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Complete loss of insulin secretion capacity in type 1A diabetes patients during long‐term follow up

AIM/INTRODUCTION: Patients with type 1 diabetes are classified into three subtypes in Japan: acute onset, fulminant and slowly progressive. Acute‐onset type 1 diabetes would be equivalent to type 1A diabetes, the typical type 1 diabetes in Western countries. The insulin secretion capacity in Japanes...

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Autores principales: Uno, Sae, Imagawa, Akihisa, Kozawa, Junji, Fukui, Kenji, Iwahashi, Hiromi, Shimomura, Iichiro
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6031490/
https://www.ncbi.nlm.nih.gov/pubmed/29034607
http://dx.doi.org/10.1111/jdi.12763
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author Uno, Sae
Imagawa, Akihisa
Kozawa, Junji
Fukui, Kenji
Iwahashi, Hiromi
Shimomura, Iichiro
author_facet Uno, Sae
Imagawa, Akihisa
Kozawa, Junji
Fukui, Kenji
Iwahashi, Hiromi
Shimomura, Iichiro
author_sort Uno, Sae
collection PubMed
description AIM/INTRODUCTION: Patients with type 1 diabetes are classified into three subtypes in Japan: acute onset, fulminant and slowly progressive. Acute‐onset type 1 diabetes would be equivalent to type 1A diabetes, the typical type 1 diabetes in Western countries. The insulin secretion capacity in Japanese patients with long‐standing type 1A diabetes is unclear. The aim of the present study was to clarify the course of endogenous insulin secretion during long‐term follow up and the factors associated with residual insulin secretion in patients with acute‐onset type 1 diabetes (autoimmune). MATERIALS AND METHODS: We retrospectively investigated endogenous insulin secretion capacity in 71 patients who fulfilled the diagnostic criteria for acute‐onset type 1 diabetes (autoimmune) in Japan. To assess the residual insulin secretion capacity, we evaluated randomly measured C‐peptide levels and the results of glucagon stimulation test in 71 patients. RESULTS: In the first year of disease, the child‐ and adolescent‐onset patients had significantly more in residual insulin secretion than the adult‐onset patients (34 patients in total). C‐peptide levels declined more rapidly in patients whose age of onset was ≤18 years than in patients whose age of onset was ≥19 years. Endogenous insulin secretion capacity stimulated by glucagon was completely lost in almost all patients at >15 years after onset (61 patients in total). CONCLUSIONS: Most patients with acute‐onset type 1 diabetes (autoimmune) completely lose their endogenous insulin secretion capacity during the disease duration in Japan. Age of onset might affect the course of insulin secretion.
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spelling pubmed-60314902018-07-11 Complete loss of insulin secretion capacity in type 1A diabetes patients during long‐term follow up Uno, Sae Imagawa, Akihisa Kozawa, Junji Fukui, Kenji Iwahashi, Hiromi Shimomura, Iichiro J Diabetes Investig Articles AIM/INTRODUCTION: Patients with type 1 diabetes are classified into three subtypes in Japan: acute onset, fulminant and slowly progressive. Acute‐onset type 1 diabetes would be equivalent to type 1A diabetes, the typical type 1 diabetes in Western countries. The insulin secretion capacity in Japanese patients with long‐standing type 1A diabetes is unclear. The aim of the present study was to clarify the course of endogenous insulin secretion during long‐term follow up and the factors associated with residual insulin secretion in patients with acute‐onset type 1 diabetes (autoimmune). MATERIALS AND METHODS: We retrospectively investigated endogenous insulin secretion capacity in 71 patients who fulfilled the diagnostic criteria for acute‐onset type 1 diabetes (autoimmune) in Japan. To assess the residual insulin secretion capacity, we evaluated randomly measured C‐peptide levels and the results of glucagon stimulation test in 71 patients. RESULTS: In the first year of disease, the child‐ and adolescent‐onset patients had significantly more in residual insulin secretion than the adult‐onset patients (34 patients in total). C‐peptide levels declined more rapidly in patients whose age of onset was ≤18 years than in patients whose age of onset was ≥19 years. Endogenous insulin secretion capacity stimulated by glucagon was completely lost in almost all patients at >15 years after onset (61 patients in total). CONCLUSIONS: Most patients with acute‐onset type 1 diabetes (autoimmune) completely lose their endogenous insulin secretion capacity during the disease duration in Japan. Age of onset might affect the course of insulin secretion. John Wiley and Sons Inc. 2017-11-24 2018-07 /pmc/articles/PMC6031490/ /pubmed/29034607 http://dx.doi.org/10.1111/jdi.12763 Text en © 2017 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Articles
Uno, Sae
Imagawa, Akihisa
Kozawa, Junji
Fukui, Kenji
Iwahashi, Hiromi
Shimomura, Iichiro
Complete loss of insulin secretion capacity in type 1A diabetes patients during long‐term follow up
title Complete loss of insulin secretion capacity in type 1A diabetes patients during long‐term follow up
title_full Complete loss of insulin secretion capacity in type 1A diabetes patients during long‐term follow up
title_fullStr Complete loss of insulin secretion capacity in type 1A diabetes patients during long‐term follow up
title_full_unstemmed Complete loss of insulin secretion capacity in type 1A diabetes patients during long‐term follow up
title_short Complete loss of insulin secretion capacity in type 1A diabetes patients during long‐term follow up
title_sort complete loss of insulin secretion capacity in type 1a diabetes patients during long‐term follow up
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6031490/
https://www.ncbi.nlm.nih.gov/pubmed/29034607
http://dx.doi.org/10.1111/jdi.12763
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