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Plasma vascular endothelial growth factor B levels are increased in patients with newly diagnosed type 2 diabetes mellitus and associated with the first phase of glucose-stimulated insulin secretion function of β-cell.

J. Endocrinol. Invest.2017 Nov;40(11):1219-1226. Epub 2017 May 18
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摘要


PURPOSE:To detect plasma vascular endothelial growth factor B (VEGF-B) in individuals with different glucose tolerance and investigate the relationship between plasma VEGF-B levels and the first phase of glucose-stimulated insulin secretion. METHODS:A cross-sectional study was conducted involving 45 patients with newly diagnosed type 2 diabetes mellitus (T2DM), 37 patients with impaired glucose regulation (IGR), and 39 Normal glucose tolerance (NGT) subjects, all of whom underwent intravenous glucose tolerance test. Plasma VEGF-B levels were assayed by ELISA. The first phase of insulin secretion was evaluated by acute insulin response (AIR), the area under the curve of the first-phase (0-10 min) insulin secretion (AUC) and glucose disposition index (GDI). RESULTS:The T2DM and IGR groups had higher plasma VEGF-B levels than the NGT group (P < 0.01). Plasma VEGF-B levels were negatively correlated with AIR, AUC, GDI, HOMA-β (P < 0.01), and positively correlated with plasma glucose, HbA1c, triglyceride, free fatty acid (FFA), fasting insulin, and HOMA-IR (P < 0.01). Logistic regression analysis revealed that higher VEGF-B levels [145.59-180.07 pg/ml, OR 3.55 (95% CI 1.05-12.02) and >180.07 pg/ml, OR 3.64 (95% CI 1.16-11.42)] were related to a greater probability of β-cell hypofunction, compared with low VEGF-B levels (<145.59 pg/ml). After adjusting for triglyceride or FFA, the association between VEGF-B levels and β-cell hypofunction disappeared (P > 0.05). CONCLUSIONS:Our study provides evidence that plasma VEGF-B levels were higher in patients with newly diagnosed T2DM, and were strongly associated with glucose and lipid metabolism and the first-phase insulin secretion function of β-cells. VEGF-B may be involved in the mechanism of β-cell dysfunction in T2DM.

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