Elevated levels of soluble E-selectin in patients with IDDM and NIDDM: relation to metabolic control

Cominacini, Luciano; Pasini, Andrea; Garbin, Ulisse; Davoli, A.; Santis, A. De; Campagnola, M.; Rigoni, Annamaria; Zenti, Maria Grazia; Moghetti, Paolo; Cascio, Vincenzo Lo

doi:10.1007/bf00402185

Cited by 143 publications

(87 citation statements)

References 9 publications

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“…Similar results were also obtained by Fasching et al [42] in 159 NIDDM patients. Contrary to our [15] and Fasching's [42] results, in another recently published paper [14], the levels of soluble adhesion molecules failed to correlate with glycaemic control. Actually soluble concentration of Eselectin was found in this study to be related not only to glycaemic control, i.e HbA 1C , but also to plasma hydroperoxides and to susceptibility of LDL to oxidation.…”

Section: Discussioncontrasting

confidence: 99%

“…Since a correlation between HbA 1C and E-selectin plasma concentration was found, a first tentative explanation of our results may be that glycaemic control per se may, somehow, affect the plasma concentration of this adhesion molecule. These results are in agreement with our previous results, in which a correlation between HbA 1C and E-selectin was found in a small group of NIDDM patients [15]. Similar results were also obtained by Fasching et al [42] in 159 NIDDM patients.…”

Section: Discussionsupporting

confidence: 94%

“…Concentrations of soluble E-selectin, ICAM-1 and VCAM-1 were estimated using the soluble E-selectin, ICAM-1 and VCAM-1 ELISA kits (British Bio-technology Products Ltd, Abingdon-Oxon, UK), as previously described [15]. The assay is standardized against purified soluble forms of recombinant E-selectin, VCAM-1 and ICAM-1.…”

Section: Methodsmentioning

confidence: 99%

“…Increased levels of E-selectin, ICAM-1 and VCAM-1 have also been found in patients with insulin-dependent diabetes and non-insulin-dependent diabetes (NIDDM) [10,[13][14][15] but it is still unclear whether this increase is related to glycaemic control. In poorly controlled diabetic patients, excess glucose causes enhanced glycation of plasma proteins.…”

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confidence: 99%

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E-Selectin plasma concentration is influenced by glycaemic control in NIDDM patients: possible role of oxidative stress

Cominacini¹,

Pasini²,

Garbin³

et al. 1997

Diabetologia

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Atherosclerosis is the major cause of death in patients with diabetes mellitus, accounting for more than 70 % of mortality in all forms of the disease [1,2]. There is plenty of evidence that monocytes are involved in the pathogenesis of atherosclerosis [3,4], the earliest morphological evidence of the disease being the binding of monocytes to the endothelium [5][6][7]. This adhesion of monocytes, a prerequisite for their recruitment and accumulation in the lesion, is probably due to the appearance of adhesion Diabetologia (1997) Summary Although elevated levels of soluble E-selectin and intercellular cell adhesion molecules-1 (ICAM-1) have been reported in non-insulin-dependent diabetes mellitus (NIDDM), it is not clear by what mechanism this elevation occurs and whether or not it is related to glycaemic control. In this study we analyse: 1) the relation of glycaemic control with the concentrations of E-selectin, vascular cell adhesion molecules-1 (VCAM-1) and ICAM-1 in NIDDM patients; 2) whether metabolic control can affect the oxidative stress (as measured by plasma hydroperoxide concentration and susceptibility of LDL to in vitro oxidation) and hence the adhesion molecule plasma concentrations. Thirty-four (19 males and 15 females) poorly controlled NIDDM patients were studied. All parameters were evaluated at the beginning of the study and after 90 days of dietary and pharmacological treatment. The treatment decreased HbA 1C (p < 0.001), E-selectin (p < 0.001), plasma hydroperoxides (p < 0.003) and the susceptibility of LDL to in vitro oxidation (lag phase) (p < 0.0001). Before treatment HbA 1C , lag phase and lipid hydroperoxides correlated with E-selectin plasma concentration (r = 0.51, -0.57 and 0.54, respectively, p < 0.01). There was also a correlation between HbA 1C and lag phase (p < 0.01) and between HbA 1C and lipid hydroperoxides (p < 0.01). In addition, the variations of HbA 1C , lag phase and lipid hydroperoxide values correlated with those for E-selectin concentration after 90 days' treatment (r = 0.54, -0.64 and 0.61, respectively, p < 0.01). In multiple linear correlation analysis, however, the partial correlation coefficients of HbA 1C (basal and variations) with Eselectin concentration (basal and variations) fell to non-significant values (r = 0.12 and 0.25, respectively) when LDL lag phase and plasma hydroperoxides were kept constant. The results indicate that the improvement of metabolic control in NIDDM patients is associated with a decrease of E-selectin plasma levels; they also suggest that glycaemic control per se is not directly implicated in determining E-selectin plasma concentration; glycaemic control could affect E-selectin concentration through its effect on oxidative stress. [Diabetologia (1997) 40: 584-589]

