Institute for Experimental and Clinical Pharmacology and Toxicology, Center of Brain, Behavior and Metabolism, University of Lübeck, 23562 Lübeck, Germany.
Institute for Pathobiochemistry, University Medical Center of Johannes Gutenberg University Mainz, 55099 Mainz, Germany.
Int J Mol Sci. 2021 May 8;22(9):4998. doi: 10.3390/ijms22094998.
The mechanisms underlying the transport of leptin into the brain are still largely unclear. While the leptin receptor has been implicated in the transport process, recent evidence has suggested an additional role of LRP2 (megalin). To evaluate the function of LRP2 for leptin transport across the blood-brain barrier (BBB), we developed a novel leptin-luciferase fusion protein (pLG), which stimulated leptin signaling and was transported in an in vitro BBB model based on porcine endothelial cells. The LRP inhibitor RAP did not affect leptin transport, arguing against a role of LRP2. In line with this, the selective deletion of LRP2 in brain endothelial cells and epithelial cells of the choroid plexus did not influence bodyweight, body composition, food intake, or energy expenditure of mice. These findings suggest that LRP2 at the BBB is not involved in the transport of leptin into the brain, nor in the development of obesity as has previously been described.
瘦素进入大脑的运输机制仍在很大程度上不清楚。虽然瘦素受体已被牵涉到运输过程中,但最近的证据表明 LRP2(巨球蛋白)具有额外的作用。为了评估 LRP2 对血脑屏障(BBB)中瘦素运输的功能,我们开发了一种新型的瘦素-荧光素酶融合蛋白(pLG),它刺激瘦素信号,并在基于猪内皮细胞的体外 BBB 模型中被运输。LRP 抑制剂 RAP 不影响瘦素的运输,这表明 LRP2 不参与瘦素的运输。与此一致的是,脑内皮细胞和脉络丛上皮细胞中 LRP2 的选择性缺失并没有影响小鼠的体重、身体成分、食物摄入或能量消耗。这些发现表明,BBB 中的 LRP2 不参与瘦素向大脑的运输,也不参与以前描述的肥胖的发展。