Circulating Concentrations of Insulin Resistance-Associated Hepatokines, Selenoprotein P and Leukocyte Cell-Derived Chemotaxin 2, during an Oral Glucose Tolerance Test in Humans
Circulating Concentrations of Insulin Resistance-Associated Hepatokines, Selenoprotein P and Leukocyte Cell-Derived Chemotaxin 2, during an Oral Glucose Tolerance Test in Humans
复制标题
DOI：
10.1248/bpb.b18-00549
复制
发表时间：
2019-03-01
影响因子：
2
通讯作者：
Takamura, Toshinari
中科院分区：
文献类型：
--
作者：
Mohri, Kensuke;Misu, Hirofumi;Takamura, Toshinari
肝细胞因子是肝源性分泌因子的统称，其以前未被认识的功能最近已被阐明。我们已经重新发现硒蛋白P（SeP）和白细胞衍生的趋化因子2（LECT 2）作为肝细胞因子参与胰岛素抵抗和高血糖的发展。本研究的目的是确定口服葡萄糖负荷是否以及如何改变人类的两种肝细胞因子。我们在75g口服葡萄糖耐量试验（OGTT）（n = 20）中检测了不同糖耐量程度的人的血清SeP和血浆LECT 2浓度。在OGTT中，血清SeP和血浆LECT 2的浓度在120分钟时与基线值相比降低，与葡萄糖耐受不良的严重程度无关。OGTT期间血清SeP的降低与胰岛素抵抗或胰岛素分泌相关的临床参数无关。在多元逐步回归分析中，选择血浆皮质醇作为解释LECT 2血浆浓度变化的变量。目前的数据揭示了口服葡萄糖对人体循环SeP和LECT 2的急性抑制作用，与葡萄糖耐受不良的严重程度无关。本研究表明，在OGTT期间，循环SeP受胰岛素和葡萄糖以外的未知临床因素的调节。
A hepatokine is a collective term for liver-derived secretory factors whose previously-unrecognized functions have been recently elucidated. We have rediscovered selenoprotein P (SeP) and leukocyte cell derived chemotaxin 2 (LECT2) as hepatokines that are involved in the development of insulin resistance and hyperglycemia. The aim of this study was to determine whether and, if so, how oral glucose loading alters the two hepatokines in humans. We measured concentrations of serum SeP and plasma LECT2 during 75g oral glucose tolerance test (OGTT) (n = 20) in people with various degrees of glucose tolerance. In OGTT, concentrations of both serum SeP and plasma LECT2 decreased at 120 min compared with the baseline values, irrespective of the severity of glucose intolerance. Decrement of serum SeP during OGTT showed no correlations to the clinical parameters associated with insulin resistance or insulin secretion. In multiple stepwise regression analyses, plasma cortisol was selected as the variable to explain the changes in plasma concentrations of LECT2. The current data reveal the acute inhibitory actions of oral intake of glucose on circulating SeP and LECT2 in humans, irrespective of the severity of glucose intolerance. This study suggests that circulating SeP is regulated by the unknown clinical factors other than insulin and glucose during OGTT.