Search

Heparan sulfate proteoglycans (HSPGs) are involved in the regulation of cell growth, apoptosis and lipid metabolism in vitro. Syndecans are the primary form of HSPGs. Syndecan-1 is involved in the processes of cell growth, differentiation, adhesion, wound healing and inflammation. Additionally, as a sinusoidal transmembrane HSPG facing the plasma compartment, syndecan-1 is a promising target to be involved in lipoprotein physiology. We aimed to examine the possible correlation of syndecan-1 and lipid profile in type 2 diabetes mellitus. In this study, serum syndecan-1 was detected by ELISA, and potential correlations between syndecan-1 and triglyceride, cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, lipoprotein a, apolipoprotein (apo) B, apoA1 and apoB/apoA1 were analyzed. Forty-one patients with type 2 diabetes and 31 age-matched, non-diabetic healthy subjects (controls) were enrolled. Syndecan-1 in patients with diabetes (26.15 ± 2.42 ng/ml) was significantly higher than that of the controls (16.85 ± 1.98 ng/ml, t = -2.98, P = 0.005). Serum syndecan-1 level correlated negatively with apoA1 (r = -0.46, P = 0.003). Multiple regression analysis showed that apoA1 (b = -0.43, P = 0.003) was a predictor of serum syndecan-1 levels in subjects with type 2 diabetes.

The peripheral neutrophils are one of the main inflammatory cells and significantly influence the damage of endothelium. Type 2 diabetes is a manifestation of an ongoing low-grade inflammation. In diabetes, impairment of neutrophil adhesion to the endothelium and migration to the site of inflammation were detected, which associated closely with adhesion molecules expressed on neutrophils and endothelial cells. To detect the expression of syndecan-1 on neutrophils in patients with type 2 diabetes mellitus, we recruited 29 patients with type 2 diabetes mellitus without any diabetic complication and 24 healthy subjects (controls). Expression of syndecan-1 was determined by flow cytometry, and potential correlations between syndecan-1 and clinical characteristics were analyzed. On neutrophils, percentage of positive syndecan-1 cells was significantly higher in subjects with diabetes (10.363 ± 1.689%) than that of the controls (3.775 ± 0.634%, P = 0.001). An association between body mass index (BMI) and percentage of positive syndecan-1 neutrophils was detected (r = 0.415, P = 0.025). When BMI was categorized into subgroups of ≤25 kg/m(2) (n = 10) and >25 kg/m(2) (n = 19), the average percentages of positive syndecan-1 neutrophils in patients with diabetes were 5.733 ± 1.842% and 12.642 ± 2.251%, respectively (t = -2.137, P = 0.042). A multiple regression analysis showed that BMI (β = 0.783, P < 0.000) was a significant predictor of positive syndecan-1 neutrophils in subjects with type 2 diabetes.

Aims: To detect the level of serum syndecan-1 of patients with type 2 diabetes., Methods: Subjects with diabetes were categorized into 4 subgroups, oral-agents, insulin therapy for 12 months. Serum syndecan-1 was detected by ELISA, and potential correlation between syndecan-1 levels and clinical characteristics was analyzed., Results: Sixty-two diabetic patients and 20 healthy subjects (controls) were enrolled. Syndecan-1 in diabetic patients (24.616+/-1.993 ng/ml) was higher than that of the controls (18.907+/-2.638 ng/ml). The average concentration of syndecan-1 in the group of oral-agents, insulin therapy for 12 months was 19.157+/-2.556 ng/ml (n=20), 24.447+/-3.173 ng/ml (n=23), 35.005+/-4.749 ng/ml (n=11), and 27.593+/-8.304 ng/ml (n=8), respectively. An association between serum syndecan-1 and intake of exogenous insulin was found (r=0.266, p=0.035). Serum syndecan-1 of insulin-therapy group (27.811+/-2.669 ng/ml) enhanced significantly compared to that of the controls (p=0.030) and that of the oral-agents group (p=0.035). Syndecan-1 of the insulin therapy for 1-12 months group enhanced predominantly compared to that of the controls (p=0.005) and the oral-agents group (p=0.005)., Conclusions: Chronic inflammation and exogenous insulin usage increases serum syndecan-1 level. Exogenous insulin can promote shedding of syndecan-1 ectodomains to the serum in a time-dependent manner.