Mittendorfer Bettina, Patterson Bruce W, Smith Gordon I, Yoshino Mihoko, Klein Samuel
Center for Human Nutrition, Washington University School of Medicine, St. Louis, MO.
Departments of Medicine and Nutrition & Exercise Physiology, University of Missouri, School of Medicine, Columbia, MO.
Diabetes Care. 2025 Jan 1;48(1):84-92. doi: 10.2337/dc24-1280.
To evaluate total, insulin-mediated, and non-insulin-mediated glucose disposal (TGD, IMGD, and NIMGD) after ingesting glucose in people with obesity and different glycemic status.
We developed and validated a new glucose tracer model in conjunction with an oral glucose tolerance test to determine IMGD, NIMGD, and TGD (sum of IMGD and NIMGD) after glucose ingestion in four groups of people: 1) lean with normal glucose tolerance (NGT), 2) obese with insulin resistance and NGT due to hyperinsulinemia (Ob-NGT group), 3) obese with insulin resistance and impaired glucose tolerance (IGT) due to inadequate hyperinsulinemia (Ob-IGT group), and 4) obese with insulin resistance and type 2 diabetes due to marked insulin insufficiency (Ob-T2D group). In addition, we evaluated the effect of intensive lifestyle therapy (ILT) that caused ∼15% weight loss on IMGD and NIMGD in people with obesity and type 2 diabetes (T2D).
IMGD progressively decreased and NIMGD progressively increased from lean to Ob-NGT to Ob-IGT to Ob-T2D. IMGD accounted for about 70%, 65%, 50%, and 20% of TGD, and NIMGD accounted for ∼40%, 35%, 50%, and 80% of TGD in lean, Ob-NGT, Ob-IGT and Ob-T2D, respectively. Although NIMGD was approximately twofold and approximately threefold higher in Ob-IGT and Ob-T2D compared with Ob-NGT, NIMGD only partially compensated for markedly impaired IMGD in the Ob-IGT and Ob-T2D. ILT in people with obesity and T2D increased IMGD and decreased NIMGD.
NIMGD is a major mechanism of postprandial TGD in people with insulin resistance and inadequate insulin secretion.
评估肥胖且血糖状态不同的人群摄入葡萄糖后的总体、胰岛素介导及非胰岛素介导的葡萄糖处置（TGD、IMGD和NIMGD）情况。
我们开发并验证了一种新的葡萄糖示踪模型，结合口服葡萄糖耐量试验，以确定四组人群摄入葡萄糖后的IMGD、NIMGD和TGD（IMGD与NIMGD之和）：1）糖耐量正常的瘦人（NGT），2）因高胰岛素血症而有胰岛素抵抗且糖耐量正常的肥胖者（Ob-NGT组），3）因高胰岛素血症不足而有胰岛素抵抗且糖耐量受损（IGT）的肥胖者（Ob-IGT组），4）因明显胰岛素不足而有胰岛素抵抗且患有2型糖尿病的肥胖者（Ob-T2D组）。此外，我们评估了导致体重减轻约15%的强化生活方式治疗（ILT）对肥胖且患有2型糖尿病（T2D）人群的IMGD和NIMGD的影响。
从瘦人到Ob-NGT组、Ob-IGT组再到Ob-T2D组，IMGD逐渐降低，NIMGD逐渐升高。在瘦人、Ob-NGT组、Ob-IGT组和Ob-T2D组中，IMGD分别约占TGD的70%、65%、50%和20%，NIMGD分别约占TGD的40%、35%、50%和80%。尽管与Ob-NGT组相比，Ob-IGT组和Ob-T2D组的NIMGD分别高出约两倍和约三倍，但在Ob-IGT组和Ob-T2D组中，NIMGD仅部分补偿了明显受损的IMGD。肥胖且患有T2D人群的ILT增加了IMGD并降低了NIMGD。
在胰岛素抵抗且胰岛素分泌不足的人群中，NIMGD是餐后TGD的主要机制。
