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Abstract CD36 may defect on platelets and/or monocytes in healthy individuals, which was defined as CD36 deficiency. However, we did not know the correlation between the molecular and protein levels completely. Here, we aim to determine the polymorphisms of the CD36 gene, RNA level, and CD36 on platelets and in plasma. The individuals were sequenced by Sanger sequencing. Bioinformational analysis was used by the HotMuSiC, CUPSAT, SAAFEC-SEQ, and FoldX. RNA analysis and CD36 protein detection were performed by qPCR, flow cytometry, and ELISA. In this study, we found c.1228_1239delATTGTGCCTATT (allele frequency = 0.0072) with the highest frequency among our cohort, and one mutation (c.1329_1354dupGATAGAAATGATCTTACTCAGTGTTG) was not present in the dbSNP database. 5 mutations located in the extracellular domain sequencing region with confirmation in deficient individuals, of which c.284T>C, c.512A>G, c.572C>T, and c.869T>C were found to have a deleterious impact on CD36 protein stability. Furthermore, the MFI of CD36 expression on platelets in the mutation-carry, deleterious-effect, and deficiency group was significantly lower than the no-mutation group (P

CD36 may defect on platelets and/or monocytes in healthy individuals, which was defined as CD36 deficiency. However, we did not know the correlation between the molecular and protein levels completely. Here, we aim to determine the polymorphisms of the CD36 gene, RNA level, and CD36 on platelets and in plasma. The individuals were sequenced by Sanger sequencing. Bioinformational analysis was used by the HotMuSiC, CUPSAT, SAAFEC-SEQ, and FoldX. RNA analysis and CD36 protein detection were performed by qPCR, flow cytometry, and ELISA. In this study, we found c.1228_1239delATTGTGCCTATT (allele frequency = 0.0072) with the highest frequency among our cohort, and one mutation (c.1329_1354dupGATAGAAATGATCTTACTCAGTGTTG) was not present in the dbSNP database. 5 mutations located in the extracellular domain sequencing region with confirmation in deficient individuals, of which c.284T>C, c.512A>G, c.572C>T, and c.869T>C were found to have a deleterious impact on CD36 protein stability. Furthermore, the MFI of CD36 expression on platelets in the mutation-carry, deleterious-effect, and deficiency group was significantly lower than the no-mutation group (P < 0.0500). In addition, sCD36 levels in type II individuals were significantly lower compared with positive controls (P = 0.0060). Nevertheless, we found the presence of sCD36 in a type I individual. RNA analysis showed CD36 RNA levels in platelets of type II individuals were significantly lower than the positive individuals (P = 0.0065). However, no significant difference was observed in monocytes (P = 0.7500). We identified the most prevalent mutation (c.1228_1239delATTGTGCCTATT) among Kunming donors. Besides, our results suggested RNA level alterations could potentially underlie type II deficiency. Furthermore, sCD36 may hold promise for assessing immune reaction risk in CD36-deficient individuals, but more studies should be conducted to validate this hypothesis. [ABSTRACT FROM AUTHOR]

