Abe Ichiro, Fujii Hideyuki, Ohishi Hanako, Sugimoto Kaoru, Minezaki Midori, Nakagawa Midori, Takahara Saori, Kudo Tadachika, Abe Makiko, Ohe Kenji, Yanase Toshihiko, Kobayashi Kunihisa
Department of Endocrinology and Diabetes Mellitus, Fukuoka University Chikushi Hospital, Chikushino, Fukuoka 818-8502, Japan.
Department of Preventive Medicine, Kyushu University Faculty of Medical Sciences, Fukuoka 812-8582, Japan.
Endocr J. 2019 Feb 28;66(2):187-192. doi: 10.1507/endocrj.EJ18-0407. Epub 2018 Dec 13.
Glucose intolerance is often observed in patients with pheochromocytoma. However, it remains controversial issue that glucose intolerance on pheochromocytoma is caused by impaired insulin secretion and/or by increased insulin resistance. We aimed to reveal the mechanism of glucose intolerance on pheochromocytoma with regard to the type and amount of catecholamines released. We evaluated 12 individuals diagnosed with pheochromocytoma and who underwent surgery to remove it. We examined glycemic parameters before and after surgery and investigated the association between the change of parameters of insulin secretion (homeostasis model assessment of β-cell function (HOMA-β)), insulin resistance (homeostasis model assessment of insulin resistance (HOMA-IR)) and that of urinary levels of metanephrine/normetanephrine before and after surgery. Overall, fasting plasma glucose, glycated hemoglobin (HbA1c), HOMA-β, and HOMA-IR were improved significantly after surgery. Regression analysis showed that the improvement in HOMA-β from before to after surgery was significantly positively associated with an improvement in urinary levels of metanephrine from before to after surgery and showed a significantly negative association with improvement in urinary levels of normetanephrine from before to after surgery. The improvement in HOMA-IR from before to after surgery was significantly positively associated with an improvement in urinary levels of normetanephrine from before to after surgery. Our results showed that pheochromocytoma extirpation improved glycemic parameters. Furthermore, the different effects elicited by excess amounts of adrenaline and noradrenaline on glucose intolerance were demonstrated.
嗜铬细胞瘤患者常出现葡萄糖耐量异常。然而,嗜铬细胞瘤导致葡萄糖耐量异常是由胰岛素分泌受损和/或胰岛素抵抗增加引起的,这一问题仍存在争议。我们旨在揭示嗜铬细胞瘤导致葡萄糖耐量异常的机制,以及所释放儿茶酚胺的类型和数量。我们评估了12例被诊断为嗜铬细胞瘤并接受手术切除的患者。我们检查了手术前后的血糖参数,并研究了胰岛素分泌参数(β细胞功能稳态模型评估(HOMA-β))、胰岛素抵抗(胰岛素抵抗稳态模型评估(HOMA-IR))的变化与手术前后尿间甲肾上腺素/去甲间肾上腺素水平变化之间的关联。总体而言,术后空腹血糖、糖化血红蛋白(HbA1c)、HOMA-β和HOMA-IR均有显著改善。回归分析显示,术后HOMA-β的改善与术后尿间甲肾上腺素水平的改善显著正相关,与术后尿去甲间肾上腺素水平的改善显著负相关。术后HOMA-IR的改善与术后尿去甲间肾上腺素水平的改善显著正相关。我们的结果表明,切除嗜铬细胞瘤可改善血糖参数。此外,还证明了过量肾上腺素和去甲肾上腺素对葡萄糖耐量异常产生的不同影响。