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Background: Visceral adiposity index (VAI) has been identified as a cardiometabolic risk marker in children and adolescents which reflects abdominal fat distribution. The aim of the present study was to evaluated the predictive capacity of VAI, a body shape index (ABSI), atherogenic index of plasma (AIP), and triglycerides and glucose index (TyG index) compared with classical anthropometric measurements to discriminate metabolic syndrome (MetS). Methods: This retrospective study included 1372 individuals. Anthropometric, clinical, and biochemical measurements were used to screen the prevalence of MetS components and to calculate VAI, ABSI, TyG index, and AIP. Results: The discriminatory capacity among the variables was assessed by the area under the receiver operating characteristic (ROC) curve (AUC). VAI was the variable with the highest AUC with 0.932 CI 95% (0.917–0.948), followed by AIP with 0.914 CI 95% (0.897–0.931), and TyG index with 0.889 CI 95% (0.871–0.908). Conclusion: VAI is a promising tool to identify MetS in the late adolescence setting. Among the novel adiposity indexes VAI, AIP, TyG index are able to determine MetS presence, while ABSI is not capable. [ABSTRACT FROM AUTHOR]

- Overweight in childhood sets the stage for a lifelong struggle with weight and eating and raises the risk of health problems, such as obesity, diabetes mellitus, hypertension, sleep apnea, and heart disease. Research from multiple disciplinary fields has identified scores of contributing factors. Efforts to integrate these factors into a single 'big picture' have been hampered by the challenges of constructing theoretical models that are both comprehensive and developmentally adaptable. This article reviews select genetic and environmental factors influencing childhood overweight and obesity, then explicates an ecological model mapping these and other factors. The Six-Cs model extends previous theoretical work on childhood weight imbalance by acknowledging dimensions of factors specific to heredity as well as the environment, to activity as well as nutrition, to resources and opportunities as well as practices, and to development from birth through adolescence. This article concludes by discussing the model's policy relevance and identifying important next steps for transdisciplinary research concerning child overweight and obesity. [ABSTRACT FROM AUTHOR]

The fat mass (FM) and obesity-associated (FTO) gene is the first obesity-susceptibility gene identified by genome-wide association scans and confirmed in several follow-up studies. Homozygotes for the risk allele (A/A) have 1.67 times greater risk of obesity than those who do not have the allele. However, it is not known whether regular exercise-induced changes in body composition are influenced by the FTO genotype. The purpose of our study was to test whether the FTO genotype is associated with exercise-induced changes in adiposity. Body composition was derived from underwater weighing before and after a 20-week endurance training program in 481 previously sedentary white subjects of the HERITAGE Family Study. FTO single-nucleotide polymorphism (SNP) rs8050136 was genotyped using Illumina GoldenGate assay. In the sedentary state, the A/A homozygotes were significantly heavier and fatter than the heterozygotes and the C/C homozygotes in men (P = 0.004) but not in women (P = 0.331; gene-by-sex interaction P = 0.0053). The FTO genotype was associated with body fat responses to regular exercise (P < 0.005; adjusted for age, sex, and baseline value of response trait): carriers of the C allele showed three times greater FM and %body fat losses than the A/A homozygotes. The FTO genotype explained 2% of the variance in adiposity changes. Our data suggest that the FTO obesity-susceptibility genotype influences the body fat responses to regular exercise. Resistance to exercise-induced reduction in total adiposity may represent one mechanism by which the FTO A allele promotes overweight and obesity. [ABSTRACT FROM AUTHOR]

Summary: Background: Childhood obesity is a nutrition‐related disease with multiple underlying aetiologies. While genetic factors contribute to obesity, the gut microbiome is also implicated through fermentation of nondigestible polysaccharides to short‐chain fatty acids (SCFA), which provide some energy to the host and are postulated to act as signalling molecules to affect expression of gut hormones. Objective To study the cumulative association of causal, regulatory, and tagged single nucleotide polymorphisms (SNPs) within genes involved in SCFA recognition and metabolism with obesity. Design Study participants were non‐Hispanic White (NHW, n = 270) and non‐Hispanic Black (NHB, n = 113) children (2‐5 years) from the Synergistic Theory and Research on Obesity and Nutrition Group (STRONG) Kids 1 Study. SNP variables were assigned values according to the additive, dominant, or recessive inheritance models. Weighted genetic risk scores (GRS) were constructed by multiplying the reassigned values by independently generated β‐coefficients or by summing the β‐coefficients. Ethnicity‐specific SNPs were selected for inclusion in GRS by cohort. Results: GRS were directly associated with body mass index (BMI) z‐score. The models explained 3.75%, 12.9%, and 26.7% of the variance for NHW/NHB, NHW, and NHB (β = 0.89 [CI: 0.43‐1.35], P = 0.0002; β = 0.78 [CI: 0.54‐1.03], P < 0.0001; β = 0.74 [CI: 0.51–0.97], P < 0.0001). Conclusion: This analysis supports the cumulative association of several candidate genetic variants selected for their role in SCFA signalling, transport, and metabolism with early‐onset obesity. These data strengthen the concept that microbiome influences obesity development through host genes interacting with SCFA. [ABSTRACT FROM AUTHOR]