Background: Our previous study suggested CD36 may be a positive regulator of hepatitis B virus (HBV) replication in vitro. Therefore, the present study aimed to investigate whether circulating soluble CD36 (sCD36) could serve as a diagnostic and prognostic biomarker for HBV-related liver diseases based on the clinic collected data. Methods: A total of 282 subjects were divided into healthy controls (HC, n = 47), chronic hepatitis B (CHB, n = 68), HBV-related liver cirrhosis (HBV-LC, n = 167). Soluble CD36 in plasma was measured by ELISA, and monocyte or platelet CD36 expression was determined by flow cytometry. Results: There was a step-wise increase of sCD36 with the progression of chronic HBV infection, and it was the highest in the HBV- LC group with liver failure (1.50, IQR:1.04–2.00) as compared with HC (0.38, IQR:0.27–0.38), CHB (0.75, IQR:0.40–1.13), and HBV-LC without liver failure (1.02, IQR,0.61–1.35) group. Circulating sCD36 was not correlated with serum HBV DNA levels, but correlated with liver function parameters. Additionally, ROC analysis confirmed sCD36 could be used to predict liver failure for HBV-LC patients, which yielded an AUC of 0.775 with 71.0% sensitivity and 72.2% specificity. Multivariate logistic regression analysis revealed sCD36 is an independent risk factor in predicting liver failure. Moreover, plasma sCD36 in HBV-LC patients was significantly correlated with prognostic indices, including MELD, MELD-Na and CHILD-PUGH scores. On the other hand, CD36 expression on monocytes or platelets was positively correlated with plasma sCD36 levels, whereas they were not strongly associated with the disease severity. Conclusion: Circulating sCD36 could be used as a novel noninvasive biomarker for predicting liver failure and prognosis in chronic HBV infected patients. [ABSTRACT FROM AUTHOR]

Non-alcoholic fatty liver disease (NAFLD) is increasingly being recognized in the pediatric population, therefore, the search for non-invasive parameters to predict progression of NAFLD is of great interest. The aim of this study was to assess serum concentration of sCD36 in children with obesity and to determine its diagnostic value in pediatric NAFLD. The study group consisted of 50 children with obesity aged 8–17.5 years, admitted to our Department because of suspected liver pathology. Selected liver diseases were excluded in the examined group. Anthropometry, laboratory tests (including the concentration of sCD36) and liver ultrasound, were performed in all subjects. NAFLD was confirmed in 16 out of 50 patients with obesity. There was significantly higher activity of ALT, AST, GGT, and increased waist-hip ratio WHR in individuals with NAFLD in comparison to non-hepatopathic children with obesity. We did not find a significant difference between sCD36 concentration in patients with obesity and NAFLD and non-hepathopathic patients with obesity. We also did not find a significant difference between sCD36 concentration in children with obesity in comparison to the control group and between mild (grade 1) vs. advanced (grade ≥2) steatosis. Correlation of sCD36 concentration with anthropometric, biochemical, and bioimpedance parameters in children with obesity was confirmed only with body fat percentage. sCD36 is not a suitable parameter to differentiate children with NAFLD from non-hepatopathic children with obesity and controls without obesity. Further studies on a larger pediatric population are needed to confirm these findings. [ABSTRACT FROM AUTHOR]

Objectives: To determine the serum levels of sCD36, a lipid metabolism-related molecule, in high-altitude and sea-level populations, and to establish the association of this parameter with cardiometabolic risk factors. Materials and methods: The study population consisted of 45 people from Carhuamayo (4100 masl) and 40 people from Mala (30 masl). Weight, height and blood pressure were measured. Hemoglobin was determined in whole blood, and glucose, lipid profile and sCD36 in serum. Results: It has been found that hemoglobin levels in the population of Carhuamayo were significantly higher, while weight, BMI and glucose level were significantly lower than those in the population of Mala. There was no significant difference between serum levels of sCD36 in both populations. A significant difference was observed between sCD36 mean serum levels of both populations based on the BMI, and a significant positive correlation between sCD36 and the weight and BMI. Conclusions: The observed sCD36 serum level is not related to the altitude and can be considered as a potential marker of metabolic syndrome.

