Diabetes Division, Department of Medicine I, St. Josef-Hospital, Ruhr-University Bochum, Bochum, Germany.
Diabetes Obes Metab. 2013 Mar;15(3):258-63. doi: 10.1111/dom.12022.
Postprandial insulin pulsatility is impaired in patients with type 2 diabetes, but the effects of exogenous insulin therapy on pulsatile insulin secretion are not known. We addressed, whether pulsatile insulin secretion is related to glycaemic control, whether basal insulin supplementation increases postprandial insulin secretion, and if so, is this accomplished by a specific improvement in pulsatile insulin secretion?
Fourteen patients with type 2 diabetes underwent a mixed meal test before and after an 8-week treatment period with insulin glargine. Glucose, insulin and C-peptide levels were measured, and insulin pulsatility was determined by deconvolution analysis.
Insulin treatment lowered fasting glycaemia from 179.6 ± 7.5 mg/dl to 117.6 ± 6.5 mg/dl (p < 0.001). Postprandial insulin and C-peptide levels increased significantly after the treatment period (p < 0.0001). The total calculated insulin secretion rate increased with insulin treatment (p = 0.0039), with non-significant increases in both pulsatile and non-pulsatile insulin secretion. Insulin pulse frequency was unchanged by the intervention. There was an inverse relationship between fasting and postprandial glycaemia and insulin pulse mass (r(2) = 0.51 and 0.56, respectively), whereas non-pulsatile insulin secretion was unrelated to either fasting or postprandial glucose concentrations (r(2) = 0.0073 and 0.031).
Hyperglycaemia in type 2 diabetes is associated with a reduction in postprandial insulin secretion, specifically through a reduction in insulin pulsatility. Reducing chronic hyperglycaemia by basal insulin therapy enhances endogenous β-cell function in the postprandial state. These data support the use of basal insulin regimens in the pharmacotherapy of overtly hyperglycaemic patients with type 2 diabetes.
2 型糖尿病患者餐后胰岛素脉冲产生受损，但外源性胰岛素治疗对脉冲式胰岛素分泌的影响尚不清楚。我们旨在研究餐后胰岛素分泌是否与血糖控制有关，基础胰岛素补充是否增加餐后胰岛素分泌，如果是，是否通过脉冲式胰岛素分泌的特异性改善来实现。
14 例 2 型糖尿病患者在接受甘精胰岛素 8 周治疗前后进行混合餐试验。检测血糖、胰岛素和 C 肽水平，并通过反卷积分析确定胰岛素脉冲。
胰岛素治疗使空腹血糖从 179.6±7.5mg/dl 降至 117.6±6.5mg/dl（p<0.001）。治疗后餐后胰岛素和 C 肽水平显著升高（p<0.0001）。胰岛素分泌率随胰岛素治疗而增加（p=0.0039），脉冲式和非脉冲式胰岛素分泌均有显著增加。干预后胰岛素脉冲频率无变化。空腹和餐后血糖与胰岛素脉冲质量呈负相关（r(2)=0.51 和 0.56），而非脉冲式胰岛素分泌与空腹或餐后血糖浓度无关（r(2)=0.0073 和 0.031）。
2 型糖尿病患者的高血糖与餐后胰岛素分泌减少有关，特别是通过减少胰岛素脉冲。通过基础胰岛素治疗降低慢性高血糖可增强餐后内源性β细胞功能。这些数据支持在 2 型糖尿病明显高血糖患者的药物治疗中使用基础胰岛素方案。
