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首页> 外文期刊>Contrast media & molecular imaging >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
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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

机译：高脂肪饮食诱导的胰岛素抵抗模型中使用18F-FDG PET和[U-13C]葡萄糖核磁共振示踪剂对心肌葡萄糖适应的早期成像生物标记

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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.
机译：背景。高脂饮食（HFD）引起全身性胰岛素抵抗，导致心肌功能障碍。我们旨在表征心肌葡萄糖实用性对HFD诱导的胰岛素抵抗的早期适应。方法。将Sprague–Dawley雄性大鼠分为两组，常规饮食或HFD随意喂养10周。我们将心脏磁共振（CMR），18F-FDG PET和离体核磁共振（NMR）代谢组学的体内成像用于碳13标记的葡萄糖（[U-13C] Glc）灌注心肌。结果。与对照组相比，HFD大鼠具有更高的射血分数和较小的左心室收缩末期容积（），而18F-FDG PET上的心肌SUVmax则在4周内显着增加（）。 [U-13C] Glc检测到增加的葡萄糖摄取被代谢为丙酮酸和乙酰辅酶A，并通过三羧酸（TCA）循环进行氧化磷酸化，然后合成为谷氨酸和谷氨酰胺，这与LC3B过表达有关。结论。葡萄糖转运蛋白，乙酰辅酶A合酶的过度表达支持了与HFD诱导的IR相关的IR升高，该IR与通过TCA循环在心肌中进行氧化磷酸化而增加的葡萄糖利用率有关。非侵入性成像生物标志物具有检测左心室功能下降之前的代谢紊乱的潜力。

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