Department of Surgical Sciences, Uppsala University, Uppsala, Sweden.
Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Diabetes. 2017 May;66(5):1286-1292. doi: 10.2337/db16-1449. Epub 2017 Feb 28.
[C]5-hydroxy-tryptophan ([C]5-HTP) positron emission tomography of the pancreas has been shown to be a surrogate imaging biomarker of pancreatic islet mass. The change in islet mass in different stages of type 2 diabetes (T2D) as measured by noninvasive imaging is currently unknown. Here, we describe a cross-sectional study where subjects at different stages of T2D development with expected stratification of pancreatic islet mass were examined in relation to individuals without diabetes. The primary outcome was the [C]5-HTP uptake and retention in pancreas, as a surrogate marker for the endogenous islet mass. We found that metabolic testing indicated a progressive loss of β-cell function, but this was not mirrored by a decrease in [C]5-HTP tracer accumulation in the pancreas. This provides evidence of retained islet mass despite decreased β-cell function. The results herein indicate that β-cell dedifferentiation, and not necessarily endocrine cell loss, constitutes a major cause of β-cell failure in T2D.
[C]5-羟色氨酸 ([C]5-HTP) 胰腺正电子发射断层扫描已被证明是胰岛质量的替代成像生物标志物。目前尚不清楚非侵入性成像测量的 2 型糖尿病 (T2D) 不同阶段的胰岛质量变化。在这里，我们描述了一项横断面研究，其中检查了处于 T2D 发展不同阶段且预期胰岛质量分层的受试者与无糖尿病个体的关系。主要结果是 [C]5-HTP 在胰腺中的摄取和保留，作为内源性胰岛质量的替代标志物。我们发现代谢测试表明 β 细胞功能逐渐丧失，但这并没有反映在胰腺中 [C]5-HTP 示踪剂积累的减少。这提供了证据表明尽管 β 细胞功能下降，但胰岛质量仍然保留。本文的结果表明，β 细胞去分化，而不一定是内分泌细胞丢失，是 T2D 中 β 细胞衰竭的主要原因。
