Corona-Meraz Fernanda-Isadora, Navarro-Hernández Rosa-Elena, Ruíz-Quezada Sandra-Luz, Madrigal-Ruíz Perla-Monserrat, Castro-Albarrán Jorge, Chavarría-Ávila Efraín, Guzmán-Ornelas Milton-Omar, Gómez-Bañuelos Eduardo, Petri Marcelo-Herón, Ramírez-Cedano Joel-Isidro, Aguilar-Aldrete María-Elena, Ríos-Ibarra Clara, Vázquez-Del Mercado Mónica
Departamento de Biología Molecular y Genómica, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Sierra Mojada No. 950 Colonia Independencia, CP 44340, Guadalajara, JAL, Mexico; Instituto de Investigación en Reumatología y del Sistema Musculo Esquelético, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Sierra Mojada No. 950 Colonia Independencia, CP 44340, Guadalajara, JAL, Mexico; UDG-CA-701, Grupo de Investigación Inmunometabolismo en Enfermedades Emergentes (GIIEE), Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Sierra Mojada No. 950 Colonia Independencia, CP 44340, Guadalajara, JAL, Mexico.
Departamento de Biología Molecular y Genómica, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Sierra Mojada No. 950 Colonia Independencia, CP 44340, Guadalajara, JAL, Mexico; Instituto de Investigación en Reumatología y del Sistema Musculo Esquelético, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Sierra Mojada No. 950 Colonia Independencia, CP 44340, Guadalajara, JAL, Mexico; UDG-CA-701, Grupo de Investigación Inmunometabolismo en Enfermedades Emergentes (GIIEE), Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Sierra Mojada No. 950 Colonia Independencia, CP 44340, Guadalajara, JAL, Mexico; Departamento de Farmacobiología, Centro Universitario de Ciencias Exactas e Ingenierías, Universidad de Guadalajara, Boulevard Marcelino García Barragán No. 1421, CP 44430, Guadalajara, JAL, Mexico.
Mediators Inflamm. 2016;2016:3085390. doi: 10.1155/2016/3085390. Epub 2016 Apr 28.
In obesity there is a subclinical chronic low-grade inflammatory response where insulin resistance (IR) may develop. Chemerin is secreted in white adipose tissue and promotes low-grade inflammatory process, where it expressed CMKLR1 receptor. The role of chemerin and CMKLR1 in inflammatory process secondary to obesity is not defined yet.
Cross-sectional study with 134 individuals classified as with and without obesity by body mass index (BMI) and IR. Body fat storage measurements and metabolic and inflammatory markers were measured by routine methods. Soluble chemerin and basal levels of insulin by ELISA and relative expression of CMKLR1 were evaluated with qPCR and 2(-ΔΔCT) method.
Differences (P < 0.05) were observed between obesity and lean individuals in body fat storage measurements and metabolic-inflammatory markers. Both CMKLR1 expression and chemerin levels were increased in obesity without IR. Soluble chemerin levels correlate with adiposity and metabolic markers (r = 8.8% to 38.5%), P < 0.05.
The increment of CMKLR1 expression was associated with insulin production. Increased serum levels of chemerin in obesity were observed, favoring a dysmetabolic response. The results observed in this study suggest that both chemerin and CMKLR1 have opposite expression in the context of low-grade inflammatory response manifested in the development of IR.
在肥胖症中存在一种亚临床慢性低度炎症反应，胰岛素抵抗（IR）可能由此产生。趋化素在白色脂肪组织中分泌，并促进低度炎症过程，在该过程中它表达CMKLR1受体。趋化素和CMKLR1在肥胖继发的炎症过程中的作用尚未明确。
对134名个体进行横断面研究，根据体重指数（BMI）和胰岛素抵抗将其分为肥胖组和非肥胖组。通过常规方法测量体脂储存量以及代谢和炎症标志物。采用酶联免疫吸附测定法（ELISA）检测可溶性趋化素和胰岛素基础水平，并用实时定量聚合酶链反应（qPCR）和2(-ΔΔCT)法评估CMKLR1的相对表达。
肥胖个体与瘦个体在体脂储存量测量以及代谢炎症标志物方面存在差异（P < 0.05）。在无胰岛素抵抗的肥胖个体中，CMKLR1表达和趋化素水平均升高。可溶性趋化素水平与肥胖及代谢标志物相关（r = 8.8%至38.5%），P < 0.05。
CMKLR1表达的增加与胰岛素分泌有关。观察到肥胖患者血清趋化素水平升高，这有利于代谢紊乱反应。本研究观察到的结果表明，在胰岛素抵抗发生过程中出现的低度炎症反应背景下，趋化素和CMKLR1具有相反的表达。
