Abstract
There is unexplained deficit in size and function of the exocrine pancreas in type 1 diabetes (T1D). We obtained pancreas from an individual with pre-T1D obtained at surgery and addressed the question, what is the relative inflammation in the exocrine and endocrine pancreas in pre-T1D in the absence of the potential confounding changes at autopsy or in brain dead organ donors. Pancreas was removed surgically from a 36 year woman for benign neuroendocrine tumors (NET). The patient had gestational diabetes at age 29 and has a 23 year old sister with T1D. Pre-operative fasting glucose of 109 mg/dl and HbA1C 5.8% revealed prediabetes with an anti-GAD 1,144 (5–250 U/ml) together with family history implying pre-T1D. There was patchy low grade immune infiltration in some, but not all, islets that met criteria for autoimmune insulitis. The exocrine pancreas showed more abundant inflammation with areas of chronic pancreatitis and acinar to ductal metaplasia, and with other areas of atrophy and fatty infiltration. In pre-T1D inflammation may be more prominent in the exocrine than the endocrine pancreas, calling into question the sequence of events and assumed islet centric basis of autoimmunity leading to T1D.
Highlights
Type 1 diabetes (T1D) is an autoimmune disease with an eventual near complete loss of beta cells [1]
In adult onset T1D [2, 3] there may be as much as a 5–10 year prediabetes phase following the detection of autoantibodies and clinical diabetes onset
Considerable e ort has been expended on arresting disease progression during the prediabetes phase of T1D, but with limited success. is is partly due to a limited understanding of the sequence of events leading to loss of beta cell function in T1D
Summary
Type 1 diabetes (T1D) is an autoimmune disease with an eventual near complete loss of beta cells [1]. E exocrine pancreas in both slowly progressive and fulminant forms of T1D have increased in ammatory cells that are comparable in subtypes to those observed in islets in the same individuals [12,13,14] as well as activation of the pancreatic duct compartment (PDG) [15], a regenerative compartment that is activated by pancreatitis. Taken together these studies have raised the possibility that in ammation originating in the. It was of particular interest in the present case where surgically resected pancreas became available from an individual with pre-T1D to evaluate the exocrine and endocrine pancreas in the pre-T1D phase
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