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Updated: Jan 20, 2026

Determining Glucose Metabolism Kinetics Using 18F-FDG Micro-PET/CT
Published on: May 2, 2017
18Fluorodeoxyglucose Accumulation in Arterial Tissues Determined by PET Signal Analysis
Rozh H Al-Mashhadi1, Lars P Tolbod2, Lars Ø Bloch3
1Department of Clinical Medicine, Aarhus University, Aarhus, Denmark; Department of Radiology, Aarhus University Hospital, Aarhus, Denmark; Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Arterial 18fluorodeoxyglucose (FDG) positron emission tomography (PET) accumulates similarly in macrophages and other arterial cells, challenging the assumption of macrophage-selective uptake in atherosclerosis imaging. This finding helps explain clinical observations in cardiovascular disease research.
Area of Science:
- Cardiovascular Imaging
- Molecular Imaging
- Atherosclerosis Research
Background:
- Arterial 18fluorodeoxyglucose (FDG) positron emission tomography (PET) is a tool for assessing atherosclerotic plaque macrophages and disease activity.
- The precise distribution of FDG within different arterial cell types remains unclear.
Purpose of the Study:
- To investigate FDG uptake patterns in various arterial tissues.
- To determine the contribution of different tissues to the overall PET signal in normal and atherosclerotic arteries.
Main Methods:
- Atherosclerosis was induced in Yucatan minipigs using a high-fat, high-cholesterol diet.
- FDG-PET and CT scans were performed, followed by histological analysis of arterial tissues.
- FDG distribution was quantified using in vivo PET signal modeling and confirmed with direct autoradiography.
Main Results:
- FDG-PET imaging in minipigs closely resembled human imaging findings.
- Quantitative modeling demonstrated comparable FDG accumulation in macrophages and other arterial tissues, including smooth muscle cells.
- Autoradiography validated these findings in both normal and atherosclerotic arteries.
Conclusions:
- FDG uptake is not selective to macrophages in arterial tissues.
- This finding provides a mechanistic explanation for clinical observations that previously seemed inconsistent with macrophage-selective FDG uptake in atherosclerosis.
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