Correlation of the Homeostasis Model Assessment Index and Adiponectin, Leptin and Insulin Levels to Body Mass Index-Associated Gene Polymorphisms in Adolescents

• Main Authors: María D. Martínez-Martínez, Hugo Mendieta-Zerón, Luis Celis, Cristian F. Layton-Tovar, Rocío Torres-García, Laura E. Gutiérrez-Pliego, Eneida Camarillo-Romero, José D. Garduño-García, María D. Camarillo-Romero
• Format: Article
• Language: English
• Published: Sultan Qaboos University 2018-12-01
• Series: Sultan Qaboos University Medical Journal
• Online Access: https://journals.squ.edu.om/index.php/squmj/article/view/2848

Objectives: This study aimed to describe correlations between glucose, insulin and adipokine levels and the homeostasis model assessment (HOMA) index with regards to the presence/absence of fat mass and obesity-associated (FTO) rs9939609 and peroxisome proliferator-activated receptor (PPAR)-y rs1801282 single nucleotide polymorphisms (SNPs) as indicators of body mass index in adolescents. Methods: This cross-sectional study was conducted between September and December 2016 in Toluca, Mexico. A total of 71 students between 14–18 years old were included. Various anthropometric and laboratory measurements were collected, including lipid profile, glucose, insulin and adipokine levels and HOMA index. The degree of association between variables was evaluated with regards to the presence/absence of the SNPs. Results: Leptin levels were significantly higher among female students (P = 0.001), although adiponectin levels did not differ significantly (P = 0.060). There were significant positive correlations between insulin levels and HOMA index with FTO (r = 0.391; P = 0.007 and r = 0.413; P = 0.005, respectively) and PPARγ (r = 0.529; P = 0.007 and r = 0.537; P = 0.007, respectively) SNPs. Leptin showed a significant positive correlation in the presence of PPARγ (r = 0.483; P = 0.007) or in the absence of both SNPs (r = 0.627; P = 0.039). However, adiponectin was significantly negatively correlated in the presence of FTO, either alone (r = −0.333; P = 0.024) or in combination with PPARγ (r = −0.616; P = 0.043). Conclusion: The presence of FTO and/or PPARγ SNPs might be related to a genetic predisposition to metabolic syndrome. Keywords: Obesity; Body Mass Index; Single Nucleotide Polymorphisms; Fat Mass and Obesity Associated Protein, Human; Peroxisome Proliferator-Activated Receptor gamma; Adipokines.