Leptin receptor Gln223Arg variant is associated with a cluster of metabolic abnormalities in response to long-term overfeeding.
Leptin receptor Gln223Arg variant is associated with a cluster of metabolic abnormalities in response to long-term overfeeding.
复制标题
瘦素受体 Gln223Arg 变异与长期过度喂养引起的一系列代谢异常有关。
DOI：
10.1046/j.1365-2796.2000.00751.x
复制
发表时间：
2000
影响因子：
11.1
通讯作者：
Bouchard,C
中科院分区：
文献类型：
--
作者：
Ukkola,O;Tremblay,A;Després,JP;Chagnon,YC;Campfield,LA;Bouchard,C
Ukkola O，Tremblay A，DespréS J-P，Chagnon YC，Campfield LA，Bouchard C(美国路易斯安那州巴吞鲁日的彭宁顿生物医学研究中心；芬兰奥卢大学；加拿大魁北克省拉瓦尔大学；美国科罗拉多州丹佛市科罗拉多大学健康科学中心)。瘦素受体Gln223Arg变异与一系列代谢异常有关，以应对长期过量饮食。研究目的：研究瘦素受体基因Gln223Arg多态在超量喂养后代谢和身体成分变化中的作用。研究对象：12对男性同卵双胞胎在100MJ 天数中摄入4.2MJ -1天，6 MJ -1天能量盈余。结果超量喂养导致GlnGln(n= 10)受试者的葡萄糖(P= 0.001百分比变化)和胰岛素(P= 0.038)曲线下面积显著高于GlnArg/ArgArg(n=ArgArg)受试者(n=OGTTS)。此外，与Gln-Arg/Arg联合基因型相比，Gln-Gln基因型与血浆瘦素(P= 0.037)和总甘油三酯(P= 0.003)水平的升高以及高密度脂蛋白胆固醇(P= 0.010)的下降显著相关。结论：携带LEPR基因多态性的GlnGln受试者长期处于正能量平衡状态时，更易发生代谢异常。这些发现提供了关于个体差异对长期食物摄入量的反应的遗传基础的新信息。
Ukkola O, Tremblay A, Després J‐P, Chagnon YC, Campfield LA, Bouchard C (Pennington Biomedical Research Center, Baton Rouge, Louisiana, USA; University of Oulu, Oulu, Finland; Laval University, Ste‐Foy, Québec, Canada; and University of Colorado Health Sciences Center, Denver, Colorado, USA). Leptin receptor Gln223Arg variant is associated with a cluster of metabolic abnormalities in response to long‐term overfeeding.J Intern Med2000;248:435–439.Objectives.The role of the leptin receptor (LEPR) gene Gln223Arg polymorphism on the metabolic and body composition changes in response to overfeeding was studied.Subjects.Twelve pairs of male monozygotic twins ate a 4.2 MJ day–1energy surplus, 6 days week–1, during a period of 100 days.Results.Overfeeding induced a significantly greater increase in glucose (P= 0.001 for percentage change) and insulin (P= 0.038) areas under the curve during oral glucose tolerance tests (OGTTs) in the GlnGln (n= 10) than in the GlnArg/ArgArg (n= 14) subjects. In addition, the GlnGln genotype was associated with a greater increase in plasma levels of leptin (P= 0.037) and total triglycerides (P= 0.003), as well as a greater decrease in high‐density lipoprotein cholesterol (P= 0.010), than for the combined GlnArg/ArgArg genotypes. Body composition changes were not different between the genotypes.Conclusions.We conclude that the GlnGln subjects of the LEPR gene polymorphism are more susceptible to metabolic abnormalities when they are exposed to long‐term positive energy balance. These findings provide new information on the genetic basis of individual differences in response to chronically elevated food intake.