Islet inflammation is associated with pancreatic fatty infiltration and hyperglycemia in type 2 diabetes

INTRODUCTION: Chronic inflammation is observed in type 2 diabetes islets, and fat deposition in the pancreas affects insulin secretion and glucose tolerance. However, the relationship between this inflammation and pancreatic fat deposition has not been elucidated. RESEARCH DESIGN AND METHODS: We examined pancreatic sections from 60 Japanese patients obtained by pancreatectomy. We evaluated pancreatic fat-cell area (%) and CD68-positive (CD68(+)) cells per islet histologically and examined the relationships between these histological findings and various clinical parameters. RESULTS: The number of CD68(+) cells per islet in the diabetes group was significantly higher than that in the normal glucose tolerance group (p=0.026). Moreover, CD68(+) cells per islet were significantly correlated with body mass index (r=0.33, p=0.0080), fasting C-peptide immunoreactivity (r=0.46, p=0.0042), homeostasis model assessment insulin resistance (r=0.38, p=0.016), C-peptide index (r=0.38, p=0.018), the area under the glucose concentration curve (AUC(glucose)) at the 75 g oral glucose tolerance test (r=0.49, p=0.0065) and fat-cell area (r=0.51, p<0.0001). In multiple regression analyses, fat-cell area (β=0.600, p=0.0027) and AUC(glucose) (β=0.453, p=0.0042) were the independent and significant determinants of CD68(+) cells per islet. CONCLUSION: The inflammation of islets is associated with pancreatic fatty infiltration and hyperglycemia, which may further aggravate glucose tolerance.