Rym Kefi1, Meriem Hechmi2, Hamza Dallali3, Sahar Elouej4, Haifa Jmel3, Yossra Ben Halima5, Majdi Nagara4, Mariem Chargui5, Sihem Ben Fadhel2, Safa Romdhane2, Ines Kamoun6, Zinet Turki6, Abdelmajid Abid7, Sonia Bahri8, Afaf Bahlous8, Ramon Gomis9, Abdelhamid Baraket10, Florin Grigorescu11, Christophe Normand11, Henda Jamoussi7, Sonia Abdelhak5. 1. Laboratory of Biomedical Genomics and Oncogenetics, Institut Pasteur de Tunis, BP 74, 13, place Pasteur, Tunis 1002, Tunisia; University of Tunis El Manar, 2092 El Manar I Tunis, Tunisia. Electronic address: rym.kefi@pasteur.rns.tn. 2. Laboratory of Biomedical Genomics and Oncogenetics, Institut Pasteur de Tunis, BP 74, 13, place Pasteur, Tunis 1002, Tunisia. 3. Laboratory of Biomedical Genomics and Oncogenetics, Institut Pasteur de Tunis, BP 74, 13, place Pasteur, Tunis 1002, Tunisia; University of Carthage, BP 77, 1054 Amilcar, Tunisia. 4. Aix Marseille-University, Faculty of Medecine La Timone, Inserm, GMGF, 27, boulevard Jean-Moulin, 13385 Marseille, France. 5. Laboratory of Biomedical Genomics and Oncogenetics, Institut Pasteur de Tunis, BP 74, 13, place Pasteur, Tunis 1002, Tunisia; University of Tunis El Manar, 2092 El Manar I Tunis, Tunisia. 6. National Institute of Nutrition and Food Technology, 11, rue Jebel Lakhdar, Bab Saadoun, 1007 Tunis, Tunisia. 7. Laboratory of Biomedical Genomics and Oncogenetics, Institut Pasteur de Tunis, BP 74, 13, place Pasteur, Tunis 1002, Tunisia; National Institute of Nutrition and Food Technology, 11, rue Jebel Lakhdar, Bab Saadoun, 1007 Tunis, Tunisia. 8. Central Laboratory of Medical Biology, Institut Pasteur de Tunis, BP 74, 13, place Pasteur, Tunis 1002, Tunisia. 9. August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Carrer del Rosselló, 149, 08036 Barcelona, Spain. 10. Laboratory of Human molecular Genetics Institut Pasteur du Maroc 1, place Louis Pasteur, Casablanca, Morocco. 11. IURC, Molecular Endocrinology Laboratory, Nutrition & Genomes, UMR-204, NUTRIPASS, Montpellier, France.
Abstract
AIM OF THE STUDY: APOA5 has been linked to metabolic syndrome (MetS) or its traits in several populations. In North Africa, only the Moroccan population was investigated. Our aim is to assess the association between APOA5 gene polymorphisms with the susceptibility to MetS and its components in the Tunisian population. MATERIALS AND METHODS: A total of 594 participants from the Tunisian population were genotyped for two polymorphisms rs3135506 and rs651821 located in APOA5 gene using KASPar technology. Statistical analyses were performed using R software. RESULTS: The SNP rs651821 increased the risk of MetS under the dominant model (OR=1.91 [1.17-3.12], P=0.008) whereas the variant rs3135506 was not associated with MetS. After stratification of the cohort following the sex, only the variant rs651821 showed a significant association with MetS among the women group. The influence of the geographic origin of the studied population on the genotype distribution of APOA5 variants showed that the variant rs651821 was significantly associated with MetS only for the Northern population. The association analyses of the variants rs651821 and rs3135506 with different quantitative traits of MetS showed a significant association only between the variant rs3135506 and triglycerides levels. CONCLUSION: This is the first study reporting the association of APOA5 gene variants with MetS in Tunisia. Our study emphasizes the role of APOA5 variants in the regulation of the triglycerides blood levels. Further studies are needed to confirm the clinical relevance of these associations and to better understand the physiopathology of the MetS.
AIM OF THE STUDY: APOA5 has been linked to metabolic syndrome (MetS) or its traits in several populations. In North Africa, only the Moroccan population was investigated. Our aim is to assess the association between APOA5 gene polymorphisms with the susceptibility to MetS and its components in the Tunisian population. MATERIALS AND METHODS: A total of 594 participants from the Tunisian population were genotyped for two polymorphisms rs3135506 and rs651821 located in APOA5 gene using KASPar technology. Statistical analyses were performed using R software. RESULTS: The SNP rs651821 increased the risk of MetS under the dominant model (OR=1.91 [1.17-3.12], P=0.008) whereas the variant rs3135506 was not associated with MetS. After stratification of the cohort following the sex, only the variant rs651821 showed a significant association with MetS among the women group. The influence of the geographic origin of the studied population on the genotype distribution of APOA5 variants showed that the variant rs651821 was significantly associated with MetS only for the Northern population. The association analyses of the variants rs651821 and rs3135506 with different quantitative traits of MetS showed a significant association only between the variant rs3135506 and triglycerides levels. CONCLUSION: This is the first study reporting the association of APOA5 gene variants with MetS in Tunisia. Our study emphasizes the role of APOA5 variants in the regulation of the triglycerides blood levels. Further studies are needed to confirm the clinical relevance of these associations and to better understand the physiopathology of the MetS.