Seino Y, Ikeda M, Kurahachi H, Taminato T, Sakurai H, Goto Y, Inoue Y, Kadowaki S, Mori K, Imura H
Diabetes. 1978 Dec;27(12):1145-50. doi: 10.2337/diab.27.12.1145.
Plasma glucagon response to glucose in diabetic subjects was observed before and after treatment. In normal subjects, plasma glucagon concentrations decreased substantially after an oral glucose load. In all diabetic patients before treatment, plasma glucagon was not suppressed and rather tended to rise paradoxically despite pronounced hyperglycemia. In diabetics treated with sulfonylurea or insulin, basal plasma glucagon concentrations were significantly lower than those in patients who were not treated. However, plasma glucagon response to an oral glucose load was not normalized by successful treatment with sulfonylurea or insulin, in spite of improvement of glucose tolerance. These results suggest that the insensitivity of the A-cell to hyperglycemia exists after treatment, and this abnormal plasma glucagon response to glucose after treatment may be caused either by impaired response of endogenous insulin to glucose, which is sustained even after treatment, or by an intrinsic defect of the A-cell.
观察了糖尿病患者治疗前后血浆胰高血糖素对葡萄糖的反应。在正常受试者中，口服葡萄糖负荷后血浆胰高血糖素浓度大幅下降。在所有未治疗的糖尿病患者中，尽管存在明显的高血糖，但血浆胰高血糖素并未受到抑制，反而有反常升高的趋势。在用磺脲类药物或胰岛素治疗的糖尿病患者中，基础血浆胰高血糖素浓度显著低于未治疗的患者。然而，尽管糖耐量有所改善，但用磺脲类药物或胰岛素成功治疗后，血浆胰高血糖素对口服葡萄糖负荷的反应并未恢复正常。这些结果表明，治疗后A细胞对高血糖不敏感，且治疗后血浆胰高血糖素对葡萄糖的这种异常反应可能是由于内源性胰岛素对葡萄糖的反应受损（即使在治疗后仍持续存在）或A细胞的内在缺陷所致。
