Vascular Cell Adhesion Molecule 1, Intercellular Adhesion Molecule 1, and Cluster of Differentiation 146 Levels in Patients with Type 2 Diabetes with Complications

Abstract

BackgroundType 2 diabetes mellitus (T2DM) is a multisystemic, chronic disease accompanied by microvascular complications involving various complicated mechanisms. Intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and cluster of differentiation-146 (CD146) are mainly expressed by endothelial cells, and facilitate the adhesion and transmigration of immune cells, leading to inflammation. In the present study, we evaluated the levels of soluble adhesion molecules in patients with microvascular complications of T2DM.MethodsSerum and whole blood samples were collected from 58 T2DM patients with microvascular complications and 20 age-matched healthy subjects. Levels of soluble ICAM-1 (sICAM-1) and soluble VCAM-1 (sVCAM-1) were assessed using enzyme-linked immunosorbent assay, while flow cytometry was used to determine CD146 levels.ResultsSerum sICAM-1 levels were lower in T2DM patients with microvascular complications than in healthy controls (P<0.05). No significant differences were found in sVCAM-1 and CD146 levels between the study and the control group. Although patients were subdivided into groups according to the type of microvascular complications that they experienced, cell adhesion molecule levels were not correlated with the complication type.ConclusionIn the study group, most of the patients were on insulin therapy (76%), and 95% of them were receiving angiotensin-converting enzyme (ACE)-inhibitor agents. Insulin and ACE-inhibitors have been shown to decrease soluble adhesion molecule levels via various mechanisms, so we suggest that the decreased or unchanged levels of soluble forms of cellular adhesion molecules in our study group may have resulted from insulin and ACE-inhibitor therapy, as well as tissue-localized inflammation in patients with T2DM.

<p>Evaluation of the Effect of Fish Oil Alone and in Combination with a Proprietary Chromium Complex on Endothelial Dysfunction, Systemic Inflammation and Lipid Profile in Type 2 Diabetes Mellitus – A Randomized, Double-Blind, Placebo-Controlled Clinical Study</p>

“…Their results are in concurrence with the highly significant reductions in ICAM-1, VCAM-1 and ET-1 in all three treatment groups in our study, with the best improvement seen in Group C. NO, a vasodilator, seems to have anti-inflammatory properties and thus decreases ICAM-1 and VCAM-1 expression. 59 In our study, as mentioned in the previous paragraph, a significant improvement in NO levels was seen. The positive effect of ω-3FA on NO levels, along with the inhibitory effect on endothelial expression of adhesion molecules, is the possible mechanism of action of ω-3FAs.…”

Dysregulation of Leukocyte Trafficking in Type 2 Diabetes: Mechanisms and Potential Therapeutic Avenues

“…However, a recent study on 58 patients with T2DM on insulin therapy and displaying microvascular complications found lower levels of serum sICAM-1 in these patients irrespective of the type of diabetic complication when compared to age-matched healthy controls ( Hocaoglu-Emre et al, 2017 ). Since the participants with T2DM were also receiving angiotensin-converting enzyme (ACE)-inhibitor agents, decreased levels of sICAM-1 might have resulted from the combination of insulin and ACE-inhibitor therapies.…”

“…Some studies have hypothesized that these discrepancies between cohorts are linked to the degree of complications and the bigger impact seems to occur in late-stage diabetic complications when other treatments such as ACE-inhibitors are used. The conflicting evidence about the levels of sCAMs in the circulation suggests that different CAMs may play different roles in the different stages of vascular complications in T2DM ( Hocaoglu-Emre et al, 2017 ).…”

Diabetes Induced Renal Complications by Leukocyte Activation of Nuclear Factor κ-B and its Regulated Genes Expression

“…For the purpose of analysis, genes were clustered functionally into proinflammatory (NF-ΚB, IL-1β, IL-6, TNF-α, VEGF), profibrotic (FN, ICAM-1, VCAM-1) and proliferative (MAPK-1, EGF) genes. Based on the fact that our candidate genes are involved in endothelial injury and extracellular mass synthesis, our suggested genes may be therapeutic or diagnostic target for diabetes complications [45][46][47][48][49][50][51][52][53][54].…”

“…Proinflammatory cytokines including NF-κB and its dependent cytokines mainly TNF-α were shown to have a direct toxic effects on renal cells, alters endothelial permeability and induces albuminuria during nephropathy progression [44][45][46][47]. Persistent leukocyte activation is established in and type 2 diabetes mellitus patients [48]. leukocyte activation has been linked to microvascular diabetic complications in response to overactivation of the inflammatory cascade and increased tissue damage [-49].…”