Department of Endocrinology and Metabolism, Tianjin Medical University General Hospital, Tianjin, China.
Department of Medical Laboratory, Tianjin Medical University General Hospital, Tianjin, China.
J Clin Endocrinol Metab. 2019 Oct 1;104(10):4341-4346. doi: 10.1210/jc.2019-00549.
Evidence indicates that there is substantial impairment/loss of β-cell function/mass even before prediabetes. Elevated plasma proinsulin is a sign of β-cell dysfunction in patients with diabetes/prediabetes. However, the dynamic changes of glucose stimulated proinsulin secretion (GSPS) among nondiabetic individuals remain obscure.
To examine GSPS and glucose-stimulated insulin secretion (GSIS) among individuals with normal glucose tolerance (NGT) and impaired glucose tolerance (IGT) and to evaluate whether impaired GSPS is an early biomarker of β-cell impairment in individuals with NGT who have subthreshold postprandial plasma glucose (PPG).
We evaluated GSPS and GSIS in 116 Chinese adults without diabetes (mean age ± SD, 33.31 ± 9.10 years; mean BMI, 25.24 ± 4.20 kg/m2) with fasting plasma glucose (FPG) < 5.6 mmol/L. Based on 2hPPG, the participants were divided into three groups: NGT1 (2hPPG < 6.67 mmol/L), NGT2 (6.67 ≤ 2hPPG < 7.78 mmol/L), and IGT (7.78 ≤ 2hPPG<11.1 mmol/L). We analyzed the association of GSIS and GSPS with commonly used indexes of β-cell function, insulin resistance and family history of diabetes.
Although not diagnosed with prediabetes, the individuals with NGT2 have clinical characteristics and high diabetes risk factors similar to those of the IGT group. However, unlike individuals with IGT, NGT2 participants did not exhibit a delayed GSIS. Instead, GSPS was impaired in NGT2 groups but not in NGT1 group.
This study suggests that impaired GSPS, but not impaired GSIS, may serve as an early biomarker to identify a subpopulation of NGT with a high risk of diabetes.
有证据表明，β细胞功能/质量的大量损害/丧失甚至发生在糖尿病前期之前。在糖尿病/糖尿病前期患者中，升高的血浆胰岛素原是β细胞功能障碍的标志。然而，非糖尿病个体中葡萄糖刺激的胰岛素原分泌（GSPS）的动态变化仍然不清楚。
检查糖耐量正常（NGT）和糖耐量受损（IGT）个体中的 GSPS 和葡萄糖刺激的胰岛素分泌（GSIS），并评估在餐后血糖（PPG）低于阈限的 NGT 个体中，受损的 GSPS 是否是β细胞受损的早期生物标志物。
我们评估了 116 名无糖尿病的中国成年人（平均年龄±标准差，33.31±9.10 岁；平均 BMI，25.24±4.20kg/m2）的 GSPS 和 GSIS，其空腹血糖（FPG）<5.6mmol/L。根据 2hPPG，参与者分为三组：NGT1（2hPPG<6.67mmol/L）、NGT2（6.67mmol/L≤2hPPG<7.78mmol/L）和 IGT（7.78mmol/L≤2hPPG<11.1mmol/L）。我们分析了 GSIS 和 GSPS 与常用的β细胞功能、胰岛素抵抗和糖尿病家族史指标的相关性。
尽管未被诊断为糖尿病前期，NGT2 个体具有与 IGT 组相似的临床特征和高糖尿病风险因素。然而，与 IGT 个体不同，NGT2 参与者没有出现 GSIS 延迟。相反，NGT2 组的 GSPS 受损，但 NGT1 组没有。
这项研究表明，受损的 GSPS，而不是受损的 GSIS，可能是识别 NGT 亚群中具有高糖尿病风险的早期生物标志物。
