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一名中年患者出现显著的高胰岛素原血症。

Prominent Hyperproinsulinemia in a Middle Age Patient.

作者信息

Yoshino Hiroshi, Kawakami Kyoko, Yoshino Kei, Yoshino Gen

机构信息

Department of Geriatrics and Cognitive Disorders, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.

Center for Diabetes, Shin-suma General Hospital, Kobe, Japan.

出版信息

Clin Med Insights Case Rep. 2021 Sep 1;14:11795476211042241. doi: 10.1177/11795476211042241. eCollection 2021.

Abstract

INTRODUCTION

Insulin is synthesized in the β-cells from preproinsulin. Preproinsulin becomes proinsulin after leaving the signal peptide. Proinsulin is separated into C-peptide and insulin by 2 enzymes. Hyperproinsulinemia is suspected to be a pancreatic β-cell defect that is augmented by the increased demand placed on the β-cell by hyperglycemia.

CASE PRESENTATION

A 39-year-old Japanese man visited to Shin-suma hospital in May 2013. Liver dysfunction, dyslipidemia, and hyperuricemia had been found in medical checkups in his workplace. Therefore, he visited Shin-suma hospital in order to receive intensive examination. Diet and exercise therapy were initiated. In November 2013, intact proinsulin and proinsulin per insulin (PI/I) ratio were evaluated as part of an ongoing study. His intact proinsulin level and PI/I ratio were markedly elevated. A 75 g oral OGTT revealed that his glucose tolerance was impaired. His glycosylated hemoglobin was 6.9%. He was diagnosed as having type 2 diabetes mellitus. Although, diet and exercise therapy continued, his hyperproinslinemia and diabetes mellitus remained. Therefore, aloguliptin was started in order to recover insulin secretion in November 2014. Thereafter, pioglitazone was added to improve insulin resistance. Finally, luseogliflozin was commenced to expect glucose-lowering effects. His HbA1c was stabilized. To the best of our knowledge, there have been few reports of patients with hyperproinsulinemia.

CONCLUSION

When the physicians face treatment resistance in diabetes mellitus, we emphasize that evaluation of proinsulin should be considered as one of the methods.

摘要

引言

胰岛素在β细胞中由胰岛素原合成。胰岛素原离开信号肽后成为胰岛素原。胰岛素原通过两种酶被分离成C肽和胰岛素。高胰岛素原血症被怀疑是一种胰腺β细胞缺陷,高血糖对β细胞的需求增加会加剧这种缺陷。

病例介绍

一名39岁的日本男性于2013年5月前往新须磨医院就诊。他在工作场所的体检中发现了肝功能障碍、血脂异常和高尿酸血症。因此,他前往新须磨医院接受进一步检查。开始了饮食和运动疗法。2013年11月,作为一项正在进行的研究的一部分,对完整胰岛素原和胰岛素原与胰岛素的比值(PI/I)进行了评估。他的完整胰岛素原水平和PI/I比值显著升高。75克口服葡萄糖耐量试验显示他的糖耐量受损。他的糖化血红蛋白为6.9%。他被诊断为2型糖尿病。尽管继续进行饮食和运动疗法,但他的高胰岛素原血症和糖尿病仍然存在。因此,2014年11月开始使用阿格列汀以恢复胰岛素分泌。此后,添加了吡格列酮以改善胰岛素抵抗。最后,开始使用鲁索格列净以期望达到降糖效果。他的糖化血红蛋白水平稳定。据我们所知,关于高胰岛素原血症患者的报道很少。

结论

当医生在糖尿病治疗中面临耐药性时,我们强调胰岛素原评估应被视为方法之一。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7125/8414601/fe8b02ffae88/10.1177_11795476211042241-fig1.jpg

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