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Published on: May 6, 2013
Aetiology of type 1 diabetes: Physiological growth in children affects disease progression
Oskar Skog1, Olle Korsgren1,2
1Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.
Insights
Type 1 diabetes (T1D) progression may be linked to impaired beta-cell mass expansion in childhood due to inflammation. This inflammation could hinder islet neogenesis, impacting glucose metabolism and disease severity.
Area of Science:
- Endocrinology
- Immunology
- Pathology
Background:
- Type 1 diabetes (T1D) is traditionally viewed as resulting from autoimmune destruction of pancreatic beta cells.
- However, the slow progression of T1D, even after autoantibody seroconversion, suggests other contributing factors.
- Inflammation, particularly in the periductal area, is frequently observed in recent-onset T1D.
Purpose of the Study:
- To explore the role of inflammation and impaired beta-cell mass expansion in T1D pathogenesis.
- To investigate the potential impact of periductal inflammation on islet neogenesis and its implications for disease progression.
- To explain the slower disease course in adults versus children with T1D.
Main Methods:
- The study reviews existing literature on T1D pathogenesis, beta-cell mass, islet neogenesis, and childhood development.
- It correlates findings from pancreatitis lesions in T1D patients with potential effects on stem cells and beta-cell regeneration.
- Comparative analysis of T1D progression in children and adults is discussed.
Main Results:
- Periductal inflammation and fibrosis are common in recent-onset T1D.
- This inflammation may negatively affect islet neogenesis by impacting ductal stem cells.
- Impaired beta-cell mass expansion during childhood could lead to earlier onset and more aggressive T1D.
Conclusions:
- Inflammation-induced impairment of beta-cell neogenesis may contribute significantly to T1D development and progression.
- Failure to achieve adequate beta-cell mass expansion in childhood could underlie the more severe T1D observed in this population.
- This hypothesis offers a potential explanation for the observed differences in T1D aggressiveness between children and adults.
Abstract:
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.
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