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Submitted on November 17, 2006
Accepted on February 11, 2008
Department of Pediatrics, University of Turku, Turku, Finland; Turku PET Centre, University of Turku, Turku, Finland; Department of Medicine, University of Turku, Turku, Finland; Department of Radiology, University of Turku, Turku, Finland; Department of Pediatrics, Central Hospital of Seinäjoki, Seinäjoki, Finland
* To whom correspondence should be addressed. E-mail: teemu.kalliokoski{at}utu.fi.
Context. Due to the restricted accessibility of pancreatic tissue in living man, direct analysis of the events preceding development of autoimmune changes in the pancreas has been problematic. In vivo imaging of insulitis might markedly increase understanding of the events and timing of the events that are necessary for the progression toward overt type 1 diabetes.
Design. To evaluate possibilities to visualize insulitis in man in vivo with positron emission tomography (PET), we studied 12 male patients (age 26 ± 7 years) with newly diagnosed type 1 diabetes (duration range 0–7 months) and 9 age and sex-matched healthy controls after an overnight fast using 2-[18F]fluoro-2-deoxy-D-glucose ([18F]FDG) and [11C]methionine. For definition of the regions of interest (ROIs) pancreas was localized with MRI or CT-PET.
Results. Glucose uptake to the pancreas was markedly higher in the patients with type 1 diabetes than in the healthy controls (22.9 ± 6.4 vs. 17.8 ± 6.0 µmol/kg·min, p = 0.039). Glucose uptake to the pancreas of the patients was inversely associated with the duration of diabetes (R = -0.58, p = 0.024), so that in patients with newly diagnosed type 1 diabetes glucose uptake was higher than in the healthy controls or patients with long duration of diabetes. Methionine uptake to the pancreas of the patients was similar as in the controls (3.7 ± 1.9 vs. 4.6 ± 2.4 µmol/kg·min, P = 0.21).
Conclusions. In patients with type 1 diabetes glucose uptake to the pancreas is enhanced at or soon after the time of diagnosis.
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| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
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