Abstract
This study aimed to determine the association of fatty acid transporter plasma soluble cluster of differentiation 36 (sCD36) with subclinical carotid atherosclerosis (SCA). A cross-sectional study was conducted in 1023 subjects, 225 with type 1 diabetes (T1D), 276 with type 2 diabetes (T2D) and 522 who were nondiabetic. Carotid atherosclerotic plaque (CAP) presence was determined using B-mode carotid ultrasound imaging. sCD36 were analysed by ELISA, and CD36 surface receptor and mRNA expression were measured by flow cytometry and real-time PCR. Logistic regression models were used to evaluate sCD36 as a biomarker of SCA. Up to 376 (36.75%) participants had at least one CAP, 76 T1D, 164 T2D and 136 without diabetes, while the remaining 647 (63.25%) did not have any CAP. There were no differences in sCD36 between patients with and without CAP in T1D (p = 0.287) or T2D (p = 0.513). Although nondiabetic subjects with plaques had lower sCD36 levels than those without (p = 0.023), the multivariate models revealed no association of sCD36 with CAP in any of the three study groups. No differences were found in surface CD36 or CD36 mRNA expression between the patients with and without CAP. sCD36 is not associated with SCA in type 1 or type 2 diabetic or in nondiabetic subjects.
Highlights
Accelerated atherosclerosis is the primary cause of the increased cardiovascular morbidity and mortality associated with type 1 (T1D) and type 2 diabetes (T2D)
DiTscauksesniotongether, our results show no differences in the fatty acid transporter soluble cluster of differentiation 36 (sCD36) concentration between subjects with and without carotid atherosclerotic plaque in the type 1 diabetes (T1D), T2D or nondiabetic contrToalkgernoutopgse.thAerll, ooufrtrheessueltsstsuhdoywgnrooudpifsfewreenrceefsrienethofe fmatatcyraocviadstcrualnasrpdoirsteearsseCDan3d6 cdoindcennottrahtaiovne ebsettawbeliesnhesducbhjercotnsicwkiitdhnaenyddiwseiathseo.uTthcearreowtidasantohearsossocclieartoiotincopflfaaqttuyeaicnidthtreanTs1pDo,rtTer2Dwiothr tnhoenpdrieasbeentciec ocornbturordl egnrooufpess.taAblllisohfetdhessuebcsltiundicyalgcraoruoptisdwatehreerforseceleorof smisaicnroavnayscouflathredgisreoauspes.anWdedaisdsensostedhathvee established chronic kidney disease
Circulating plasma sCD36 concentration does not appear to be a biomarker of the presence or burden of subclinical nonstenotic carotid atherosclerosis
Summary
Accelerated atherosclerosis is the primary cause of the increased cardiovascular morbidity and mortality associated with type 1 (T1D) and type 2 diabetes (T2D). There is solid evidence from experimental, clinical and epidemiological studies showing that hyperglycemia and its associated metabolic disturbances are linked to an increased inflammatory response that contributes through different pathways to the inflammatory response involved in the pathogenesis of the atherosclerotic process [2,3]. The cluster of differentiation 36 (CD36) is an 88-kDa transmembrane glycoprotein expressed in many cell types, and plays an essential role in lipid metabolism, angiogenesis and inflammation. This fatty acid transporter is related to several disease conditions such as cancer biology, insulin resistance, stroke, diabetes nephropathy and atherosclerosis [4,5]. Previous studies demonstrated the involvement of CD36 in the progression of atherosclerosis, and that deletion or blockage of the CD36-induced signalling pathway decreased the development of atherosclerotic lesions in mice [7,8]
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