O C Martínez-Ramírez1, D A Salazar-Piña2, Ramos-García M de Lorena2, C Castro-Hernández3, L Casas-Ávila4, J A Portillo-Jacobo2, J Rubio3. 1. Facultad de Nutrición, Universidad Autónoma del Estado de Morelos, Río Iztacihuatl S/N. Col. Vista Hermosa, C.P. 62350, Mexico, Mexico. celeste.martinez@uaem.mx. 2. Facultad de Nutrición, Universidad Autónoma del Estado de Morelos, Río Iztacihuatl S/N. Col. Vista Hermosa, C.P. 62350, Mexico, Mexico. 3. Departamento de Medicina Genómica y Toxicología Ambiental, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Apartado Postal 70228, C.P. 04510, Ciudad de México, Mexico. 4. Departamento de Genética, Instituto Nacional de Rehabilitación, C.P. 14389, Ciudad de México, Mexico.
Abstract
Chronic low-grade inflammation is strongly related to the etiology of diabetes mellitus type 2 (T2DM), and the expression of inflammatory cytokines may be modulated by polymorphisms located in the regulatory regions of the NFκβ, IL-1β, IL-6, TNFα, and LPL genes. We considered it particularly important to investigate the relationship of gene polymorphisms involved in chronic inflammation with the risk of T2DM or uncontrolled biochemical parameters. METHODS: We included 199 individuals with a T2DM diagnosis and 213 individuals without a T2DM diagnosis. Restriction fragment length polymorphism (RFLP) analyses were used to assess polymorphisms. RESULTS: We found a risk association between T2DM and uncontrolled biochemical parameters in a Mexican population for the genotypes del/del of NFκβ, -174 and -572 of IL-6, C/C of IL-1β, -308 and -238 of TNFα, and T/T of LPL. In subjects without diabetes (controls), we found an association between the G/C genotype of the -572 polymorphism and the G/C and C/C genotypes of the -597 polymorphism of IL-6 with the risk of glucose levels > 131 mg/dL. Genotype C/C of polymorphism -174 of the IL-6 gene was associated with high triglyceride levels, and levels > 5.8% of HbA1c were associated with the G/A genotype of TNFα -308. CONCLUSION: Here, we describe for the first time the relationship of T2DM risk and uncontrolled biochemical parameters with polymorphisms in the NFκβ, IL-6, TNFα, IL-1β, and LPL genes in a Mexican population. We also showed that for the population included in this study, there is an additive effect of the polymorphisms of the studied genes that considerably increases the risk of developing T2DM.We also showed that there are interactions between genes related to chronic inflammation that affect the risk of T2DM.
Chronic low-grade inflammation is strongly related to the etiology of diabetes mellitus type 2 (T2DM), and the expression of inflammatory cytokines may be modulated by polymorphisms located in the regulatory regions of the NFκβ, IL-1β, IL-6, TNFα, and LPL genes. We considered it particularly important to investigate the relationship of gene polymorphisms involved in chronic inflammation with the risk of T2DM or uncontrolled biochemical parameters. METHODS: We included 199 individuals with a T2DM diagnosis and 213 individuals without a T2DM diagnosis. Restriction fragment length polymorphism (RFLP) analyses were used to assess polymorphisms. RESULTS: We found a risk association between T2DM and uncontrolled biochemical parameters in a Mexican population for the genotypes del/del of NFκβ, -174 and -572 of IL-6, C/C of IL-1β, -308 and -238 of TNFα, and T/T of LPL. In subjects without diabetes (controls), we found an association between the G/C genotype of the -572 polymorphism and the G/C and C/C genotypes of the -597 polymorphism of IL-6 with the risk of glucose levels > 131 mg/dL. Genotype C/C of polymorphism -174 of the IL-6 gene was associated with high triglyceride levels, and levels > 5.8% of HbA1c were associated with the G/A genotype of TNFα -308. CONCLUSION: Here, we describe for the first time the relationship of T2DM risk and uncontrolled biochemical parameters with polymorphisms in the NFκβ, IL-6, TNFα, IL-1β, and LPL genes in a Mexican population. We also showed that for the population included in this study, there is an additive effect of the polymorphisms of the studied genes that considerably increases the risk of developing T2DM.We also showed that there are interactions between genes related to chronic inflammation that affect the risk of T2DM.
Authors: L Guariguata; D R Whiting; I Hambleton; J Beagley; U Linnenkamp; J E Shaw Journal: Diabetes Res Clin Pract Date: 2013-12-01 Impact factor: 5.602
Authors: Imtiyaz A Bhat; Niyaz A Naykoo; Iqbal Qasim; Farooq A Ganie; Qaiser Yousuf; Bashir A Bhat; Roohi Rasool; S A Aziz; Zafar Amin Shah Journal: Meta Gene Date: 2014-01-17