Eriksson J, Nakazato M, Miyazato M, Shiomi K, Matsukura S, Groop L
Fourth Department of Medicine, Helsinki University Central Hospital, Finland.
Diabetologia. 1992 Mar;35(3):291-3. doi: 10.1007/BF00400933.
To study whether abnormal secretion of islet amyloid polypeptide is involved in the development of insulin resistance and impaired insulin secretion in Type 2 (non-insulin-dependent) diabetes mellitus, we measured islet amyloid polypeptide concentrations in 56 first-degree relatives of Type 2 diabetic subjects and in 10 healthy control subjects. Fasting islet amyloid polypeptide concentrations were similar in control subjects, glucose-tolerant and glucose-intolerant relatives (8 +/- 1, 9 +/- 1 and 11 +/- 2 fmol/ml; p = NS). The area under the islet amyloid polypeptide curve measured during an oral glucose load was larger in glucose-intolerant relatives (115 +/- 13 fmol/ml) compared to glucose tolerant relatives and control subjects (88 +/- 3 and 79 +/- 12 fmol/ml; p less than 0.05). The insulin response during the oral glucose load was inversely correlated with the rate of glucose disposal measured during a euglycaemic hyperinsulinaemic clamp (r = -0.725; p less than 0.01), while no significant correlation was observed between the corresponding values for islet amyloid polypeptide and glucose disposal (r = -0.380; p = NS). Hypersecretion of islet amyloid polypeptide is observed in glucose-intolerant first-degree relatives of patients with Type 2 diabetes. Since these patients are characterized by insulin resistance and abnormal first-phase insulin secretion, the putative role of islet amyloid polypeptide in the development of these abnormalities remains to be established. It is however, unlikely that islet amyloid polypeptide is involved in the development of insulin resistance as insulin-resistant relatives with normal glucose-tolerance showed normal islet amyloid polypeptide concentrations.
为研究胰岛淀粉样多肽异常分泌是否参与2型（非胰岛素依赖型）糖尿病患者胰岛素抵抗及胰岛素分泌受损的发生过程，我们检测了56例2型糖尿病患者的一级亲属及10例健康对照者的胰岛淀粉样多肽浓度。空腹时，对照者、糖耐量正常及糖耐量异常的亲属的胰岛淀粉样多肽浓度相似（分别为8±1、9±1和11±2 fmol/ml；p=无显著性差异）。口服葡萄糖负荷期间测得的胰岛淀粉样多肽曲线下面积，糖耐量异常的亲属（115±13 fmol/ml）大于糖耐量正常的亲属及对照者（分别为88±3和79±12 fmol/ml；p<0.05）。口服葡萄糖负荷期间的胰岛素反应与正常血糖高胰岛素钳夹期间测得的葡萄糖处置率呈负相关（r=-0.725；p<0.01），而胰岛淀粉样多肽与葡萄糖处置的相应值之间未观察到显著相关性（r=-0.380；p=无显著性差异）。在2型糖尿病患者糖耐量异常的一级亲属中观察到胰岛淀粉样多肽分泌过多。由于这些患者具有胰岛素抵抗和异常的第一相胰岛素分泌特征，胰岛淀粉样多肽在这些异常发生过程中的假定作用仍有待确定。然而，胰岛淀粉样多肽不太可能参与胰岛素抵抗的发生，因为糖耐量正常的胰岛素抵抗亲属的胰岛淀粉样多肽浓度正常。
