Genetic polymorphisms in genes related to risk‐taking behaviours predicting body mass index trajectory among Mexican American adolescents

Zhao, Hua; Wilkinson, Anna V.; Shen, Jie; Wu, Xifeng; Chow, Wong Ho

doi:10.1111/ijpo.12151

Cited by 13 publications

(8 citation statements)

References 30 publications

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“…For example, the effects of metabolic biomarkers 42 and environmental endocrine disruptors (EEDs) on children's BMI were not considered in our study. Second, because this analysis is based on cross-sectional data, we cannot make causal inferences.…”

Section: Study Strengths and Limitationsmentioning

confidence: 99%

Polygenic risk, adherence to a healthy lifestyle, and childhood obesity

et al. 2018

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Summary Background Both polygenic and unhealthy lifestyle factors contribute to individual‐level risk of obesity during childhood. The extent to which increased polygenic risk can be offset by healthy lifestyle is unknown. Objective To examine whether increased polygenic risk of obesity is modified by a healthy lifestyle during childhood. Methods A total of 997 children (418 boys and 579 girls) who had complete DNA genotyping and body mass index (BMI) were eligible for the study were analyzed from an established prospective puberty cohort. The polygenic risk score (PRS) was computed based on 11 BMI‐increasing single nucleotide polymorphisms (SNPs) derived from a published genome‐wide association study (GWAS) for child obesity. Seven lifestyle factors were selected to determine a composite healthy lifestyle, such as food responsiveness, slowness in eating, satiety responsiveness, physical activity, screen time, sleep duration, and sugar‐sweetened beverages consumption, and which was classified as healthy (P75) lifestyle. Linear and logistic regression analyses were conducted. Results Children carrying additional BMI susceptibility alleles increased the BMI by 0.11 kg/m2, after adjusting gender, age and socio‐economic status (SES). A healthy lifestyle was associated with a substantially lower risk of obesity than an unhealthy lifestyle, regardless of the polygenic risk category. Among children at high polygenic risk, a healthy lifestyle was associated with an 85% lower risk of obesity than an unhealthy lifestyle (odds ratio, 0.15; 95% CI, 0.04 to 0.59; p = 0.007). Conclusions Our findings suggest that increased polygenic risk might be largely offset by healthy lifestyle as early as in childhood.

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Section: Study Strengths and Limitationsmentioning

confidence: 99%

Polygenic risk, adherence to a healthy lifestyle, and childhood obesity

et al. 2018

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“…Recent studies suggest that genetic effects on obesity‐related phenotypes, like body mass index (BMI), may differ across life stages . To date, few genetic studies have focused on the effects of genetics across childhood , or Hispanic/Latinos , including Chileans, although they shoulder a high burden of obesity. These observations highlight the need to characterize the relevance of established genetic loci from infancy into adulthood.…”

Section: Introductionmentioning

confidence: 99%

Genetic determinants of BMI from early childhood to adolescence: the Santiago Longitudinal Study

et al. 2018

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Summary Background While the genetic contribution to obesity is well established, few studies have examined how genetic variants influence standardized body mass index Z‐score (BMIz) in Hispanics/Latinos, especially across childhood and adolescence. Objectives We estimated the effect of established BMIz loci in Chilean children of the Santiago Longitudinal Study (SLS). Methods We examined associations with BMIz at age 10 for 15 loci previously identified in European children. For significant loci, we performed association analyses at ages 5 and 16 years, for which we have smaller sample sizes. We tested associations of unweighted genetic risk scores (GRSs) for previously identified tag variants (GRS_EUR) and from the most significant variants in SLS at each locus (GRS_SLS). Results We generalized five variants at age 10 (P < 0.05 and directionally consistent), including rs543874 that reached Bonferroni‐corrected significance. The effect on BMIz was greatest at age 10 for all significant loci, except FTO, which exhibited an increase in effect from ages 5 to 16. Both GRSs were associated with BMIz (P < 0.0001), but GRS_SLS explained a much greater proportion of the variation (13.63%). Conclusion Our results underscore the importance of conducting genetic investigations across life stages and selecting ancestry appropriate tag variants in future studies for disease prediction and clinical evaluation.

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“…Previous studies have shown that HTR2A agonist could increase lipid accumulation and 5-HT suppress lipolysis in 3T3-L1 adipocytes and a genetic variant in HTR2A associated with obesity [ 6 , 7 ]. In this research, HTR2A was upregulated in Day-4 and Day-9 compared to Day-0, so it was chosen for functional analyses.…”

Section: Resultsmentioning

confidence: 99%

“…HTR2A agonist treatment increased lipid accumulation and 5-HT suppressed lipolysis using 3T3-L1 adipocytes [ 6 ]. It has been identified as a genetic variant, namely, rs17069005 in HTR2A gene associated with obesity at last follow-up [ 7 ], but the role of HTR2A in mediating the effects on cattle adipocyte differentiation remains unexplored.…”

Section: Introductionmentioning

confidence: 99%

RNA-Seq Analysis Reveals a Positive Role of HTR2A in Adipogenesis in Yan Yellow Cattle

Yun

Jin

Cao

et al. 2018

IJMS

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In this study, we performed high throughput RNA sequencing at the primary bovine preadipocyte (Day-0), mid-differentiation (Day-4), and differentiated adipocyte (Day-9) stages in order to characterize the transcriptional events regulating differentiation and function. The preadipocytes were isolated from subcutaneous fetal bovine adipose tissues and were differentiated into mature adipocytes. The adipogenic characteristics of the adipocytes were detected during various stages of adipogenesis (Day-0, Day-4, and Day-9). We used RNA sequencing (RNA-seq) to investigate a comprehensive transcriptome information of adipocytic differentiation. Compared to the pre-differentiation stage (Day-0), 2510 genes were identified as differentially expressed genes (DEGs) at the mid-differentiation stage (Day-4). We found 2446 DEGs in the mature adipocytic stage relative to the mid-differentiation stage. Some adipogenesis-related transcription factors, CCAAT-enhancer-binding protein α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ) were differentially expressed at Day-0, Day-4, and Day-9. We further investigated the adipogenic function of 5-hydroxytryptamine receptor 2A (HTR2A) in adipogenesis. Overexpression of HTR2A stimulated the differentiation of preadipocytes, and knockdown of HTR2A had opposite effects. Furthermore, functional enrichment analysis of DEGs revealed that the PI3K-Akt signaling pathway was the significantly enriched pathway, and HTR2A regulated adipogenesis by activating or inhibiting phosphorylation of phospho-AKT (Ser473). In summary, the present study provides the first comparative transcription of various periods of adipocytes in cattle, which presents a solid foundation for further study into the molecular mechanism of fat deposition and the improvement of beef quality in cattle.

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Genetic polymorphisms in genes related to risk‐taking behaviours predicting body mass index trajectory among Mexican American adolescents

Cited by 13 publications

References 30 publications

Polygenic risk, adherence to a healthy lifestyle, and childhood obesity

Polygenic risk, adherence to a healthy lifestyle, and childhood obesity

Genetic determinants of BMI from early childhood to adolescence: the Santiago Longitudinal Study

RNA-Seq Analysis Reveals a Positive Role of HTR2A in Adipogenesis in Yan Yellow Cattle

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