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Pancreatic 18F-FDG uptake is increased in type 2 diabetes patients compared to non-diabetic controls
Guido J Bakker1, Manon C Vanbellinghen1, Torsten P Scheithauer2,3
1Department of Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Introduction:
Increasing evidence indicates that the development of type 2 diabetes is driven by chronic low grade beta-cell inflammation. However, it is unclear whether pancreatic inflammation can be noninvasively visualized in type 2 diabetes patients. We aimed to assess pancreatic 18F-FDG uptake in type 2 diabetes patients and controls using 18F-fluorodeoxylglucose positron emission tomography/computed tomography (18F-FDG PET/CT).
Material And Methods:
In this retrospective cross-sectional study, we enrolled 20 type 2 diabetes patients and 65 controls who had undergone a diagnostic 18F-FDG PET/CT scan and obtained standardized uptake values (SUVs) of pancreas and muscle. Pancreatic SUV was adjusted for background uptake in muscle and for fasting blood glucose concentrations.
Results:
The maximum pancreatic SUVs adjusted for background muscle uptake (SUVmax.m) and fasting blood glucose concentration (SUVglucose) were significantly higher in diabetes patients compared to controls (median 2.86 [IQR 2.24-4.36] compared to 2.15 [IQR 1.51-2.83], p = 0.006 and median 2.76 [IQR 1.18-4.34] compared to 1.91 [IQR 1.27-2.55], p<0.001, respectively). In linear regression adjusting for age and body mass index, diabetes remained the main predictor of SUVmax.m and SUVglucose.
Conclusion:
Pancreatic 18F-FDG uptake adjusted for background muscle uptake and fasting blood glucose concentration was significantly increased in type 2 diabetes patients.
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