Pancreatic .sup.18F-FDG uptake is increased in type 2 diabetes patients compared to non-diabetic controls

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 .sup.18 F-FDG uptake in type...

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Veröffentlicht in:PloS one 2019-03, Vol.14 (3), p.e0213202
Hauptverfasser: Bakker, Guido J, Vanbellinghen, Manon C, Scheithauer, Torsten P, Verchere, C. Bruce, Stroes, Erik S, Timmers, Nyanza K. L. M, Herrema, Hilde, Nieuwdorp, Max, Verberne, Hein J, van Raalte, Daniël H
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Sprache:eng
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Zusammenfassung: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 .sup.18 F-FDG uptake in type 2 diabetes patients and controls using .sup.18 F-fluorodeoxylglucose positron emission tomography/computed tomography (.sup.18 F-FDG PET/CT). In this retrospective cross-sectional study, we enrolled 20 type 2 diabetes patients and 65 controls who had undergone a diagnostic .sup.18 F-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. The maximum pancreatic SUVs adjusted for background muscle uptake (SUV.sub.max.m) and fasting blood glucose concentration (SUV.sub.glucose) 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
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0213202