Determinants of visfatin in type 2 diabetes patients with diabetic kidney disease: Relationship to inflammation, adiposity and undercarboxylated osteocalcin.

BACKGROUND: Visfatin is a proinflammatory molecule with possible actions on glucose metabolism. Interactions to bone metabolism and undercarboxylated osteocalcin (uOC) in diabetic patients (T2DP) with diabetic kidney disease (DKD) have not been reported. MATERIALS AND METHODS: We included 51 incident T2DP with DKD. History, laboratory evaluation, anthropometry, visfatin, uOC were obtained. Fifteen T2DP without DKD were used as controls. RESULTS: Visfatin was similar in DKD patients and controls: 1.56(0.97-3.03) versus 2.04(1.08-3.21) ng/mL, p = 0.51. In controls, visfatin positively correlated with diabetes duration (r = 0.63, p = 0.01) and negatively with uOC (r = -0.57, p = 0.03). In multivariate regression, diabetes duration remained significant (p = 0.01). In patients with DKD, visfatin was positively linked to C reactive protein (r = 0.27, p = 0.05), tricipital skin fold (TSF) (r = 0.41, p = 0.004) and leukocytes (r = 0.37, p = 0.01); the latter two parameters predicted visfatin in multivariate model (p = 0.001). In normoalbuminuric patients, visfatin was linked to body mass index (r = 0.32, p = 0.04), waist circumference (r = 0.42, p < 0.0001), LDL cholesterol (r = 0.33, p = 0.03), serum glucose (r = 0.36, p = 0.03) and glycated hemoglobin (r = 0.41, p = 0.007); there was a trend towards negative correlation to uOC (r = -0.28, p = 0.07); only glycaemia remained significant in multivariate analysis (p = 0.04). Albuminuric patients displayed a positive correlation of visfatin to waist to hip ratio (r = 0.41, p = 0.04) and leukocytes (r = 0.56, p = 0.04); the latter remained significant in multivariate regression (p = 0.005). CONCLUSION: The main determinant of visfatin in T2D patients with DKD is inflammation; in normoalbuminuric patients, a positive link to adiposity and altered glycemic control and a trend towards a negative correlation to uOC was observable; the latter relationship was evident in patients without DKD.

Relationship of endothelial cell selective adhesion molecule to markers of oxidative stress in type 2 diabetes.

BACKGROUND: Endothelial dysfunction is an important contributor to micro and macrovascular complications of type 2 diabetes (T2D) and is reflected by increased systemic oxidative stress. Endothelial cell selective adhesion molecule (ESAM) influences endothelial function. We aimed to assess, for the first time to our knowledge, the relationship of soluble ESAM to markers of systemic oxidative stress. MATERIALS AND METHODS: ESAM, malondialdehyde (MDA) level and catalase activity were determined in 54 T2D patients and 43 controls. RESULTS: T2D patients had significantly higher ESAM when compared to controls (16.07 ± 5.77 µg/L versus 8.57 ± 5.28 µg/L, p < 0.0001), they also had higher MDA level (3.88 ± 1.50 µmol/L vs. 1.58 ± 0.72 µmol/L, p < 0.0001) and lower catalase activity (3.07 (2.63-3.44) U/mg vs. 8.72 (4.55-10.46) U/mg, p < 0.0001). In T2D patients ESAM was inversely related to catalase activity (r = -0.27, p = 0.04), relationship to MDA level was direct but not significant (r = 0.16, p = 0.24). MDA concentration correlated inversely to catalase activity (r = -0.28, p = 0.04). In multiple regression catalase activity remained significantly correlated to ESAM (p = 0.02) and MDA level was significantly related to glycated hemoglobin (p = 0.01); there was trend towards a positive correlation of MDA level to ESAM (p = 0.08). When patients were divided according to oxidative stress, those with increased oxidative stress (defined as MDA concentration > 2.98 µmol/L and catalase activity < 3.38 U/mg) had higher ESAM than the rest of the patients (17.99 ± 5.02 µg/L vs. 14.29 ± 5.94 µg/L p = 0.01). CONCLUSION: ESAM is higher in T2D than in controls and parallels oxidative stress: ESAM is inversely related to catalase activity and higher ESAM is found in T2D patients with increased oxidative stress.