The effect of cigarette smoking on soluble adhesion molecules in middle‐aged patients with Type 2 diabetes mellitus

Abstract

Our present study shows that levels of adhesion molecules were higher in diabetic smokers than diabetic non-smokers or non-diabetic smokers, and that cessation after chronic smoking did not restore the levels of sICAM-1 and sE-selectin, though sP-selectin levels were restored. These data suggest a possible mechanism for accelerated atherosclerosis induced by smoking in patients with diabetes.

The markers of inflammation and endothelial dysfunction in correlation with glycated haemoglobin are present in type 2 diabetes mellitus patients but not in their relatives

“…Moreover, a close relationship between increased urinary albumin excretion, endothelial dysfunction, and inflammation and death risk in diabetic patients has been described [34]. On the other hand, diabetic patients who were smokers had higher concentrations of E-selectin, ICAM-1 and VCAM-1 than non-smokers as has been shown in one report [7].…”

“…Several studies of the biomarkers of endothelial dysfunction have been done in patients with diabetes mellitus or insulin resistance. Although most of them have demonstrated an increased concentration of E-selectin, P-selectin, ICAM-1 and VCAM-1, there is a broad heterogeneity in the results; mainly in regard to which factor is more highly altered [2,7,[9][10][11][12]. Furthermore, the results in patients with impaired glucose tolerance are discordant [8,12] and some studies have described, in the general population, an increased risk of diabetes mellitus in people with higher biomarkers of endothelial dysfunction [2,13,29,30].…”

“…Several of these substances, such as E-selectin, P-selectin, soluble intercellular cell adhesion molecule-1 (ICAM-1), soluble vascular cell adhesion molecule-1 (VCAM-1), interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1) have been studied in patients with type 2 diabetes mellitus and insulin-resistance, showing that these substances are probably implicated in the pathophysiology of the disease [2,[7][8][9][10][11][12]. On the other hand, high glycated haemoglobin impairs nitric oxide-mediated vascular responses by a mechanism involving superoxide anions but not cyclooxygenase derivatives [13].…”

Long-term effects of green tea ingestion on atherosclerotic biological markers in smokers

“…P-selectin, which is induced by platelet activation, acts on the adhesion of white blood cells to endothelial cells in the early phase of inflammatory process. In addition, it has been reported that the plasma concentrations of P-selectin in smokers were higher than those of non-smokers [5]. Smoking also induces atherosclerosis through induction of oxidative stress and subsequent elevation of oxidized LDL [6].…”

Association of hsCRP and soluble fraction of E-selectin with diabetic and non-diabetic individuals

“…[9] E-selectin is a leukocyte adhesion molecule specific to endothelial cells, and soluble E-selectin is a marker of endothelial activation. [10][11][12][13] It may reflect a variety of pathophysiological conditions related to inflammation.…”