Abstract
A higher titer of IA-2Ab reflects a reduced pancreatic size in the patients with Type 1 diabetes (T1D), especially in those with the acute-onset form of the disease. The potential mechanisms underlying the reduced pancreatic size might differ between acute-onset T1D and slowly progressive insulin-dependent diabetes mellitus. The authors investigated the relationship between islet autoimmunity and pancreatic size in the Japanese patients with T1D.
Highlights
Type 1 diabetes (T1D) is caused by autoimmune-mediated selective destruction of insulin-producing β-cells [1]
We reported that the pancreatic volume assessed by computed tomography (CT) was significantly reduced in the newly diagnosed acute-onset T1D patients, but not in the virus-induced fulminant T1D patients, when compared to non-diabetic controls [15]
C-peptide index (CPI) was significantly lower in acute-onset T1D than in slowly progressive insulin-dependent diabetes mellitus (SPIDDM)
Summary
Type 1 diabetes (T1D) is caused by autoimmune-mediated selective destruction of insulin-producing β-cells [1]. Reduced pancreas size has recently been observed in both adults with newly diagnosed acute-onset T1D [12] and islet autoantibodypositive non-diabetic donors [14] This observation suggests that the atrophy of the pancreas is likely to begin before the onset of T1D. We reported that the pancreatic volume assessed by CT was significantly reduced in the newly diagnosed acute-onset T1D patients, but not in the virus-induced fulminant T1D patients, when compared to non-diabetic controls (non-DCs) [15]. These findings suggest that the autoimmune process contributes to the pathogenesis of reduced PV in acute-onset T1D
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