Pancreatic 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 18F-FDG uptake in type 2 diab...

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Published inPloS one Vol. 14; no. 3; p. e0213202
Main Authors 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.
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 2019
Public Library of Science (PLoS)
Subjects
Aged
Beta cells
Biology and Life Sciences
Blood
Blood Glucose - analysis
Blood levels
Body mass
Body mass index
Body size
Computed tomography
Cross-Sectional Studies
Diabetes
Diabetes mellitus
Diabetes mellitus (non-insulin dependent)
Diabetes Mellitus, Type 2 - metabolism
Diabetes Mellitus, Type 2 - pathology
Diagnostic systems
Family medical history
Fasting
Female
Fluorine isotopes
Fluorodeoxyglucose F18 - chemistry
Fluorodeoxyglucose F18 - metabolism
Glucose
Humans
Hyperglycemia
Inflammation
Insulin
Internal medicine
Laboratories
Linear Models
Male
Medical imaging
Medicine and Health Sciences
Metabolism
Middle Aged
Muscles
Muscles - metabolism
Nuclear medicine
Pancreas
Pancreas - metabolism
Pancreatic cancer
Patients
Physical Sciences
Positron emission
Positron emission tomography
Positron Emission Tomography Computed Tomography
Radiopharmaceuticals - chemistry
Radiopharmaceuticals - metabolism
Research and Analysis Methods
Retrospective Studies
Tomography
Netherlands
Online AccessGet full text
ISSN1932-6203
1932-6203
DOI10.1371/journal.pone.0213202

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Abstract 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.
AbstractList 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.
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.
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.
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).INTRODUCTIONIncreasing 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.MATERIAL AND METHODSIn 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.RESULTSThe 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.CONCLUSIONPancreatic 18F-FDG uptake adjusted for background muscle uptake and fasting blood glucose concentration was significantly increased in type 2 diabetes patients.
IntroductionIncreasing 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 methodsIn 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.ResultsThe 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.ConclusionPancreatic 18F-FDG uptake adjusted for background muscle uptake and fasting blood glucose concentration was significantly increased in type 2 diabetes patients.
Author Bakker, Guido J.
Verchere, C. Bruce
Nieuwdorp, Max
van Raalte, Daniël H.
Herrema, Hilde
Timmers, Nyanza K. L. M.
Verberne, Hein J.
Scheithauer, Torsten P.
Vanbellinghen, Manon C.
Stroes, Erik S.
AuthorAffiliation 6 ICaR, Amsterdam University Medical Centers, Amsterdam, The Netherlands
7 Department of Radiology and Nuclear Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands
4 Department of Surgery and Department of Pathology and Laboratory Medicine, BC Children’s Hospital, University of British Columbia, Vancouver, British Columbia, Canada
1 Department of Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands
Mahidol University, THAILAND
3 Diabetes Center, Department of Internal Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands
2 Department of Experimental Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands
5 Wallenberg Laboratory, Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
AuthorAffiliation_xml – name: 2 Department of Experimental Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands
– name: 5 Wallenberg Laboratory, Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
– name: Mahidol University, THAILAND
– name: 7 Department of Radiology and Nuclear Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands
– name: 4 Department of Surgery and Department of Pathology and Laboratory Medicine, BC Children’s Hospital, University of British Columbia, Vancouver, British Columbia, Canada
– name: 1 Department of Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands
– name: 3 Diabetes Center, Department of Internal Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands
– name: 6 ICaR, Amsterdam University Medical Centers, Amsterdam, The Netherlands
Author_xml – sequence: 1
  givenname: Guido J.
  orcidid: 0000-0002-2819-9395
  surname: Bakker
  fullname: Bakker, Guido J.
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  givenname: Manon C.
  surname: Vanbellinghen
  fullname: Vanbellinghen, Manon C.
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  givenname: Daniël H.
  surname: van Raalte
  fullname: van Raalte, Daniël H.
BackLink https://www.ncbi.nlm.nih.gov/pubmed/30889184$$D View this record in MEDLINE/PubMed
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CitedBy_id crossref_primary_10_1053_j_semnuclmed_2020_04_002
crossref_primary_10_2214_AJR_20_24567
crossref_primary_10_3390_s21206820
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Snippet Increasing evidence indicates that the development of type 2 diabetes is driven by chronic low grade beta-cell inflammation. However, it is unclear whether...
Introduction Increasing evidence indicates that the development of type 2 diabetes is driven by chronic low grade beta-cell inflammation. However, it is...
IntroductionIncreasing evidence indicates that the development of type 2 diabetes is driven by chronic low grade beta-cell inflammation. However, it is unclear...
Introduction Increasing evidence indicates that the development of type 2 diabetes is driven by chronic low grade beta-cell inflammation. However, it is...
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SubjectTerms Aged
Beta cells
Biology and Life Sciences
Blood
Blood Glucose - analysis
Blood levels
Body mass
Body mass index
Body size
Computed tomography
Cross-Sectional Studies
Diabetes
Diabetes mellitus
Diabetes mellitus (non-insulin dependent)
Diabetes Mellitus, Type 2 - metabolism
Diabetes Mellitus, Type 2 - pathology
Diagnostic systems
Family medical history
Fasting
Female
Fluorine isotopes
Fluorodeoxyglucose F18 - chemistry
Fluorodeoxyglucose F18 - metabolism
Glucose
Humans
Hyperglycemia
Inflammation
Insulin
Internal medicine
Laboratories
Linear Models
Male
Medical imaging
Medicine and Health Sciences
Metabolism
Middle Aged
Muscles
Muscles - metabolism
Nuclear medicine
Pancreas
Pancreas - metabolism
Pancreatic cancer
Patients
Physical Sciences
Positron emission
Positron emission tomography
Positron Emission Tomography Computed Tomography
Radiopharmaceuticals - chemistry
Radiopharmaceuticals - metabolism
Research and Analysis Methods
Retrospective Studies
Tomography
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Title Pancreatic 18F-FDG uptake is increased in type 2 diabetes patients compared to non-diabetic controls
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