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神经性厌食症患者对胰岛素诱导的低血糖症的胰高血糖素分泌受损。

Impaired glucagon secretion to insulin-induced hypoglycemia in anorexia nervosa.

作者信息

Fujii S, Tamai H, Kumai M, Takaichi Y, Nakagawa T, Aoki T T

机构信息

Department of Psychosomatic Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.

出版信息

Acta Endocrinol (Copenh). 1989 May;120(5):610-5. doi: 10.1530/acta.0.1200610.

DOI:10.1530/acta.0.1200610
PMID:2658451
Abstract

In order to clarify the role played by pancreatic alpha-cell dysfunction in the impaired glucose recovery from hypoglycemia in patients with anorexia nervosa, the response of pancreatic alpha-cells to insulin-induced hypoglycemia was investigated in 16 patients with anorexia nervosa before and after treatment. The results were compared with those obtained after loading with arginine. Before treatment, despite comparable falls in plasma glucose levels, glucagon secretion was significantly reduced in the anorectic patients compared with control subjects. In addition, glucose recovery from hypoglycemia in the patients was attenuated. However, after treatment, both glucagon secretory activity and plasma glucose recovery following insulin-induced hypoglycemia were restored to normal. Plasma glucagon responses to arginine infusion were not significantly different in the untreated anorectic patients and control subjects. However, the plasma insulin response in the patients was significantly lower than in the control group. These results suggest that the impaired recovery of plasma glucose levels from insulin-induced hypoglycemia in patients with anorexia nervosa is primarily attributable to impaired pancreatic alpha-secretory capability. In addition, this abnormality in pancreatic alpha-cell function is reversible with treatment leading to improved nutrition and weight gain.

摘要

为了阐明神经性厌食症患者低血糖后血糖恢复受损过程中胰腺α细胞功能障碍所起的作用,对16例神经性厌食症患者治疗前后胰腺α细胞对胰岛素诱导的低血糖的反应进行了研究。将结果与精氨酸负荷后获得的结果进行比较。治疗前,尽管血浆葡萄糖水平下降程度相当,但与对照组相比,厌食症患者的胰高血糖素分泌显著减少。此外,患者低血糖后的血糖恢复减弱。然而,治疗后,胰岛素诱导的低血糖后胰高血糖素分泌活性和血浆葡萄糖恢复均恢复正常。未经治疗的厌食症患者和对照组对精氨酸输注的血浆胰高血糖素反应无显著差异。然而,患者的血浆胰岛素反应显著低于对照组。这些结果表明,神经性厌食症患者胰岛素诱导的低血糖后血浆葡萄糖水平恢复受损主要归因于胰腺α细胞分泌能力受损。此外,胰腺α细胞功能的这种异常可通过治疗逆转,从而改善营养状况和体重增加。

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