OBJECTIVE: To explore the correlations between the degree of coronary artery stenosis with blood lipid, C-reactive protein (CRP), homocysteine (Hcy), gamma-glutamyl transpeptidase (GGT), soluble cluster determinant 36 (sCD36), and fibrinogen (Fib) levels in elderly patients with coronary heart disease. PATIENTS AND METHODS: The Gensini scores for the coronary artery stenosis were analyzed in patients with single-vessel, double-vessel, and multi-vessel coronary artery diseases in observation group and normal people in control group. Changes in blood lipid-associated parameters, including total cholesterol (TC), triacylglycerol (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C), CRP, Hcy, GGT, sCD36, and Fib were compared between the two groups. The correlations between the Gensini score with changes of the blood-associated parameters, CRP, Hcy, GGT, sCD36, and Fib were analyzed. Finally, univariate and multivariate logistic regression analyses were conducted to determine the risk factors for coronary artery stenosis in elderly patients with coronary heart disease. RESULTS: The Gensini score was significantly higher in coronary heart disease patients with multi-vessel, double-vessel, and single-vessel coronary artery diseases compared with that in normal people (p<0.05). The levels of the blood lipid-associated parameters TC, TG, and LDL-C in observation group were substantially higher than those in control group (p<0.05), and the level of HDL-C was notably lower than that in control group (p<0.05). Subjects in observation group had markedly higher levels of CRP, Hcy, GGT, sCD36, and Fib than control group (p<0.05). The Gensini score for the degree of coronary artery stenosis was positively correlated with the levels of the blood lipid-associated parameters TC and TG, CRP, Hcy, GGT, sCD36, and Fib (p<0.05) and negatively associated with the level of HDL-C (p<0.05). Blood lipid-associated parameters, CRP, Hcy, GGT, sCD36, and Fib were the independent risk factors for coronary artery stenosis in elderly patients with coronary heart disease patients. CONCLUSIONS: The elevations of blood lipid, CRP, Hcy, GGT, sCD36, and Fib levels are closely associated with coronary artery stenosis, and serve as the independent risk factors for coronary artery stenosis. [ABSTRACT FROM AUTHOR]

Introduction: Introduction: CD36 is a membrane protein that functions as a lingual receptor for lipids. The soluble CD36 fraction (sCD36) may correlate oral fatty acid fat taste sensitivity to body mass index (BMI) and adiposity. Objectives: to determine if the oral fatty acid taste sensitivity in healthy young individuals of both sexes is related to serum sCD36 levels, adiposity and BMI. Methods: a cross-sectional study was conducted in 72 healthy young individuals (18-25 years). Serum sCD36 was quantified for all subjects. Oral fatty acid taste sensitivity was determined using an ascending series of the three-alternate forced choice methodology. Additionally, BMI was calculated using anthropometry, and adiposity was determined by bioelectric impedance analysis. Results: there was a positive correlation between BMI and the oral fatty acid taste sensitivity threshold (r = 0.277, p < 0.05) and a negative correlation between BMI and serum sCD36 levels (r = -0.035, p < 0.01). Adiposity negatively correlated with the sCD36 levels only in women (r = -0.359, p < 0.05). The threshold for oral sensitivity to fatty acids in overweight individuals was 1.0 (IQR 1.16) mM vs 0.2 (IQR 0.29) mM in healthy weight individuals (p < 0.05), while sCD36 levels were 26.1 pg/ml (IQR 32.9) and 77.97 pg/ml (IQR 560.66) in overweight and normal weight individuals, respectively (p < 0.05). Conclusions: BMI positively correlates with the oral sensitivity threshold of fatty acids and negatively correlates with serum sCD36 levels. The threshold of oral sensitivity to fatty acids was significantly higher in overweight subjects, while sCD36 levels were significantly higher in the group of normal weight individuals. [ABSTRACT FROM AUTHOR]

Soluble receptors are widely understood to be freestanding moieties formed via cleavage from their membrane-bound counterparts. They have unique structures, are found among various receptor families, and have intriguing mechanisms of generation and release. Soluble receptors’ ability to exhibit pleiotropic action by receptor modulation or by exhibiting a dual role in cytoprotection and neuroinflammation is concentration dependent and has continually mystified researchers. Here, we have compiled findings from preclinical and clinical studies to provide insights into the role of soluble/decoy receptors, focusing on the soluble cluster of differentiation 36, the soluble cluster of differentiation 163, and soluble lipoprotein-related protein 1 (sCD36, sCD163, and sLRP1, respectively) and the functions they could likely serve in the management of stroke, as they would notably regulate the bioavailability of the hemoglobin and heme after red blood cell lysis. The key roles that these soluble receptors play in inflammation, oxidative stress, and the related pharmacotherapeutic potential in improving stroke outcomes are described. The precise pleiotropic physiological functions of soluble receptors remain unclear, and further scientific investigation/validation is required to establish their respective role in diagnosis and therapy.

