Kumai M, Tamai H, Fujii S, Nakagawa T, Aoki T T
Department of Psychosomatic Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Am J Clin Nutr. 1988 Feb;47(2):239-42. doi: 10.1093/ajcn/47.2.239.
Patients with anorexia nervosa frequently manifest impaired glucose tolerance. However, alterations in pancreatic glucagon secretion have also been associated with alterations in diabetes mellitus. For this reason, pancreatic alpha- and beta-cell responses to glucose load were measured in 25 anorexic patients both before and after treatment. The baseline glucose challenge failed to suppress plasma glucagon levels in the patients. However, in the control subjects and patients after treatment, glucagon levels were suppressed after glucose ingestion. Plasma glucose levels during the baseline challenge were significantly higher than those of the control subjects; however, after treatment glucose responses were nearly normal. Finally, insulin responses at baseline and after treatment were lower in the patients than in control subjects. These results suggest that the impaired glucose tolerance manifested by anorexic patients may be attributable to significant alterations in both pancreatic alpha- and beta-cell secretions and in pancreatic alpha-cell and glucose interrelationships.
神经性厌食症患者常表现出葡萄糖耐量受损。然而，胰腺胰高血糖素分泌的改变也与糖尿病的改变有关。因此，对25名厌食症患者在治疗前后均测量了胰腺α细胞和β细胞对葡萄糖负荷的反应。在这些患者中，基线葡萄糖激发试验未能抑制血浆胰高血糖素水平。然而，在对照组受试者和治疗后的患者中，葡萄糖摄入后胰高血糖素水平受到抑制。基线激发试验期间的血浆葡萄糖水平显著高于对照组受试者；然而，治疗后葡萄糖反应接近正常。最后，患者在基线和治疗后的胰岛素反应低于对照组受试者。这些结果表明，厌食症患者表现出的葡萄糖耐量受损可能归因于胰腺α细胞和β细胞分泌以及胰腺α细胞与葡萄糖相互关系的显著改变。
