Xinyi Zhang, Huiying Liu, Chenyu Li, Ying Wei, Xuan Kan, Xiaoxiao Liu, Xinyi Han, Zhenghao Zhao, Tianfeng An, Zhong-Ze Fang, Shifeng Ma, Rongxiu Zheng, Jing Li
{"title":"青少年腹部肥胖:血浆中溶血磷脂酰胆碱浓度与胰岛素抵抗的关系。","authors":"Xinyi Zhang, Huiying Liu, Chenyu Li, Ying Wei, Xuan Kan, Xiaoxiao Liu, Xinyi Han, Zhenghao Zhao, Tianfeng An, Zhong-Ze Fang, Shifeng Ma, Rongxiu Zheng, Jing Li","doi":"10.1038/s41390-024-03652-z","DOIUrl":null,"url":null,"abstract":"<p><strong>Backgroud: </strong>This study aimed to explore the associations of lysophosphatidylcholines (LPCs) with insulin resistance (IR) and abdominal obesity among children and adolescents.</p><p><strong>Methods: </strong>A cross-sectional study was conducted on 612 young individuals, aged 7 to 18 years in Tianjin City, China. LC-MS metabolomic analysis was used to measure LPCs levels. The Homeostasis Model Assessment was used to estimate IR. Waist circumference measurements were used to assess abdominal obesity. Logistic regression models were employed to explore the relationships between LPCs and IR and abdominal obesity. Mediation analyses were performed to analyze whether LPCs affected IR through abdominal obesity.</p><p><strong>Results: </strong>Compared to their counterparts, five specific LPCs were significantly different in youth with IR. The levels of LPC 24:0 and 26:0 were significantly associated with IR after adjustment. Both decreased levels of LPC 24:0 and 26:0 associated with the increased risks of IR (OR: 0.64, 95%CI: 0.38-0.95; OR: 0.66, 95%CI: 0.40-1.00), and the ORs for abdominal obesity were 0.68 (95%CI: 0.38-1.00) and 0.51 (95%CI: 0.28-0.90), respectively. Mediation analysis indicated that abdominal obesity mediated the association between LPC 26:0 and IR, with a total effect (c) of -0.109 (P < 0.05), a direct effect (c') of -0.055 (P > 0.05), and an indirect effect through obesity (a × b) path with \"a\" of -0.125 (P < 0.05) and \"b\" of 0.426 (P < 0.05).</p><p><strong>Conclusion: </strong>Overall findings suggest that decreased levels of LPC 24:0 and 26:0 were associated with increased risks of IR and abdominal obesity. Importantly, addressing abdominal obesity may mediate the impact of IR driven by LPC 26:0.</p>","PeriodicalId":19829,"journal":{"name":"Pediatric Research","volume":null,"pages":null},"PeriodicalIF":3.1000,"publicationDate":"2024-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Abdominal obesity in youth: the associations of plasma Lysophophatidylcholine concentrations with insulin resistance.\",\"authors\":\"Xinyi Zhang, Huiying Liu, Chenyu Li, Ying Wei, Xuan Kan, Xiaoxiao Liu, Xinyi Han, Zhenghao Zhao, Tianfeng An, Zhong-Ze Fang, Shifeng Ma, Rongxiu Zheng, Jing Li\",\"doi\":\"10.1038/s41390-024-03652-z\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Backgroud: </strong>This study aimed to explore the associations of lysophosphatidylcholines (LPCs) with insulin resistance (IR) and abdominal obesity among children and adolescents.</p><p><strong>Methods: </strong>A cross-sectional study was conducted on 612 young individuals, aged 7 to 18 years in Tianjin City, China. LC-MS metabolomic analysis was used to measure LPCs levels. The Homeostasis Model Assessment was used to estimate IR. Waist circumference measurements were used to assess abdominal obesity. Logistic regression models were employed to explore the relationships between LPCs and IR and abdominal obesity. Mediation analyses were performed to analyze whether LPCs affected IR through abdominal obesity.</p><p><strong>Results: </strong>Compared to their counterparts, five specific LPCs were significantly different in youth with IR. The levels of LPC 24:0 and 26:0 were significantly associated with IR after adjustment. Both decreased levels of LPC 24:0 and 26:0 associated with the increased risks of IR (OR: 0.64, 95%CI: 0.38-0.95; OR: 0.66, 95%CI: 0.40-1.00), and the ORs for abdominal obesity were 0.68 (95%CI: 0.38-1.00) and 0.51 (95%CI: 0.28-0.90), respectively. Mediation analysis indicated that abdominal obesity mediated the association between LPC 26:0 and IR, with a total effect (c) of -0.109 (P < 0.05), a direct effect (c') of -0.055 (P > 0.05), and an indirect effect through obesity (a × b) path with \\\"a\\\" of -0.125 (P < 0.05) and \\\"b\\\" of 0.426 (P < 0.05).