Hatim Boughanem1, Borja Bandera-Merchán2, Pablo Hernández-Alonso2,3,4, Noelia Moreno-Morales5, Francisco José Tinahones2,3, José Lozano6, Sonsoles Morcillo2,3, Manuel Macias-Gonzalez2,3. 1. Instituto de Investigación Biomédica de Málaga (IBIMA), Facultad de Ciencias, Universidad de Málaga, 29010 Málaga, Spain. 2. Unidad de Gestión Clínica de Endocrinología y Nutrición del Hospital Virgen de la Victoria, Instituto de Investigación Biomédica de Málaga (IBIMA), Universidad de Málaga, 29010 Málaga, Spain. 3. Centro de Investigación Biomédica en Red de Fisiopatología de la Obesidad y la Nutrición, CIBERObn, 28029 Madrid, Spain. 4. Human Nutrition Unit, Faculty of Medicine and Health Sciences, Sant Joan Hospital, Institut d'Investigació Sanitària Pere Virgili, Rovira i Virgili University, 43201 Reus, Spain. 5. Department of Physiotherapy, School of Health Sciences, University of Malaga-Instituto de Investigación Biomédica de Málaga (IBIMA), 29010 Málaga, Spain. 6. Departamento de Bioquímica y Biología Molecular, Facultad de Ciencias, Universidad de Málaga, 29010 Málaga, Spain.
Abstract
Background: The interaction between obesity and genetic traits on high density lipoprotein (HDL) levels has been extensively studied. The variance of serum HDL has a strong genetic heritability, although the studied variant only explains a small part of this variation. The goal of this study was to investigate the associations between the apolipoprotein type 2 (APOA2) rs3813627 single nucleotide polymorphism (SNP) and anthropometric and biochemical variables, though body mass index (BMI). Methods: This study included 153 subjects (91 overweight/obese (BMI³25 kg/m2) and 62 non-obese individuals (BMI < 25 kg/m2)). The APOA2 rs3813627 SNP was selected and genotyped. Genotype analysis was performed to analyze the associations between APOA2 SNPs and anthropometric and biochemical variables through BMI. Results: The APOA2 rs3813627 TT genotype was associated with low HDL levels in comparison with the APOA2 rs3813627 GG and GT genotype in overweight/obese individuals, but not in the non-obese subjects (p < 0.05). The same trend was observed in the apolipoprotein type 1 (APOA1) protein levels (p < 0.05). Correlation analysis revealed a negative correlation between HDL and APOA1 levels and APOA2 rs3813627 SNP under recessive model (p < 0.05). The odds ratio for low HDL levels was 3.76 and 3.94 for low APOA1 levels. The mediation analysis of APOA2 rs3813627 SNP through BMI showed a full mediation on HDL and partial mediation on APOA1 levels (p < 0.05). Bioinformatic analysis showed that rs3813627 lies in the APOA2 promoter and overlaps motifs for several bound transcription factors. Conclusion: On the basis of these data, the APOA2 rs3813627 SNP is associated with low HDL and APOA1 levels susceptibility, and this effect was mediated by an increased BMI.
Background: The interaction between obesity and genetic traits on high density lipoprotein (HDL) levels has been extensively studied. The variance of serum HDL has a strong genetic heritability, although the studied variant only explains a small part of this variation. The goal of this study was to investigate the associations between the apolipoprotein type 2 (APOA2) rs3813627 single nucleotide polymorphism (SNP) and anthropometric and biochemical variables, though body mass index (BMI). Methods: This study included 153 subjects (91 overweight/obese (BMI³25 kg/m2) and 62 non-obese individuals (BMI < 25 kg/m2)). The APOA2rs3813627 SNP was selected and genotyped. Genotype analysis was performed to analyze the associations between APOA2 SNPs and anthropometric and biochemical variables through BMI. Results: The APOA2rs3813627 TT genotype was associated with low HDL levels in comparison with the APOA2rs3813627 GG and GT genotype in overweight/obese individuals, but not in the non-obese subjects (p < 0.05). The same trend was observed in the apolipoprotein type 1 (APOA1) protein levels (p < 0.05). Correlation analysis revealed a negative correlation between HDL and APOA1 levels and APOA2rs3813627 SNP under recessive model (p < 0.05). The odds ratio for low HDL levels was 3.76 and 3.94 for low APOA1 levels. The mediation analysis of APOA2rs3813627 SNP through BMI showed a full mediation on HDL and partial mediation on APOA1 levels (p < 0.05). Bioinformatic analysis showed that rs3813627 lies in the APOA2 promoter and overlaps motifs for several bound transcription factors. Conclusion: On the basis of these data, the APOA2rs3813627 SNP is associated with low HDL and APOA1 levels susceptibility, and this effect was mediated by an increased BMI.