Objectives: To determine the serum levels of sCD36, a lipid metabolism-related molecule, in high-altitude and sea-level populations, and to establish the association of this parameter with cardiometabolic risk factors. Materials and methods: The study population consisted of 45 people from Carhuamayo (4100 masl) and 40 people from Mala (30 masl). Weight, height and blood pressure were measured. Hemoglobin was determined in whole blood, and glucose, lipid profile and sCD36 in serum. Results: It has been found that hemoglobin levels in the population of Carhuamayo were significantly higher, while weight, BMI and glucose level were significantly lower than those in the population of Mala. There was no significant difference between serum levels of sCD36 in both populations. A significant difference was observed between sCD36 mean serum levels of both populations based on the BMI, and a significant positive correlation between sCD36 and the weight and BMI. Conclusions: The observed sCD36 serum level is not related to the altitude and can be considered as a potential marker of metabolic syndrome. [ABSTRACT FROM AUTHOR]

Uremic toxin (UT) retention in chronic kidney disease (CKD) affects biological systems. We aimed to identify the associations between UT, inflammatory biomarkers and biomarkers of the uremic cardiovascular response (BUCVR) and their impact on cardiovascular status as well as their roles as predictors of outcome in CKD patients. CKD patients stages 3, 4 and 5 (n = 67) were recruited and UT (indoxyl sulfate/IS, p-cresil sulfate/pCS and indole-3-acetic acid/IAA); inflammatory biomarkers [Interleukin-6 (IL-6), high sensitivity C reactive protein (hsCRP), monocyte chemoattractant protein-1 (MCP-1), soluble vascular adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 (sICAM-1) and soluble Fas (sFas)] and BUCVRs [soluble CD36 (sCD36), soluble receptor for advanced glycation end products (sRAGE), fractalkine] was measured. Patients were followed for 5.2 years and all causes of death was used as the primary outcome. Artery segments collected at the moment of transplantation were used for the immunohistochemistry analysis in a separate cohort. Estimated glomerular filtration rate (eGFR), circulating UT, plasma biomarkers of systemic and vascular inflammation and BUCVR were strongly interrelated. Patients with plaque presented higher signs of UT-induced inflammation and arteries from CKD patients presented higher fractalkine receptor (CX3CR1) tissue expression. Circulating IS (p = 0.03), pCS (p = 0.007), IL-6 (p = 0.026), sFas (p = 0.001), sCD36 (p = 0.01) and fractalkine (p = 0.02) were independent predictors of total mortality risk in CKD patients. Our results reinforce the important role of uremic toxicity in the pathogenesis of cardiovascular disease (CVD) in CKD patients through an inflammatory pathway.

