Frier B M, Corrall R J, Ashby J P, Adrian T E, Bloom S R
Horm Metab Res. 1981 Apr;13(4):191-5. doi: 10.1055/s-2007-1019218.
Following acute insulin-induced hypoglycaemia, an abnormal pattern of insulin secretion in response to a meal has been demonstrated in six healthy volunteers. This is characterized by an initial impairment in insulin secretion and late hyperinsulinaemia. Postprandial gastrointestinal hormone levels were normal following hypoglycaemia in these subjects. In four other subjects, the administration of intravenous glucose prior to the meal partially reversed the abnormal pattern of secretion. In two patients with a total pre-ganglionic sympathectomy, the pattern of blood glucose, plasma insulin and C-peptide was similar to that observed following hypoglycaemia in normal subjects. It is unlikely that an abnormal entero-insular axis or an elevation of plasma catecholamine levels are primarily responsible for this phenomenon. This effect of hypoglycaemia on postprandial insulin secretion may be caused by glucopenia of the pancreatic beta cells.
在六名健康志愿者中，已证实在急性胰岛素诱导的低血糖之后，其对进餐的胰岛素分泌模式异常。这表现为胰岛素分泌初期受损及后期高胰岛素血症。这些受试者在低血糖后餐后胃肠激素水平正常。在另外四名受试者中，进餐前静脉输注葡萄糖部分逆转了异常分泌模式。在两名接受节前交感神经切除术的患者中，血糖、血浆胰岛素和C肽的模式与正常受试者低血糖后观察到的相似。肠 - 胰岛轴异常或血浆儿茶酚胺水平升高不太可能是这一现象的主要原因。低血糖对餐后胰岛素分泌的这种影响可能是由胰腺β细胞的低血糖症引起的。
