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Contrast Media & Molecular Imaging
Volume 2018, Article ID 8751267, 10 pages
https://doi.org/10.1155/2018/8751267
Research Article

Early Imaging Biomarker of Myocardial Glucose Adaptations in High-Fat-Diet-Induced Insulin Resistance Model by Using 18F-FDG PET and [U-13C]glucose Nuclear Magnetic Resonance Tracer

1Center for Advanced Molecular Imaging and Translation (CAMIT), Linkou Chang Gung Memorial Hospital, Taoyuan, Taiwan
2Department of Medical Imaging and Intervention, Imaging Core Lab, Institute for Radiological Research, Linkou Chang Gung Memorial Hospital and Chang Gung University, Taoyuan, Taiwan
3Clinical Metabolomics Core Laboratory, Linkou Chang Gung Memorial Hospital, Taoyuan, Taiwan
4Metabolomics Core Laboratory, Healthy Aging Research Center, Chang Gung University, Taoyuan, Taiwan
5Department and Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan
6Healthy Aging Research Center, Chang Gung University, Taoyuan, Taiwan
7Kidney Research Center, Linkou Chang Gung Memorial Hospital, Taoyuan, Taiwan
8Heart Failure Center, Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial Hospital, Keelung, Taiwan

Correspondence should be addressed to Gigin Lin; wt.gro.hmgc@nilnigig

Received 9 March 2018; Revised 31 May 2018; Accepted 4 June 2018; Published 12 July 2018

Academic Editor: Anxo Fernández-Ferreiro

Copyright © 2018 Yi-Hsiu Chung et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background. High-fat diet (HFD) induces systemic insulin resistance leading to myocardial dysfunction. We aim to characterize the early adaptations of myocardial glucose utility to HFD-induced insulin resistance. Methods. Male Sprague–Dawley rats were assigned into two groups, fed a regular chow diet or HFD ad libitum for 10 weeks. We used in vivo imaging of cardiac magnetic resonance (CMR), 18F-FDG PET, and ex vivo nuclear magnetic resonance (NMR) metabolomic analysis for the carbon-13-labeled glucose ([U-13C]Glc) perfused myocardium. Results. As compared with controls, HFD rats had a higher ejection fraction and a smaller left ventricular end-systolic volume (), with SUVmax of myocardium on 18F-FDG PET significantly increased in 4 weeks (). The [U-13C]Glc probed the increased glucose uptake being metabolized into pyruvate and acetyl-CoA, undergoing oxidative phosphorylation via the tricarboxylic acid (TCA) cycle, and then synthesized into glutamic acid and glutamine, associated with overexpressed LC3B (). Conclusions. HFD-induced IR associated with increased glucose utility undergoing oxidative phosphorylation via the TCA cycle in the myocardium is supported by overexpression of glucose transporter, acetyl-CoA synthase. Noninvasive imaging biomarker has potentials in detecting the metabolic perturbations prior to the decline of the left ventricular function.