Background: Our previous study suggested CD36 may be a positive regulator of hepatitis B virus (HBV) replication in vitro . Therefore, the present study aimed to investigate whether circulating soluble CD36 (sCD36) could serve as a diagnostic and prognostic biomarker for HBV-related liver diseases based on the clinic collected data., Methods: A total of 282 subjects were divided into healthy controls (HC, n  = 47), chronic hepatitis B (CHB, n  = 68), HBV-related liver cirrhosis (HBV-LC, n  = 167). Soluble CD36 in plasma was measured by ELISA, and monocyte or platelet CD36 expression was determined by flow cytometry., Results: There was a step-wise increase of sCD36 with the progression of chronic HBV infection, and it was the highest in the HBV- LC group with liver failure (1.50, IQR:1.04-2.00) as compared with HC (0.38, IQR:0.27-0.38), CHB (0.75, IQR:0.40-1.13), and HBV-LC without liver failure (1.02, IQR,0.61-1.35) group. Circulating sCD36 was not correlated with serum HBV DNA levels, but correlated with liver function parameters. Additionally, ROC analysis confirmed sCD36 could be used to predict liver failure for HBV-LC patients, which yielded an AUC of 0.775 with 71.0% sensitivity and 72.2% specificity. Multivariate logistic regression analysis revealed sCD36 is an independent risk factor in predicting liver failure. Moreover, plasma sCD36 in HBV-LC patients was significantly correlated with prognostic indices, including MELD, MELD-Na and CHILD-PUGH scores. On the other hand, CD36 expression on monocytes or platelets was positively correlated with plasma sCD36 levels, whereas they were not strongly associated with the disease severity., Conclusion: Circulating sCD36 could be used as a novel noninvasive biomarker for predicting liver failure and prognosis in chronic HBV infected patients., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Cai, Xiao, Luo, Zheng, Li, Lei, Zhong, Chen, Yang, Tang and Zhou.)

Abstract: Inflammation, oxidative stress, and platelet activation are involved in type 2 diabetes and its complications. Soluble CD36 (sCD36) has been proposed to early identify diabetics at risk of accelerated atherothrombosis. We aimed at characterizing the platelet contribution to sCD36 in diabetes, by correlating its concentration with the extent of platelet-mediated inflammation and in vivo lipid peroxidation and investigating the effects of low-dose aspirin on these processes. A cross-sectional comparison of sCD36, soluble CD40L (sCD40L) reflecting platelet-mediated inflammation, urinary 11-dehydro-TxB2, and 8-iso-PGF2α, in vivo markers of platelet activation and lipid peroxidation, was performed among 200 diabetic patients (94 of them on aspirin 100mg/day) and 47 healthy controls. sCD36 levels (median [IQR]: 0.72 [0.31–1.47] vs 0.26 [0.2–0.37], P =0.003) and urinary 11-dehydro-TxB2 levels (666 [293–1336] vs 279 [160–396], P ≤0.0001) were significantly higher in diabetic patients not on aspirin (n =106) than in healthy subjects. These variables were significantly lower in aspirin-treated diabetics than untreated patients (P <0.0001). Among patients not on aspirin, those with long-standing diabetes (>1year) had significantly higher sCD36 levels in comparison to patients with diabetes duration <1year (1.01 [0.62–1.86] vs 0.44 [0.22–1.21], P =0.001). sCD36 linearly correlated with sCD40L (rho=0.447; P =0.0001). On multiple regression analysis, 11-dehydro-TxB2 (β =0.360; SEM=0.0001, P =0.001), 8-iso-PGF2α (β =0.469; SEM=0.0001, P <0.0001), and diabetes duration (β =0.244; SEM=0.207, P =0.017) independently predicted sCD36 levels. sCD36, platelet activation, inflammation, and oxidative stress are increased in type 2 diabetes. Future studies are needed to elucidate if the incomplete down-regulation of sCD36 by low-dose aspirin implies that sCD36 may be derived from tissues other than platelets or if additional antiplatelet strategies in diabetes are necessary to interrupt CD36-dependent platelet activation. [Copyright &y& Elsevier]

