Interactions of several single nucleotide polymorphisms and high body mass index on serum lipid traits

BioFactors ◽  
2013 ◽  
Vol 39 (3) ◽  
pp. 315-325 ◽  
Author(s):  
Rui-Xing Yin ◽  
Dong-Feng Wu ◽  
Lin Miao ◽  
Lynn Htet Htet Aung ◽  
Xiao-Li Cao ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Single Nucleotide Polymorphisms ◽  
Body Mass ◽  
Serum Lipid ◽  
High Body Mass Index ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
High Body

The Multiplex Genotyping Method for Single-Nucleotide Polymorphisms of Genes Associated with Obesity and Body Mass Index

2019 ◽  
Vol 55 (10) ◽  
pp. 1282-1293
Author(s):  
E. A. Trifonova ◽  
A. A. Popovich ◽  
K. V. Vagaitseva ◽  
A. V. Bocharova ◽  
M. M. Gavrilenko ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Single Nucleotide Polymorphisms ◽  
Body Mass ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Genotyping Method ◽  
Multiplex Genotyping

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

2018 ◽  
Vol 18 (3) ◽  
pp. 291
Author(s):  
María D. Martínez-Martínez ◽  
Hugo Mendieta-Zerón ◽  
Luis Celis ◽  
Cristian F. Layton-Tovar ◽  
Rocío Torres-García ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Single Nucleotide Polymorphisms ◽  
Body Mass ◽  
Peroxisome Proliferator ◽  
Model Assessment ◽  
Homa Index ◽  
Nucleotide Polymorphisms ◽  
Homeostasis Model Assessment ◽  
Single Nucleotide ◽  
Peroxisome Proliferator Activated Receptor

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.

scholarly journals 2125 What genes are involved in the brain food reward circuitry: Findings from a large candidate gene analysis

2018 ◽  
Vol 2 (S1) ◽  
pp. 36-36
Author(s):  
Ying Meng ◽  
Susan W. Groth ◽  
Joyce A. Smith ◽  
Harriet Kitzman
Keyword(s):  
Body Mass Index ◽  
Single Nucleotide Polymorphisms ◽  
Body Mass ◽  
Food Reward ◽  
African American Adolescents ◽  
Overweight And Obesity ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Reward Circuitry ◽  
The Brain

OBJECTIVES/SPECIFIC AIMS: The food reward circuitry regulates hedonic eating especially in relation to palatable hypercaloric foods, which can lead to chronic overeating and consequent overweight and obesity. Evidence supports that there is considerable overlap within the brain reward circuitry between palatable hypercaloric food intake and substance addiction. The goal of this study was to identify associations between addiction-related genes and body mass index. We hypothesized that addiction-related genes potentially participate in the food reward circuitry if they are associated with obesity traits. METHODS/STUDY POPULATION: A secondary analysis was conducted with 1093 African American adolescents and young adults from the New Mother’s Study. Anthropometric, genetic, demographic and lifestyle measurements were available at the 18-year follow-up assessments. A total of 1350 single nucleotide polymorphisms mapped to 127 addiction-related genes were assessed. A total of 186 ancestry informative markers were used to adjust for population stratification. Generalized estimating equation models were used to identify genetic associations, including additive, dominant, and recessive models, and control for correlations within families. RESULTS/ANTICIPATED RESULTS: The participants ranged from 15 to 23 years of age. Of them, 42.7% were overweight or obese. Significant associations with body mass index were identified for 13 single nucleotide polymorphisms mapped to 11 addiction-related genes, including LEP (p 0.027–<0.001). Most of these genes are involved in dopaminergic, opioidergic, serotonergic pathways, and stress. DISCUSSION/SIGNIFICANCE OF IMPACT: Our results support the role of dopaminergic and opioidergic pathways in the food reward circuitry, and suggest a potential involvement of serotonergic pathways and genes related to stress in the food reward circuitry. Further investigation of the identified genes will facilitate delineation and understanding of the brain food reward system and its relationship with obesity.

scholarly journals Functional Single-Nucleotide Polymorphisms in the Secretogranin III (SCG3) Gene that Form Secretory Granules with Appetite-Related Neuropeptides Are Associated with Obesity

2007 ◽  
Vol 92 (3) ◽  
pp. 1145-1154 ◽  
Author(s):  
Atsushi Tanabe ◽  
Takahiro Yanagiya ◽  
Aritoshi Iida ◽  
Susumu Saito ◽  
Akihiro Sekine ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Single Nucleotide Polymorphisms ◽  
Body Mass ◽  
Secretory Granules ◽  
P Value ◽  
Nucleotide Polymorphisms ◽  
Hypothalamic Area ◽  
Single Nucleotide ◽  
Association Analyses ◽  
Control Subjects

Abstract Context: Genetic factors are important for the development of obesity. However, the genetic background of obesity still remains unclear. Objective: Our objective was to search for obesity-related genes using a large number of gene-based single-nucleotide polymorphisms (SNPs). Design and Setting: We conducted case-control association analyses using 94 obese patients and 658 controls with 62,663 SNPs selected from the SNP database. SNPs that possessed P ≤ 0.02 were further analyzed using 796 obese and 711 control subjects. One SNP (rs3764220) in the secretogranin III (SCG3) gene showed the lowest P value (P = 0.0000019). We sequenced an approximately 300-kb genomic region around rs3764220 and discovered SNPs for haplotype analyses. SCG3 was the only gene within a haplotype block that contained rs3764220. The functions of SCG3 were studied. Patients: Obese subjects (body mass index ≥ 30 kg/m2, n = 890) and control subjects (general population; n = 658, body mass index ≤ 25kg/m2; n = 711) were recruited for this study. Results: Twelve SNPs in the SCG3 gene including rs3764220 were in almost complete linkage disequilibrium and significantly associated with an obesity phenotype. Two SNPs (rs16964465, rs16964476) affected the transcriptional activity of SCG3, and subjects with the minor allele seemed to be resistant to obesity (odds ratio, 9.23; 95% confidence interval, 2.77–30.80; χ2 = 19.2; P = 0.0000067). SCG3 mRNA and immunoreactivity were detected in the paraventricular nucleus, lateral hypothalamic area, and arcuate nucleus, and the protein coexisted with orexin, melanin-concentrating hormone, neuropeptide Y, and proopiomelanocortin. SCG3 formed a granule-like structure together with these neuropeptides. Conclusions: Genetic variations in the SCG3 gene may influence the risk of obesity through possible regulation of hypothalamic neuropeptide secretion.

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