</p><p><strong>Conclusion: </strong>Overall findings suggest that decreased levels of LPC 24:0 and 26:0 were associated with increased risks of IR and abdominal obesity. Importantly, addressing abdominal obesity may mediate the impact of IR driven by LPC 26:0.</p>\",\"PeriodicalId\":19829,\"journal\":{\"name\":\"Pediatric Research\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":3.1000,\"publicationDate\":\"2024-10-19\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Pediatric Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1038/s41390-024-03652-z\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"PEDIATRICS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pediatric Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41390-024-03652-z","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"PEDIATRICS","Score":null,"Total":0}
引用次数: 0
摘要
背景:本研究旨在探讨溶血磷脂酰胆碱(LPCs)与儿童和青少年胰岛素抵抗(IR)和腹部肥胖的关系:方法:对中国天津市 612 名 7 至 18 岁的青少年进行了横断面研究。采用 LC-MS 代谢组学分析法测量 LPCs 水平。采用平衡模型评估法估算IR。腰围测量用于评估腹部肥胖。采用逻辑回归模型探讨 LPCs 与 IR 和腹部肥胖之间的关系。进行中介分析以分析 LPCs 是否通过腹部肥胖影响 IR:与同龄人相比,患有IR的青少年体内有五种特定的LPCs存在显著差异。经调整后,LPC 24:0和26:0的水平与IR显著相关。LPC 24:0和26:0水平的降低均与IR风险的增加有关(OR:0.64,95%CI:0.38-0.95;OR:0.66,95%CI:0.40-1.00),腹部肥胖的OR分别为0.68(95%CI:0.38-1.00)和0.51(95%CI:0.28-0.90)。中介分析表明,腹型肥胖在 LPC 26:0 与 IR 的关系中起中介作用,总效应(c)为-0.109(P 0.05),通过肥胖(a × b)路径产生的间接效应 "a "为-0.125(P 结论:LPC 26:0 与 IR 的关系中,腹型肥胖起中介作用:总体研究结果表明,LPC 24:0 和 26:0 水平的降低与 IR 和腹部肥胖风险的增加有关。重要的是,解决腹部肥胖问题可能会介导 LPC 26:0 对 IR 的影响。
Abdominal obesity in youth: the associations of plasma Lysophophatidylcholine concentrations with insulin resistance.
Backgroud: This study aimed to explore the associations of lysophosphatidylcholines (LPCs) with insulin resistance (IR) and abdominal obesity among children and adolescents.
Methods: A cross-sectional study was conducted on 612 young individuals, aged 7 to 18 years in Tianjin City, China. LC-MS metabolomic analysis was used to measure LPCs levels. The Homeostasis Model Assessment was used to estimate IR. Waist circumference measurements were used to assess abdominal obesity. Logistic regression models were employed to explore the relationships between LPCs and IR and abdominal obesity. Mediation analyses were performed to analyze whether LPCs affected IR through abdominal obesity.
Results: Compared to their counterparts, five specific LPCs were significantly different in youth with IR. The levels of LPC 24:0 and 26:0 were significantly associated with IR after adjustment. Both decreased levels of LPC 24:0 and 26:0 associated with the increased risks of IR (OR: 0.64, 95%CI: 0.38-0.95; OR: 0.66, 95%CI: 0.40-1.00), and the ORs for abdominal obesity were 0.68 (95%CI: 0.38-1.00) and 0.51 (95%CI: 0.28-0.90), respectively. Mediation analysis indicated that abdominal obesity mediated the association between LPC 26:0 and IR, with a total effect (c) of -0.109 (P < 0.05), a direct effect (c') of -0.055 (P > 0.05), and an indirect effect through obesity (a × b) path with "a" of -0.125 (P < 0.05) and "b" of 0.426 (P < 0.05).
Conclusion: Overall findings suggest that decreased levels of LPC 24:0 and 26:0 were associated with increased risks of IR and abdominal obesity. Importantly, addressing abdominal obesity may mediate the impact of IR driven by LPC 26:0.
期刊介绍:
Pediatric Research publishes original papers, invited reviews, and commentaries on the etiologies of children''s diseases and
disorders of development, extending from molecular biology to epidemiology. Use of model organisms and in vitro techniques
relevant to developmental biology and medicine are acceptable, as are translational human studies