Recently, soluble CD36 (sCD36) levels were reported to be elevated in type 2 diabetes, and to be tightly correlated with insulin resistance. Our aim was to obtain further insight into the relationship between insulin sensitivity, low-grade inflammation and sCD36.We studied glucose-tolerant (n=90) and glucose-intolerant (n=57) moderately obese men. Insulin sensitivity was measured by the frequent sample intravenous glucose tolerance test, and sCD36 by an in-house ELISA assay.In glucose-intolerant subjects, sCD36 was negatively associated with insulin sensitivity and positively with interleukin-6 (IL-6), fasting glucose, fasting triglycerides, fat-free mass and platelet count. On multiple linear regression analyses, insulin sensitivity contributed 22% of sCD36 variance, independent of age, body mass index (BMI) and IL-6, in glucose-intolerant subjects. The level of sCD36 in subjects with glycosylated haemoglobin (HbA1C) above the mean was higher than in those with HbA1C values below the mean.Insulin sensitivity is a predictor of sCD36 in men with impaired glucose tolerance. IL-6 is related to sCD36 but does not predict sCD36 independent of insulin sensitivity and BMI. [ABSTRACT FROM PUBLISHER]

This study assessed the association of CD5L and soluble CD36 (sCD36) with the risk of a cardiovascular event (CVE), including CV death and all-cause mortality in CKD. We evaluated the association of CD5L and sCD36 with a predefined composite CV endpoint (unstable angina, myocardial infarction, transient ischemic attack, cerebrovascular accident, congestive heart failure, arrhythmia, peripheral arterial disease [PAD] or amputation by PAD, aortic aneurysm, or death from CV causes) and all-cause mortality using Cox proportional hazards regression, adjusted for CV risk factors. The analysis included 1,516 participants free from pre-existing CV disease followed up for 4 years. The median age was 62 years, 38.8% were female, and 26.8% had diabetes. There were 98 (6.5%) CVEs and 72 (4.8%) deaths, of which 26 (36.1%) were of CV origin. Higher baseline CD5L concentration was associated with increased risk of CVE (HR, 95% CI, 1.17, 1.0-1.36), and all-cause mortality (1.22, 1.01-1.48) after adjusting for age, sex, diabetes, systolic blood pressure, dyslipidemia, waist circumference, smoking, and CKD stage. sCD36 showed no association with adverse CV outcomes or mortality. Our study showed for the first time that higher concentrations of CD5L are associated with future CVE and all-cause mortality in individuals with CKD.

Soluble receptors are widely understood to be freestanding moieties formed via cleavage from their membrane-bound counterparts. They have unique structures, are found among various receptor families, and have intriguing mechanisms of generation and release. Soluble receptors' ability to exhibit pleiotropic action by receptor modulation or by exhibiting a dual role in cytoprotection and neuroinflammation is concentration dependent and has continually mystified researchers. Here, we have compiled findings from preclinical and clinical studies to provide insights into the role of soluble/decoy receptors, focusing on the soluble cluster of differentiation 36, the soluble cluster of differentiation 163, and soluble lipoprotein-related protein 1 (sCD36, sCD163, and sLRP1, respectively) and the functions they could likely serve in the management of stroke, as they would notably regulate the bioavailability of the hemoglobin and heme after red blood cell lysis. The key roles that these soluble receptors play in inflammation, oxidative stress, and the related pharmacotherapeutic potential in improving stroke outcomes are described. The precise pleiotropic physiological functions of soluble receptors remain unclear, and further scientific investigation/validation is required to establish their respective role in diagnosis and therapy. [ABSTRACT FROM AUTHOR]

