Research Article: Pancreatic 18F-FDG uptake is increased in type 2 diabetes patients compared to non-diabetic controls

Date Published: March 19, 2019

Publisher: Public Library of Science

Author(s): Guido J. Bakker, Manon C. Vanbellinghen, Torsten P. Scheithauer, C. Bruce Verchere, Erik S. Stroes, Nyanza K. L. M. Timmers, Hilde Herrema, Max Nieuwdorp, Hein J. Verberne, Daniël H. van Raalte, Naeti Suksomboon.


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).

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.

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. Pancreatic 18F-FDG uptake adjusted for background muscle uptake and fasting blood glucose concentration was significantly increased in type 2 diabetes patients.

Partial Text

Hyperglycemia and type 2 diabetes (T2D) are driven by a decline in beta-cell function and mass against a background of insulin resistance [1,2]. Beta-cell dysfunction is present before diabetes onset [3,4] and worsens over time, determining the progressive course of the disease [5,6]. The underlying pathophysiological mechanisms of beta-cell dysfunction are yet to be unraveled. However, increasing evidence indicates that chronic low-grade Langerhans islet inflammation is involved. Several studies have linked increased presence and a pro-inflammatory phenotype of islet macrophages to beta-cell inflammation, dysfunction and apoptosis, likely mediated through secretion of pro-inflammatory cytokines such as interleukin-1β and tumor necrosis factor-α [7–13]. In keeping with this idea, various anti-inflammatory therapies have been shown to modestly improve beta-cell function in type 2 diabetes patients [14]. Taken together, these lines of evidence suggest a role for islet inflammation in the development of type 2 diabetes.

To our knowledge, this is the first study to show that type 2 diabetes patients have significantly increased background-corrected pancreatic 18F-FDG uptake compared to non-diabetic controls. This association persisted after adjustment for BMI and age as well as after correction for prevailing glucose concentrations. Our study is in line with previous evidence that suggest an important role for beta-cell inflammation in T2D development. In addition, this study suggests that pancreatic inflammation—possibly reflecting islet inflammation—can be imaged in vivo and paves the way for prospective studies that investigate the role of inflammation on beta-cell function and diabetes development over time and modulating effects of anti-inflammatory therapies.




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