Gutniak M, Grill V, Efendić S
J Clin Endocrinol Metab. 1986 Jan;62(1):77-83. doi: 10.1210/jcem-62-1-77.
We assessed the effects of insulin and normalization of blood glucose on plasma levels of somatostatin-like immunoreactivity (SLI) in patients with noninsulin-dependent diabetes mellitus (NIDDM). In one series of experiments, normalization of blood glucose was achieved by Biostator-controlled feedback infusion of insulin. This procedure reduced plasma SLI levels by 34% [from 17.1 +/- 2.1 (+/- SEM) to 11.3 +/- 1.9 pg/ml; P less than 0.05], concomitant with a significant reduction in plasma glucagon and C-peptide and an evanescent decrease in plasma gastric inhibitory peptide (GIP) levels. An ensuing mixed meal elicited a rise in SLI that reached the same levels during infusion of insulin as during uncontrolled hyperglycemia; the incremental increase was, however, 45% higher (P less than 0.005) during insulin infusion. Furthermore feedback insulin infusion enhanced GIP and decreased C-peptide responses, but did not affect the glucagon response to the meal. To further evaluate the influence of insulin of SLI levels, we compared the effects of normo- and hyperglycemia during constant hyperinsulinemia by varying the rate of glucose infusion (glucose clamping). Basal SLI levels decreased significantly only during the normoglycemic clamp. The SLI response to a meal was more pronounced during the normoglycemic than the hyperglycemic clamp. The patterns of glucagon and GIP were similar during the two clamp conditions, while both basal and stimulated C-peptide levels were lower during the normoglycemic clamp. To investigate the temporal relationship between changes in blood glucose and SLI levels, patients were studied during a prolonged (270-min) period of normoglycemic clamp and fasting. After attaining normoglycemia, SLI levels continued to decline for 150 min, whereas glucagon and GIP levels did not change. We conclude that in patients with NIDDM, insulin significantly lowers basal SLI levels if normoglycemia is concomitantly attained; this action of insulin was partially dissociated from its hypoglycemic action; hyperglycemia per se inhibits a meal-induced SLI response, and insulin effects on SLI are not secondary to changes in glucagon or GIP levels.
我们评估了胰岛素及血糖正常化对非胰岛素依赖型糖尿病（NIDDM）患者血浆中类生长抑素免疫反应性物质（SLI）水平的影响。在一系列实验中，通过生物人工肾控制的胰岛素反馈输注实现血糖正常化。此操作使血浆SLI水平降低了34%[从17.1±2.1（±标准误）降至11.3±1.9 pg/ml；P<0.05]，同时血浆胰高血糖素和C肽显著降低，血浆胃抑制肽（GIP）水平短暂下降。随后的混合餐引发SLI升高，在胰岛素输注期间达到的水平与未控制的高血糖期间相同；然而，在胰岛素输注期间，增量升高高出45%（P<0.005）。此外，反馈性胰岛素输注增强了GIP反应并降低了C肽反应，但不影响胰高血糖素对餐食的反应。为进一步评估胰岛素对SLI水平的影响，我们通过改变葡萄糖输注速率（葡萄糖钳夹）比较了持续高胰岛素血症期间正常血糖和高血糖状态的影响。仅在正常血糖钳夹期间基础SLI水平显著降低。与高血糖钳夹相比，正常血糖钳夹期间对餐食的SLI反应更明显。在两种钳夹条件下，胰高血糖素和GIP的模式相似，而在正常血糖钳夹期间基础和刺激后的C肽水平均较低。为研究血糖变化与SLI水平之间的时间关系，在正常血糖钳夹和禁食的延长（270分钟）期间对患者进行了研究。达到正常血糖后，SLI水平持续下降150分钟，而胰高血糖素和GIP水平未改变。我们得出结论，在NIDDM患者中，如果同时实现正常血糖，胰岛素可显著降低基础SLI水平；胰岛素的这一作用部分与其降血糖作用分离；高血糖本身抑制餐食诱导的SLI反应，胰岛素对SLI的作用并非继发于胰高血糖素或GIP水平的变化。