• Relative expression of the cd36 gene associated with the development of hepatic steatosis. • Chronic sucrose intake associated with the development of obesity and fatty liver non-alcoholic disease. • Specific tissue involvement of the expression of Cd36 mRNA in rats with obesity and hepatic steatosis. Obesity is considered a global epidemic and is mainly associated with the development of diabetes, cardiovascular diseases and Non-Alcoholic Fatty Liver (NAFLD). The pathogenesis between obesity and hepatic steatosis is partially known, but could involve differentiated or tissue-specific participation of the expression of Cd36 mRNA that codes for a receptor which is a transporter of free fatty acids (FFA) in different tissues, favoring the lipids storage. This relative expression was evaluated in adipose and liver tissue in rats with steatosis after consumption of sucrose for 30 and 40 weeks. Ten Wistar rats were divided into two experimental groups (St-30 and St-40), which received a standard diet plus 30 % sucrose in their water intake. These rats showed a significant increase in abdominal fat, serum biochemical determinations, HOMA-IR; as well as, changes in adipocytes size and mild portal hepatitis and grade 2 hepatic steatosis. The relative expression of Cd36 mRNA increased in liver tissue after 30 (4.5-fold) and 40 (8.5-fold) weeks of sucrose ingestión but no in adipose tissue; with respect to control group (P < 0.05). This expression was associated with a significant increase in the levles of sCD36 in serum, which is indicator of the presence of the FFA transporter in the hepatocyte membrane causing lipids accumulation. The above shows the link between the adipose and hepatic tissue for the accumulation of steatotic fat in the liver through time, mediated by the relative expression of cd36 mRNA that encodes for the FFA transporter. [ABSTRACT FROM AUTHOR]

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.

The aim of this study was to determine whether plasma concentrations of sCD36 (soluble CD36) are associated with the presence of type 1 or type 2 diabetes. Plasma levels of sCD36 were analysed in 1023 subjects (225 type 1 diabetes (T1D) patients, 276 type 2 diabetes (T2D) patients, and 522 non-diabetic control subjects) using an enzyme-linked immunosorbent assay (ELISA). Multinomial and logistic regression models were performed to evaluate associations with sCD36 and its association with diabetes types. There were no significant differences in sCD36 (p = 0.144) among study groups, neither in head-to-head comparisons: non-diabetic versus T1D subjects (p = 0.180), non-diabetic versus T2D subjects (p = 0.583), and T1D versus T2D patients (p = 0.151). In the multinomial model, lower sCD36 concentrations were associated with older age (p < 0.001), tobacco exposure (p = 0.006), T2D (p = 0.020), and a higher-platelets count (p = 0.004). However, in logistic regression models of diabetes, sCD36 showed only a weak association with T2D. The current findings show a weak association of circulating sCD36 with type 2 diabetes and no association with T1D. [ABSTRACT FROM AUTHOR]

Uremic toxin (UT) retention in chronic kidney disease (CKD) affects biological systems. We aimed to identify the associations between UT, inflammatory biomarkers and biomarkers of the uremic cardiovascular response (BUCVR) and their impact on cardiovascular status as well as their roles as predictors of outcome in CKD patients. CKD patients stages 3, 4 and 5 (n = 67) were recruited and UT (indoxyl sulfate/IS, p-cresil sulfate/pCS and indole-3-acetic acid/IAA); inflammatory biomarkers [Interleukin-6 (IL-6), high sensitivity C reactive protein (hsCRP), monocyte chemoattractant protein-1 (MCP-1), soluble vascular adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 (sICAM-1) and soluble Fas (sFas)] and BUCVRs [soluble CD36 (sCD36), soluble receptor for advanced glycation end products (sRAGE), fractalkine] was measured. Patients were followed for 5.2 years and all causes of death was used as the primary outcome. Artery segments collected at the moment of transplantation were used for the immunohistochemistry analysis in a separate cohort. Estimated glomerular filtration rate (eGFR), circulating UT, plasma biomarkers of systemic and vascular inflammation and BUCVR were strongly interrelated. Patients with plaque presented higher signs of UT-induced inflammation and arteries from CKD patients presented higher fractalkine receptor (CX3CR1) tissue expression. Circulating IS (p = 0.03), pCS (p = 0.007), IL-6 (p = 0.026), sFas (p = 0.001), sCD36 (p = 0.01) and fractalkine (p = 0.02) were independent predictors of total mortality risk in CKD patients. Our results reinforce the important role of uremic toxicity in the pathogenesis of cardiovascular disease (CVD) in CKD patients through an inflammatory pathway. [ABSTRACT FROM AUTHOR]