Genetic Susceptibility To Obesity Research Articles

High Prevalence of Positive Genetic Obesity Variants in Postoperative Bariatric Surgery Patients with Weight Regain Presenting for Medical Obesity Intervention.

Genetic obesity susceptibility in postoperative bariatric surgery weight regain (PBSWR) remains largely unexplored. A retrospective case series of adult (N = 27) PBSWR patients who had undergone genetic obesity testing was conducted between Sept. 2020 and March 2022. frequency of genetic variants in patients experiencing weight regain following bariatric surgery. prevalence of obesity-related comorbidities, nadir BMI achieved post-bariatric surgery, and percent total body weight loss (%TBWL) achieved with obesity pharmacotherapies. Heterozygous mutations were identified in 22 (81%) patients, with the most prevalent mutations occurring in CEP290, RPGR1P1L, and LEPR genes (3 patients each). Median age was 56years (interquartile range (IQR) 46.8-65.5), 88% female. Types of surgery were 67% RYGB, 19% SG, 4% gastric band, and 13% revisions. Median nadir BMI postoperatively was 34.0kg/m2 (IQR 29.0-38.5). A high prevalence of metabolic derangements was noted; patients presented median 80months (IQR 39-168.5) postoperative for medical weight management with 40% weight regain. BMI at initiation of anti-obesity medication (AOMs) was 41.7kg/m2 (36.8-44.4). All received AOM and required at least 3 AOMs for weight regain. Semaglutide (N = 21), topiramate (N = 14), and metformin (N = 12) were most prescribed. Median %TBWL for the cohort at the first, second, and third visit was 1.7, 5.0, and 6.5 respectively. Fourteen (52%) achieved 5%TBWL, 10 (37%) achieved 10%TBWL, and 4 (15%) achieved 15%TBWL with combination AOMs and supervised medical intervention. An unusually high prevalence of genetic obesity variants in PBSWR was found, warranting further research.

Association between genetic obesity susceptibility and mother-reported eating behaviour in children up to 5years.

Many genetic polymorphisms identified by genome-wide association studies for adult body mass index (BMI) have been suggested to regulate food intake. The objective was to study the associations between a genetic obesity risk score, appetitive traits, and growth of children up to age 5years, with a longitudinal design. In 1142 children from the Etude des Déterminants pre et post natals de la santé de l'ENfant (EDEN) birth cohort, a combined obesity risk-allele score (BMI genetic risk score [GRS]) was related to appetitive traits (energy intake up to 12mo, a single item on appetite from 4mo to 3y, a validated appetite score at 5y) using Poisson regressions with robust standard errors. The potential mediation of appetitive traits on the association between BMI-GRS and growth was assessed by the Sobel test. Children with a high BMI-GRS were more likely to have high energy intake at 1year and high appetite at 2 and 5years. High energy intake in infancy and high appetite from 1year were related to higher subsequent BMI. High 2-year appetite seemed to partially mediate the associations between BMI-GRS and BMI from 2 to 5years (all P≤0.05). Genetic susceptibility to childhood obesity seems to be partially explained by appetitive traits in infancy, followed by an early childhood rise in BMI.

Interaction of smoking and obesity susceptibility loci on adolescent BMI: The National Longitudinal Study of Adolescent to Adult Health.

BackgroundAdolescence is a sensitive period for weight gain and risky health behaviors, such as smoking. Genome-wide association studies (GWAS) have identified loci contributing to adult body mass index (BMI). Evidence suggests that many of these loci have a larger influence on adolescent BMI. However, few studies have examined interactions between smoking and obesity susceptibility loci on BMI. This study investigates the interaction of current smoking and established BMI SNPs on adolescent BMI. Using data from the National Longitudinal Study of Adolescent to Adult Health, a nationally-representative, prospective cohort of the US school-based population in grades 7 to 12 (12–20 years of age) in 1994–95 who have been followed into adulthood (Wave II 1996; ages 12–21, Wave III; ages 18–27), we assessed (in 2014) interactions of 40 BMI-related SNPs and smoking status with percent of the CDC/NCHS 2000 median BMI (%MBMI) in European Americans (n = 5075), African Americans (n = 1744) and Hispanic Americans (n = 1294).ResultsTwo SNPs showed nominal significance for interaction (p < 0.05) between smoking and genotype with %MBMI in European Americans (EA) (rs2112347 (POC5): β = 1.98 (0.06, 3.90), p = 0.04 and near rs571312 (MC4R): β 2.15 (−0.03, 4.33) p = 0.05); and one SNP showed a significant interaction effect after stringent correction for multiple testing in Hispanic Americans (HA) (rs1514175 (TNNI3K): β 8.46 (4.32, 12.60), p = 5.9E-05). Stratifying by sex, these interactions suggest a stronger effect in female smokers.ConclusionsOur study highlights potentially important sex differences in obesity risk by smoking status in adolescents, with those who may be most likely to initiate smoking (i.e., adolescent females), being at greatest risk for exacerbating genetic obesity susceptibility.Electronic supplementary materialThe online version of this article (doi:10.1186/s12863-015-0289-6) contains supplementary material, which is available to authorized users.

Progressive influence of body mass index-associated genetic markers in rural Gambians

BackgroundIn populations of European ancestry, the genetic contribution to body mass index (BMI) increases with age during childhood but then declines during adulthood, possibly due to the cumulative effects of...

Associations between genetic obesity susceptibility and early postnatal fat and lean mass: an individual participant meta-analysis.

Patterns of body size and body composition associated with genetic obesity susceptibility inform the mechanisms that increase obesity risk. To test associations between genetic obesity susceptibility, represented by a combined obesity risk-allele score, and body size or body composition at birth to age 5 years. A total of 3031 children from 4 birth cohort studies in England, France, and Spain were included in a meta-analysis. A combined obesity risk-allele score was calculated from genotypes at 16 variants identified by genome-wide association studies of adult body mass index (BMI). Outcomes were age- and sex-adjusted SD scores (SDS) for weight, length/height, BMI, fat mass, lean mass, and percentage of body fat at birth as well as at ages 1, 2 to 3, and 4 to 5 years. The obesity risk-allele score was not associated with infant size at birth; at age 1 year it was positively associated with weight (β [SE], 0.020 [0.008] SDS per allele; P = .009) and length (β [SE], 0.020 [0.008] SDS per allele; P = .01), but not with BMI (β [SE], 0.013 [0.008] SDS per allele; P = .11). At age 2 to 3 years these associations were stronger (weight: β [SE], 0.033 [0.008] SDS per allele; P < .001; height: β [SE], 0.025 [0.008] SDS per allele; P < .001) and were also seen for BMI (β [SE], 0.024 [0.008] SDS per allele; P = .003). The obesity risk-allele score was positively associated with both postnatal fat mass (1 year: β [SE], 0.032 [0.017] SDS per allele; P = .05; 2-3 years: β [SE], 0.049 [0.018] SDS per allele; P = .006; and 4-5 years: β [SE], 0.028 [0.011] SDS per allele; P = .009) and postnatal lean mass (1 year: β [SE], 0.038 [0.014] SDS per allele; P = .008; 2-3 years: β [SE], 0.064 [0.017] SDS per allele; P < .001; and 4-5 years: β [SE], 0.047 [0.011] SDS per allele; P < .001), but not with the percentage of body fat (P > .15 at all ages). Genetic obesity susceptibility appears to promote a normally partitioned increase in early postnatal, but not prenatal, growth. These findings suggest that symmetrical rapid growth may identify infants with high life-long susceptibility for obesity.