Brunasso Alessandro, Dalla Man Chiara, Poli Simone, Prompers Jeanine J, Herzig David, Kreis Roland, Bally Lia, Schiavon Michele
Department of Information Engineering, University of Padova, Padova, Italy.
Magnetic Resonance Methodology, Institute of Diagnostic and Interventional Neuroradiology, University of Bern, Bern, Switzerland.
Am J Physiol Endocrinol Metab. 2025 Jul 1;329(1):E102-E116. doi: 10.1152/ajpendo.00511.2024. Epub 2025 May 26.
Despite extensive research on liver metabolism, mathematical models describing hepatic glucose kinetics are currently limited due to the lack of organ-level data. Here, we propose a model of postprandial hepatic glucose kinetics exploiting liver deuterium metabolic imaging (DMI) data combined with plasma isotope dilution analysis in humans. We used data from 10 individuals who had previously undergone Roux-en-Y gastric bypass surgery (RYGB) and 10 healthy controls (HCs). The experimental setting included a labeled oral glucose tolerance test comprising 60 g of [6,6'-H]-glucose in combination with liver DMI at 7 T. The hepatic glucose tracer signal was frequently quantified over 150 min, whereas peripheral plasma insulin and glucose tracer concentrations were measured in venous blood. The model was able to describe both liver and peripheral glucose tracer data well and provided estimates of postprandial glucose appearance and disposal in both the liver and the systemic circulation. The model predicted that almost all the ingested glucose had appeared in the liver in RYGB, but not in HC (89.0% vs. 64.0%, = 0.008) after 150 min, whereas total hepatic disposal (RYGB = 26.4% vs. HC = 29.7%) and first-pass extraction (RYGB = 10.7% vs. HC = 11.4%) were similar between populations. The fraction of glucose eliminated in the periphery was greater in RYGB (49.9% vs. 25.3%, = 0.003). Finally, no differences were observed in hepatic blood flow and GLUT2 transport rates. Although further studies are needed to validate and extend the model to include endogenous glucose production and disposal, it can be used to quantify parameters, and possibly reveal defects, of hepatic glucose handling. The proposed hepatic model allows, for the first time, to describe postprandial liver glucose tracer kinetics in humans, allowing to estimate exogenous glucose appearance and disposal in the liver, as well as glucose transport and hepatic blood flow rate. The model may become a useful tool in clinical research by supporting the identification of metabolic defects at the hepatic level without requiring invasive procedures.
尽管对肝脏代谢进行了广泛研究,但由于缺乏器官水平的数据,目前描述肝脏葡萄糖动力学的数学模型仍很有限。在此,我们提出了一种餐后肝脏葡萄糖动力学模型,该模型利用肝脏氘代谢成像(DMI)数据并结合人体血浆同位素稀释分析。我们使用了来自10名先前接受过Roux-en-Y胃旁路手术(RYGB)的个体和10名健康对照(HC)的数据。实验设置包括一项标记口服葡萄糖耐量试验,其中包含60克[6,6'-H]-葡萄糖,并在7T下进行肝脏DMI。在150分钟内频繁定量肝脏葡萄糖示踪剂信号,而在静脉血中测量外周血浆胰岛素和葡萄糖示踪剂浓度。该模型能够很好地描述肝脏和外周葡萄糖示踪剂数据,并提供了餐后肝脏和全身循环中葡萄糖出现和处置的估计值。该模型预测,150分钟后,几乎所有摄入的葡萄糖在RYGB个体中都出现在肝脏中,而在HC个体中则不然(89.0%对64.0%,P = 0.008),而总体肝脏处置(RYGB = 26.4%对HC = 29.7%)和首过提取(RYGB = 10.7%对HC = 11.4%)在不同人群之间相似。RYGB个体中外周消除的葡萄糖比例更高(49.9%对25.3%,P = 0.003)。最后,在肝血流量和GLUT2转运速率方面未观察到差异。尽管需要进一步研究来验证并扩展该模型以纳入内源性葡萄糖生成和处置,但它可用于量化肝脏葡萄糖处理的参数,并可能揭示其中的缺陷。所提出的肝脏模型首次能够描述人体餐后肝脏葡萄糖示踪剂动力学,从而能够估计外源性葡萄糖在肝脏中的出现和处置,以及葡萄糖转运和肝血流量。该模型可能通过支持在不进行侵入性操作的情况下识别肝脏水平的代谢缺陷,而成为临床研究中的一个有用工具。