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionsupporting

confidence: 94%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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E-Selectin plasma concentration is influenced by glycaemic control in NIDDM patients: possible role of oxidative stress

Cominacini¹,

Pasini²,

Garbin³

et al. 1997

Diabetologia

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“…Cell adhesion molecules are thought to be involved in the development of vascular complications in diabetes mellitus and show increased expression levels in patients with both Type I and Type II diabetes [10]. E-selectin is a cell adhesion molecule that contributes to monocyte adhesion to endothelium [29] and is expressed by endothelial cells at the site of atheroscrelotic lesions [30].…”

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confidence: 99%

Detection of monocyte-derived microparticles in patients with Type II diabetes mellitus

et al. 2002

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Patients with diabetes mellitus develop hypercoagulability, platelet hyperaggregability and premature atherosclerosis [1±4]. Atherosclerosis is the major cause of death in patients with diabetes mellitus, leading to a high mortality rate in all forms of the disease [5]. Classical risk factors, including hyperlipidaemia, hypertension, and obesity, do not completely account for the increased incidence of atherosclerosis associated with diabetes [6]. Recent reports suggest that increased expression of endothelial adhesion Diabetologia (2002) Results. The concentration of MDMPs in diabetic patients was higher than in normal subjects. We found no differences in the binding of anti-GPIIb/IIIa and anti-GPIb monoclonal antibodies between groups. There were differences, however, in the concentrations of PDMPs, plt-CD62P, and plt-CD63 between Type II (non-insulin-dependent) diabetes mellitus patients and control subjects (PDMPs: 585 25 vs 263 9, p < 0.01; plt-CD62P: 28.1 % 1.4 % vs 9.4 % 0.6 %, p < 0.001; plt-CD63: 28.1 % 1.4 % vs 8.6 % 0.5 %, p < 0.001). Amounts of MDMPs correlated positively with these platelet activation markers, and the relation between PDMP and MDMP was the most significant. The concentration of MDMP in patients who had diabetes complicated with nephropathy, retinopathy, or neuropathy was higher than in those without diabetes-related complications. The increase in MDMP was particularly significant in patients with nephropathy. Concentrations of sE-selectin were higher in Type II diabetes patients than in control subjects, and correlated with MDMP, PDMP, plt-CD62P, and plt-CD63 levels in nephropathy patients. Conclusion/interpretation. In Type II diabetes patients, we detected increased activation of monocytes, which could have been stimulated by activated platelets and PDMPs. Because the activation of monocytes is associated with vascular endothelial damage, high concentrations of MDMPs could indicate vascular complications in diabetes patients, especially those who have diabetes-related nephropathy. [Diabetologia (2002) 45:550±555]

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Relationship between circulating vascular cell adhesion molecule-1 and microvascular complications in Type 2 diabetes mellitus

et al. 1998

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The soluble form of the vascular cell adhesion molecule-1 (VCAM-1) is detectable in human sera and is elevated in diabetic patients, with unknown clinical significance. In the present study, the relationship between serum soluble VCAM-1 and diabetic microvascular complications (retinopathy, nephropathy, and neuropathy) was evaluated in 95 Japanese patients with Type 2 diabetes mellitus (DM). Serum soluble VCAM-1 concentration was higher in patients with more advanced stages of retinopathy as well as nephropathy. There was a significant correlation between soluble VCAM-1 and log10 (urinary albumin excretion) in 69 patients with normal serum creatinine levels (r = 0.51, p < 0.0001) and a significant correlation between soluble VCAM-1 and log10 (serum creatinine) in all the patients (r = 0.83, p < 0.0001). Soluble VCAM-1 concentration was also elevated in patients with neuropathy. There was a significant correlation between soluble VCAM-1 concentration and the number of microvascular complications (r = 0.59, p < 0.0001). However, multivariate regression analysis revealed that only diabetic nephropathy, was associated with the soluble VCAM-1 concentration. The elevation of circulating VCAM-1 level in diabetic nephropathy may result from underlying systemic endothelial dysfunction, increased VCAM-1 production in damaged renal tubular or glomerular epithelial cells and/or decreased renal clearance of this molecule, depending on the stage of nephropathy.

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Elevated levels of soluble E-selectin in patients with IDDM and NIDDM: relation to metabolic control

Cited by 143 publications

References 9 publications

E-Selectin plasma concentration is influenced by glycaemic control in NIDDM patients: possible role of oxidative stress

E-Selectin plasma concentration is influenced by glycaemic control in NIDDM patients: possible role of oxidative stress

Detection of monocyte-derived microparticles in patients with Type II diabetes mellitus

Relationship between circulating vascular cell adhesion molecule-1 and microvascular complications in Type 2 diabetes mellitus

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