Prominent Hyperproinsulinemia in a Middle Age Patient

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 incre...

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Main Authors: Hiroshi Yoshino, Kyoko Kawakami, Kei Yoshino, Gen Yoshino
Format: Article
Language:English
Published: SAGE Publishing 2021-09-01
Series:Clinical Medicine Insights: Case Reports
Online Access:https://doi.org/10.1177/11795476211042241
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spelling doaj-b0f3a58463e44388b812b088ef2572142021-09-02T02:33:39ZengSAGE PublishingClinical Medicine Insights: Case Reports1179-54762021-09-011410.1177/11795476211042241Prominent Hyperproinsulinemia in a Middle Age PatientHiroshi Yoshino0Kyoko Kawakami1Kei Yoshino2Gen Yoshino3Center for Diabetes, Shin-suma General Hospital, Kobe, JapanCenter for Diabetes, Shin-suma General Hospital, Kobe, JapanDivision of Diabetes and Endocrinology, Department of Internal of Medicine, Kobe University Graduate School of Medicine, Kobe, JapanCenter for Diabetes, Shin-suma General Hospital, Kobe, JapanIntroduction: 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.https://doi.org/10.1177/11795476211042241
collection DOAJ
language English
format Article
sources DOAJ
author Hiroshi Yoshino
Kyoko Kawakami
Kei Yoshino
Gen Yoshino
spellingShingle Hiroshi Yoshino
Kyoko Kawakami
Kei Yoshino
Gen Yoshino
Prominent Hyperproinsulinemia in a Middle Age Patient
Clinical Medicine Insights: Case Reports
author_facet Hiroshi Yoshino
Kyoko Kawakami
Kei Yoshino
Gen Yoshino
author_sort Hiroshi Yoshino
title Prominent Hyperproinsulinemia in a Middle Age Patient
title_short Prominent Hyperproinsulinemia in a Middle Age Patient
title_full Prominent Hyperproinsulinemia in a Middle Age Patient
title_fullStr Prominent Hyperproinsulinemia in a Middle Age Patient
title_full_unstemmed Prominent Hyperproinsulinemia in a Middle Age Patient
title_sort prominent hyperproinsulinemia in a middle age patient
publisher SAGE Publishing
series Clinical Medicine Insights: Case Reports
issn 1179-5476
publishDate 2021-09-01
description 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.
url https://doi.org/10.1177/11795476211042241
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