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Aetiology of type 1 diabetes: Physiological growth in children affects disease progression
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.ORCID iD: 0000-0001-9713-722X
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology. University of Gothenburg, Institute of Biomedicine, Gothenburg, Sweden.ORCID iD: 0000-0002-8524-9547
2018 (English)In: Diabetes, obesity and metabolism, ISSN 1462-8902, E-ISSN 1463-1326, Vol. 20, no 4, p. 775-785Article in journal (Refereed) Published
Abstract [en]

The prevailing view is that type 1 diabetes (T1D) develops as a consequence of a severe decline in β-cell mass resulting from T-cell-mediated autoimmunity; however, progression from islet autoantibody seroconversion to overt diabetes and finally to total loss of C-peptide production occurs in most affected individuals only slowly over many years or even decades. This slow disease progression should be viewed in relation to the total β-cell mass of only 0.2 to 1.5 g in adults without diabetes. Focal lesions of acute pancreatitis with accumulation of leukocytes, often located around the ducts, are frequently observed in people with recent-onset T1D, and most patients display extensive periductal fibrosis, the end stage of inflammation. An injurious inflammatory adverse event, occurring within the periductal area, may have negative implications for islet neogenesis, dependent on stem cells residing within or adjacent to the ductal epithelium. This could in part prevent the 30-fold increase in β-cell mass that would normally occur during the first 20 years of life. This increase occurs in order to maintain glucose metabolism during the physiological increases in insulin production that are required to balance the 20-fold increase in body weight during childhood and increased insulin resistance during puberty. Failure to expand β-cell mass during childhood would lead to clinically overt T1D and could help to explain the apparently more aggressive form of T1D occurring in growing children when compared with that observed in affected adults.

Place, publisher, year, edition, pages
2018. Vol. 20, no 4, p. 775-785
Keywords [en]
islet, type 1 diabetes, β-cell function
National Category
Endocrinology and Diabetes
Identifiers
URN: urn:nbn:se:uu:diva-342884DOI: 10.1111/dom.13144ISI: 000427114800003PubMedID: 29083510OAI: oai:DiVA.org:uu-342884DiVA, id: diva2:1185323
Funder
Ernfors FoundationSwedish Child Diabetes FoundationSwedish Diabetes AssociationTore Nilsons Stiftelse för medicinsk forskningÅke Wiberg FoundationNovo NordiskEU, FP7, Seventh Framework Programme, PEVNET 261441EU, FP7, Seventh Framework Programme, HumEn HEALTH-F4-2013-602889Available from: 2018-02-23 Created: 2018-02-23 Last updated: 2018-06-08Bibliographically approved

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Skog, OskarKorsgren, Olle

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