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13.12.2018 | Original Article Open Access

Glucagon-like peptide-1 receptor expression after myocardial infarction: Imaging study using 68Ga-NODAGA-exendin-4 positron emission tomography

Journal of Nuclear Cardiology
MSc Mia Ståhle, MD, PhD Ville Kytö, MSc Max Kiugel, MSc Heidi Liljenbäck, MSc Olli Metsälä, MSc Meeri Käkelä, PhD Xiang-Guo Li, MSc Vesa Oikonen, MD, PhD Pekka Saukko, MD, PhD Pirjo Nuutila, MD, PhD Juhani Knuuti, PhD Anne Roivainen, MD, PhD Antti Saraste
Wichtige Hinweise

Electronic supplementary material

The online version of this article (https://​doi.​org/​10.​1007/​s12350-018-01547-1) contains supplementary material, which is available to authorized users.
The authors of this article have provided a PowerPoint file, available for download at SpringerLink, which summarises the contents of the paper and is free for re-use at meetings and presentations. Search for the article DOI on


The study was conducted within the Finnish Centre of Excellence in Cardiovascular and Metabolic Diseases supported by the Academy of Finland, University of Turku, Turku University Hospital and Åbo Akademi University, and further financially supported by the Finnish Foundation for Cardiovascular Research, the Sigrid Jusélius Foundation, the Instrumentarium Science Foundation, the Finnish Cultural Foundation, State Research Funding of Turku University Hospital, Jalmari and Rauha Ahokas Foundation, and Ida Montin Foundation.



Activation of glucagon-like peptide-1 receptor (GLP-1R) signaling protects against cardiac dysfunction and remodeling after myocardial infarction (MI). The aim of the study was to evaluate 68Ga-NODAGA-exendin-4 positron emission tomography (PET) for assessment of GLP-1R expression after MI in rats.

Methods and Results

Rats were studied at 3 days, 1 and 12 weeks after permanent coronary ligation or a sham-operation. Rats were injected with 68Ga-NODAGA-exendin-4 and scanned with PET and contrast-enhanced computed tomography (CT) followed by digital autoradiography and histology of left ventricle tissue sections. 68Ga-NODAGA-exendin-4 PET/CT showed focally increased tracer uptake in the infarcted regions peaking at 3 days and continuing at 1 week after MI. Pre-treatment with an unlabeled exendin-4 peptide significantly reduced 68Ga-NODAGA-exendin-4 uptake. By autoradiography, 68Ga-NODAGA-exendin-4 uptake was 8.6-fold higher in the infarcted region and slightly increased also in the remote, non-infarcted myocardium at 1 week and 12 weeks post-MI compared with sham. Uptake of 68Ga-NODAGA-exendin-4 correlated with the amount of CD68-positive macrophages in the infarcted area and alpha-smooth muscle actin staining in the remote myocardium.


68Ga-NODAGA-exendin-4 PET detects up-regulation of cardiac GLP-1R expression during healing of MI in rats and may provide information on the activated repair mechanisms after ischemic myocardial injury.

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