Levels of soluble cell adhesion molecules in type 2 diabetes mellitus patients with macrovascular complications

Abstract

Objective Type 2 diabetes mellitus (T2DM) is a main risk factor for development of cardiovascular diseases (CVDs) and endothelial dysfunction. This study aimed to investigate serum levels of soluble vascular cell adhesion molecule 1 (sVCAM-1), intercellular adhesion molecule 1 (sICAM-1), and endothelium selectin (sE-selectin) in T2DM patients with macrovascular complications. Methods A cross-sectional study of 21 controls, 30 T2DM patients without CVDs, and 30 T2DM patients with CVDs was conducted. Serum levels of soluble adhesion molecules including sVCAM-1, sICAM-1, and sE-selectin were determined using ELISA. Results Serum levels of sVCAM-1, sICAM-1, and sE-selectin were higher in T2DM patients than in controls. Levels of serum sVCAM-1 were higher in T2DM patients with CVDs compared with T2DM patients without CVDs. In T2DM patients with CVDs, significant positive associations were observed between sVCAM-1, sICAM-1, and sE-selectin levels (r = 0.575, p = 0.001 and r = 0.378, p = 0.040). Conclusions Circulating levels of soluble adhesion molecules were elevated in T2DM patients, regardless of whether the patients had cardiovascular complications. Only sVCAM-1 was considered a useful marker for the prediction of CVDs in T2DM patients.

Amelioration of Endothelial Dysfunction and Inflammation in Type 2 Diabetic Patients after Black Seed Oil Supplementation.

“…It was observed in the present study that hsCRP and sICAM-1 levels were elevated in diabetic patients compared to healthy volunteers, which are following previous studies that demonstrated the increased level of these markers in diabetic patients and their association with future diabetic complications and mortality [20,23]. At the current work, a statistically significant reduction in hsCRP levels in the intervention group was found following randomized controlled trials which demonstrated the beneficial effect of NS on the CRP level of patients with different disease states [34].…”

“…There is also a link between the levels of ICAM-1 and diabetic neuropathy [22]. So, both CRP and soluble adhesion molecules can be considered as attractive early predictors of diabetic complications and therapeutic targets for diabetic patients [23].…”

Evaluation of irisin, retinol-binding protein 4, and leptin serum levels as biomarkers of macrovascular complications involvement in Saudi type 2 diabetes mellitus. A case-control study

“… 1 Kingdom of Saudi Arabia (KSA) has the second-highest rate of T2DM prevalence in the Middle East. 2 The inflammatory process is one of the T2DM pathophysiological mechanisms. Throughout glycemic control deterioration, various factors affect the endothelium leading to endothelial dysfunction that deteriorates with insulin resistance (IR); these conditions are associated with T2DM macrovascular complications (MVC).…”

Bioinformatics analysis of potential key genes and mechanisms in type 2 diabetes mellitus

“…The functional enrichment analysis indicated that the DEGs were primarily involved in the defense response, secretory vesicle, identical protein binding, cell adhesion, extracellular matrix, structural molecule activity, neutrophil degranulation and extracellular matrix organization. Neutrophil degranulation [52], innate immune system [53], platelet degranulation [54], extracellular matrix organization [55], diseases of glycosylation [56], platelet activation, signaling and aggregation [57], hemostasis [58], secretion [59], secretory vesicle [60], transmembrane transporter activity [61], cell adhesion [62], localization of cell [63], extracellular matrix [55], intrinsic component of plasma membrane [64], structural molecule activity [65], signaling receptor binding [66], have been highly noted in T2DM. Reports indicate that HIF1A [67], HLA-DRB1 [68], CHI3L1 [69], ADORA2A [70], ADRB2 [71], CLU (clusterin) [72], AGT (angiotensinogen) [73], VCAM1 [74], PPARA (peroxisome proliferator activated receptor alpha) [75], APOL1 [76], ZFP36 [77], PPM1B [78], SOCS1 [79], SNCA (synuclein alpha) [80], CTSS (cathepsin S) [81], IL6R [82], CFB (complement factor B) [83], DEFB1 [84], VNN1 [85], RAB27A [86], DPP4 [87], RARRES2 [88], CASP1 [89], LCN2 [90], REG3A [91], CD74 [92], PCSK2 [93], CHGB (chromogranin B) [94], TTR (transthyretin) [95], LRG1 [96], ALB (albumin) [97], DPP7 [98], APOH (apolipoprotein H) [99], CTSD (cathepsin D) [100], GCG (glucagon) [101], KCNQ1 [102], NR4A1 [103], PLIN5 [104], ALDH2 [105], ANG (angiogenin) [106], CLDN7 [107], PRLR (prolactin receptor) [108], SOD2 [109], MLXIPL (MLX interacting protein like) [110], CTSD (cathepsin D) [111], PECAM1 [112], ADA (adenosine deaminase) [113], MFGE8 […”