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Aetiology of type 1 diabetes: Physiological growth in children affects disease progression

Journal article
Authors O. Skog
Olle Korsgren
Published in Diabetes, obesity and metabolism
Volume 20
Issue 4
Pages 775-785
ISSN 1462-8902
Publication year 2018
Published at Institute of Biomedicine
Pages 775-785
Language en
Keywords beta-cell function, islet, type 1 diabetes, beta-cell function, pancreatic-islet tissue, infiltrating t-cells, body-mass index, animal-models, hla genotypes, recent-onset, c-peptide, staphylococcus-aureus, insulin-resistance, Endocrinology & Metabolism
Subject categories Endocrinology and Diabetes


The prevailing view is that type 1 diabetes (T1D) develops as a consequence of a severe decline in beta-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 beta-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 beta-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 beta-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.

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