Author/Authors :
Chung, Yi-Hsiu Linkou Chang Gung Memorial Hospital - Taoyuan, Taiwan , Lu, Kuan-Ying Department of Medical Imaging and Intervention - Imaging Core Lab - Institute for Radiological Research - Linkou Chang Gung Memorial Hospital and Chang Gung University - Taoyuan, Taiwan , Chiu, Shao-Chieh Linkou Chang Gung Memorial Hospital - Taoyuan, Taiwan , Lo, Chi-Jen Chang Gung University - Taoyuan, Taiwan , Hung, Li-Man Department and Graduate Institute of Biomedical Sciences - College of Medicine - Chang Gung University - Taoyuan, Taiwan , Huang, Jiung-Pang Department and Graduate Institute of Biomedical Sciences - College of Medicine - Chang Gung University - Taoyuan, Taiwan , Cheng, Mei-Ling Department and Graduate Institute of Biomedical Sciences - College of Medicine - Chang Gung University - Taoyuan, Taiwan , Wang, Chao-Hung Department of Internal Medicine - Chang Gung Memorial Hospital - Keelung, Taiwan , Tsai, Cheng-Kun Linkou Chang Gung Memorial Hospital - Taoyuan, Taiwan , Lin, Yu-Chun Department of Medical Imaging and Intervention - Imaging Core Lab - Institute for Radiological Research - Linkou Chang Gung Memorial Hospital and Chang Gung University - Taoyuan, Taiwan , Chang, Shang-Hung Department and Graduate Institute of Biomedical Sciences - College of Medicine - Chang Gung University - Taoyuan, Taiwan , Lin, Gigin Department of Medical Imaging and Intervention - Imaging Core Lab - Institute for Radiological Research - Linkou Chang Gung Memorial Hospital and Chang Gung University - Taoyuan, Taiwan
Abstract :
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 (P < 0.05), with SUVmax of myocardium on 18F-FDG PET significantly increased in 4
weeks (P < 0.005). 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 (P < 0.05). 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.
Keywords :
Glucose , 18F-FDG , PET , Magnetic , HFD
