Vascular endothelial growth factor B improves impaired glucose tolerance through insulin-mediated inhibition of glucagon secretion
作者机构：Department of PathophysiologySchool of Basic MedicineBinzhou Medical UniversityYantai 264000Shandong ProvinceChina Department of Rheumatology and ImmunologyYantaishan HospitalYantai 264000Shandong ProvinceChina Department of SurgeryYantaishan HospitalYantai 264000Shandong ProvinceChina School of Public Health and ManagementBinzhou Medical UniversityYantai 264000Shandong ProvinceChina The First School of Clinical MedicineBinzhou Medical UniversityYantai 264000Shandong ProvinceChina
出 版 物：《World Journal of Diabetes》 (世界糖尿病杂志（英文版）（电子版）)
年 卷 期：2023年第14卷第11期
页 面：1643-1658页
核心收录：
学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学]
基 金：Supported by the National Natural Science Foundation of China,No.31771284 Basic Research Project of Yantai Science and Technology Innovation and Development Plan,No.2022JCYJ026 Natural Science Foundation of Shandong province,No.ZR202111250163 Yantai Science and Technology Plan Project,No.2022YD062
主 题：Vascular endothelial growth factor B Insulin-mediated Glucagon secretion Prediabetes Impaired glucose tolerance
摘 要：BACKGROUND Impaired glucose tolerance(IGT)is a homeostatic state between euglycemia and hyperglycemia and is considered an early high-risk state of *** IGT occurs,insulin sensitivity decreases,causing a reduction in insulin secretion and an increase in glucagon ***,vascular endothelial growth factor B(VEGFB)has been demonstrated to play a positive role in improving glucose metabolism and insulin ***,we constructed a mouse model of IGT through high-fat diet feeding and speculated that VEGFB can regulate hyperglycemia in IGT by influencing insulin-mediated glucagon secretion,thus contributing to the prevention and cure of *** To explore the potential molecular mechanism and regulatory effects of VEGFB on insulin-mediated glucagon in mice with *** We conducted in vivo experiments through systematic VEGFB knockout and pancreatic-specific VEGFB *** and glucagon secretions were detected via enzyme-linked immunosorbent assay,and the protein expression of phosphoinositide 3-kinase(PI3K)/protein kinase B(AKT)was determined using western ***,mRNA expression of forkhead box protein O1,phosphoenolpyruvate carboxykinase,and glucose-6 phosphatase was detected via quantitative polymerase chain reaction,and the correlation between the expression of proteins was analyzed via *** In mice with IGT and VEGFB knockout,glucagon secretion increased,and the protein expression of PI3K/AKT decreased ***,in mice with VEGFB overexpression,glucagon levels declined,with the activation of the PI3K/AKT signaling *** VEGFB/vascular endothelial growth factor receptor 1 can promote insulin-mediated glucagon secretion by activating the PI3K/AKT signaling pathway to regulate glucose metabolism disorders in mice with IGT.
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