after lysing of cells with methanol/chloroform binary solvent. The circulating PCSK9 level was measured using ELISA technique. The SREBP-2 expression level was estimated using theRT-qPCR technique.ResultsData showed significant correlations between LDL-C, TG and sdLDL-C levels (r=0.34, p=0.001; r=0.2, p=0.04). The circulating PCSK9 level was correlated to LDL-C (r=0.29, p=0.04), but not to sdLDL-C (r=-0.08, p=0.57). Also, cellular LDL-C value was not related to serum LDL-C level (r=-0.12, p=0.39). Furthermore, there was an inverse correlation between cellular LDL-C/protein value and estimated de novo cholesterol/protein value (r= -0.5, p=0.001). Similar results were observed for cellular LDL-C/protein value and SREBP-2 expression level (r= -0.52, p=0.004).ConclusionsWe concluded that the serum sdLDL-C value is not related to circulating PCSK9. Furthermore, SREBP-2 regulatory system was able to elevate the cellular cholesterol level after reducing LDL influx. We suggest to investigate the cellular sdLDL fate and lipid synthesis pathways in PCSK9-targeting studies.
Background. Cholesterol homeostasis is dependent upon the sterol regulatory element binding protein 2 (SREBP-2) regulatory system and the functioning of plasma proprotein convertase subtilisin/kexin type 9 (PCSK9). Many studies have also reported that low density lipoprotein receptor (LDLR) levels in cellular membranes are related to the functioning of these proteins.
Background &Aims:
It is well-known that the coronary artery stenosis is related to lipid
profile. This is a descriptive cross-sectional study to investigate the relationship between the serum
fat-soluble vitamins (A, E and D), circulating proprotein convertase subtilisin/kexin type 9
(PCSK9), and lipid profile in the study population.
Methods:
A total of 120 overweight subjects were participated in this study. The circulating
PCSK9 and vitamin D were measured by ELISA technique. The serum vitamin A and vitamin E
amounts were simultaneously measured by the HPLC method. The Serum Small Dense LDLCholesterol
(sdLDL-C) values were evaluated using heparin-Mg2+ precipitation technique. The lipid
profile was measured by routine laboratory techniques.
Results:
The serum vitamin E values correlated significantly to vitamin A (r= 0.47, P= 0.0001),
VLDL-C (r= 0.30, P= 0.002), total cholesterol (r= 0.309, P= 0.001), PCSK9 (r= 0.233, P= 0.01)
and total triglyceride (r= 0.61, P= 0.0001) values. The circulating PCSK9 values correlated significantly
to LDL-C (r= 0.17, P= 0.05) and total cholesterol (r= 0.23, P= 0.009) values. However, there
were not correlations between the levels of serum D and A vitamins, the serum LDL-C, sdLDL-C
and total cholesterol values.
Conclusion:
The data showed the correlations between serum vitamin E and PCSK9-related LDLC
values lower than the normal range. Furthermore, the results suggested a nutritional need on the
patents considering supplementation or fortification of vitamin E for the overweight subjects with
higher LDL-C levels.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.