Chu You-Hsiang, Tai Ying-Hsuan, Yeh Chun-Chang, Tsou Mei-Yung, Lee Herng-Sheng, Ho Shung-Tai, Li Min-Hui, Lin Tso-Chou, Lu Chih-Cherng
Department of Anesthesiology, Taipei Veterans General Hospital; Graduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan.
Department of Anesthesiology, Taipei Veterans General Hospital; School of Medicine, National Yang-Ming University, Taipei; Department of Anesthesiology, Shuang Ho Hospital, Taipei Medical University, New Taipei City; Department of Anesthesiology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Chin J Physiol. 2020 May-Jun;63(3):128-136. doi: 10.4103/CJP.CJP_32_20.
Glucose ingestion attenuates the water ingestion-induced increase in the total peripheral vascular resistance and orthostatic tolerance. We investigated the gastrointestinal physiology of glucose by examining the effect of glucose ingestion on the functional expression of focal adhesion kinase (FAK) in red blood cell (RBC) membrane. This study was performed in 24 young, healthy subjects. Blood samples were collected at 5 min before and 25 min and 50 min after an ingestion of 10% glucose water 500 mL, water 500 mL, or normal saline 500 mL. We determined glucose and osmolality in plasma, and phosphorylation of aquaporin 1 (AQP1), glucose transporter 1 (Glut1), and FAK in RBC membrane. Our results showed that glucose ingestion reduced the rise of peripheral vascular resistance after water ingestion and upregulated the serine phosphorylation of Glut1. It also lowered both the serine phosphorylation of FAK and tyrosine phosphorylation of AQP1, compared with the ingestion of either water or saline. In an ex vivo experiment, glucose activated the Glut1 receptor and subsequently reduced the expression of FAK compared with 0.8% saline alone. We concluded that glucose activates Glut1 and subsequently lowers the functional expression of FAK, a cytoskeleton protein of RBCs. The functional change in the RBC membrane proteins in connection with the attenuation of osmopressor response may elucidate the pathophysiology of glucose in postprandial hypotension.
摄入葡萄糖可减弱饮水诱导的总外周血管阻力增加和体位性耐力。我们通过研究摄入葡萄糖对红细胞（RBC）膜中粘着斑激酶（FAK）功能表达的影响，来探究葡萄糖的胃肠生理学。本研究在24名年轻健康受试者中进行。在摄入500 mL 10%葡萄糖水、500 mL水或500 mL生理盐水之前5分钟、之后25分钟和50分钟采集血样。我们测定了血浆中的葡萄糖和渗透压，以及RBC膜中水通道蛋白1（AQP1）、葡萄糖转运蛋白1（Glut1）和FAK的磷酸化水平。我们的结果表明，摄入葡萄糖可降低饮水后外周血管阻力的升高，并上调Glut1的丝氨酸磷酸化水平。与摄入水或生理盐水相比，它还降低了FAK的丝氨酸磷酸化水平和AQP1的酪氨酸磷酸化水平。在一项体外实验中，与单独使用0.8%生理盐水相比，葡萄糖激活了Glut1受体，随后降低了FAK的表达。我们得出结论，葡萄糖激活Glut1，随后降低RBCs细胞骨架蛋白FAK的功能表达。与渗透压反应减弱相关的RBC膜蛋白功能变化可能阐明了葡萄糖在餐后低血压中的病理生理学机制。
