Matsuyama T, Tanaka R, Shima K, Tarui S
Endocrinol Jpn. 1978 Dec;25(6):529-32. doi: 10.1507/endocrj1954.25.529.
Effects of somatostatin on extrapancreatic glucagon secretion in totally depancreatized dogs were examined. Somatostatin infusion at a rate of 3 microgram/min showed a rapid decrease of total glucagon-like immunoreactive materials (total GLI) measured by nonspecific antiserum, AGS 10, and gut glucagon immunoreactivity (gut GI) measured by specific antiserum, AGS 18, in systemic blood. Gut GLI calculated as the difference between total GLI and GI did not decrease significantly within 30 min. No changes of blood glucose were noted. Significant decreases of all glucagon fractions were observed when the rate of somatostatin infusion was increased to 10 microgram/min and prolonged for 90 min, whereas again blood glucose did not change at all. It is concluded that somatostatin inhibits both gut GI and GLI secretion, although gut GLI remains in circulation longer than gut GI. Suppression of gut GI is not effective for the reduction of blood glucose once an extreme hyperglycemia is brought about by insulin deficiency.
研究了生长抑素对完全胰腺切除犬胰腺外胰高血糖素分泌的影响。以3微克/分钟的速率输注生长抑素,可使通过非特异性抗血清AGS 10测定的总胰高血糖素样免疫反应物质(总GLI)以及通过特异性抗血清AGS 18测定的肠道胰高血糖素免疫反应性(肠道GI)在全身血液中迅速降低。计算得出的肠道GLI(即总GLI与GI的差值)在30分钟内未显著降低。未观察到血糖变化。当生长抑素输注速率增至10微克/分钟并持续90分钟时,所有胰高血糖素组分均显著降低,而血糖再次完全未发生变化。得出结论:生长抑素抑制肠道GI和GLI的分泌,尽管肠道GLI在循环中的存留时间比肠道GI更长。一旦因胰岛素缺乏导致极度高血糖,抑制肠道GI对降低血糖无效。