INSULIN REGULATES THE SERUM LEVELS OF LOW-MOLECULAR WEIGHT INSULIN-LIKE GROWTH FACTOR-BINDING PROTEIN
INSULIN REGULATES THE SERUM LEVELS OF LOW-MOLECULAR WEIGHT INSULIN-LIKE GROWTH FACTOR-BINDING PROTEIN
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DOI：
10.1210/jcem-66-2-266
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发表时间：
1988-02-01
影响因子：
5.8
通讯作者：
SEPPALA, M
中科院分区：
文献类型：
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作者：
SUIKKARI, AM;KOIVISTO, VA;SEPPALA, M
通过 RIA 方法测量了 88 名 1 型糖尿病患者、9 名 2 型糖尿病患者、7 名胰岛素瘤患者、19 名正常受试者（均在禁食过夜后）和 82 名正常受试者早餐后的 34K 胰岛素样生长因子 (IGF) 结合蛋白血清水平。此外，在每个禁食组的一些受试者中研究了 2 至 3 小时血糖正常稳态高胰岛素血症对血清 IGF 结合蛋白和 IGF-1 水平的影响。与正常受试者相比，接受常规胰岛素注射治疗的 I 型糖尿病患者的平均血清 IGF 结合蛋白水平高出 4 倍（P < 0.001），连续皮下注射胰岛素治疗的患者高出 2.5 倍（P < 0.001），2 型糖尿病患者的平均血清 IGF 结合蛋白水平高出 2 倍（P < 0.05）。在胰岛素瘤患者中，平均 IGF 结合蛋白水平比正常水平低 63% (P < 0.001)，并且在肿瘤切除后恢复正常。糖尿病患者IGF结合蛋白水平与胰岛素剂量呈轻微负相关（r = -0.22；P < 0.05）。正常受试者餐后血清胰岛素浓度比空腹状态高2倍（P < 0.001），IGF结合蛋白水平比空腹状态低29%（P < 0.05）。 1 型和 2 型糖尿病患者、胰岛素瘤患者和正常受试者的血清 IGF-I 浓度几乎相同。在稳态正常血糖高胰岛素血症期间，各组的IGF结合蛋白水平下降了40-70%（P<0.001），而IGF-I水平仅在2型糖尿病患者中下降（P<0.05）。结合蛋白的下降与基线水平密切相关（r = 0.94；P < 0.001）。在任何组中均未发现血清 IgF-I 和结合蛋白水平之间存在相关性。总之，1）1型和2型糖尿病患者血清34K IGF结合蛋白水平升高，而胰岛素瘤患者血清34K IGF结合蛋白水平降低； 2)急性高胰岛素血症降低血清结合蛋白浓度，但不降低IGF-I浓度； 3)这些数据表明血清胰岛素浓度在调节血清34K IGF结合蛋白浓度中发挥作用。
The serum levels of 34K insulin-like growth factor (IGF)-binding protein were measured by RIA in 88 type 1 diabetic patients, 9 patients with type 2 diabetes, 7 patients with insulinoma, 19 normal subjects (all after an overnight fast), and 82 normal subjects after a breakfast meal. In addition, the effect of 2- to 3-h euglycemic steady state hyperinsulinemia on serum IGF-binding protein and IGF-1 levels was studied in some subjects in each of the fasted groups. Compared with normal subjects, the mean serum IGF-binding protein levels were 4-fold (P < 0.001) higher in type I diabetic patients treated with conventional insulin injections, 2.5-fold (P < 0.001) higher in those treated with continuous sc insulin infusion, and 2-fold (P < 0.05) higher in patients with type 2 diabetes. In the patients with insulinoma, the mean IGF-binding protein level was 63% below normal (P < 0.001), and it normalized after removal of the tumor. There was a slight negative correlation between the IGF-binding protein level and insulin dose in the diabetic patients (r = -0.22; P < 0.05). In normal subjects, serum insulin concentrations were 2-fold higher (P < 0.001) and the IGF-binding protein level was 29% lower after a meal (P < 0.05) than in the fasting state. Serum IGF-I concentrations were virtually identical in the type 1 and 2 diabetic patients, insulinoma patients, and normal subjects. During steady state euglycemic hyperinsulinemia, the IGF-binding protein level fell by 40-70% in each group (P < 0.001), whereas the IGF-I level declined (P < 0.05) in the type 2 diabetic patients only. The decline of binding protein was closely related to the baseline level (r = 0.94; P < 0.001). No correlation was found between serum IgF-I and binding protein levels in any group. In conclusion, 1) serum 34K IGF-binding protein levels are elevated in type 1 and 2 diabetic patients and decreased in patients with insulinoma; 2) the serum binding protein, but not IGF-I concentration is decreased by acute hyperinsulinemia; and 3) these data suggest that the serum insulin concentration plays a role in regulation of the serum 34K IGF-binding protein concentration.