Genetic Variation and Obesity in Australian Women: A Prospective Study

Abstract

Genetic variation and obesity in Australian women: a prospective study. Obes Res. 2001;9:733-740. Objective: A number of candidate genes have been implicated in the pathogenesis of obesity in humans. This study examines associations between longitudinal changes in body mass and composition and the presence of polymorphisms in the ␤-3 adrenergic receptor, tumor necrosis factor-␣, leptin, and leptin receptor (Lepr) in a cohort of Australian women. Research Methods and Procedures: Healthy white Australian women (n ϭ 335) were randomly selected from the Barwon region of Victoria and underwent baseline anthropometry and double-energy X-ray absorptiometry for assessment of body mass and adiposity. These measurements were repeated again at 2-year follow-up. Genomic DNA was extracted and used for polymerase chain reaction-based genotyping of all polymorphisms. Results: The Pro1019Pro Lepr polymorphism was associated with longitudinal increases in body weight (p ϭ 0.02), fat mass (p ϭ 0.05), and body mass index (p ϭ 0.01) in this study, and individuals homozygous for the A allele at this locus had a greater propensity to gain body fat over time. The largest effects on body composition seemed to be in individuals already obese at baseline. Changes in body weight, fat mass, percent body fat, and body mass index over a 2-year period were not associated with genetic variation in the ␤-3 adrenergic receptor (Trp64Arg), tumor necrosis factor-␣ promoter, or leptin genes in non-obese or obese women. Discussion: These results suggest that a Lepr polymorphism is involved in the regulation of body mass and adiposity in obese Australian white women, which may have implications for the treatment of obesity in this population.

Polymorphisms inFasGene Is Associated with HIV-Related Lipoatrophy in Thai Patients

“…29 Several studies have reported that people with this SNP showed an increased risk of developing obesity and glucose intolerance, 32,33 whereas other studies failed to find any correlation between this mutation and body mass index. 45,46 The results for ApoC3 -455 were also not consistent with those of the Italian cohort, which showed an association of the 4 Kruskal-Wallis test. 5 The first measurement after patients started antiretroviral therapy.…”

“…Almost half of the patients started ART immediately after being diagnosed with HIV infection. Median CD4 count per microliter pre-ART was 45 and that post-ART (after 1 year) was 210.5. The mean followup period was 4.85 years (SD = 2.42).…”

Genetic Influences on Change in BMI from Middle to Old Age: A 29-Year Follow-up Study of Twin Sisters

“…For instance, while the Pro1019Pro Lepr polymorphism in particular associated with both high adiposity and longitudinal gains in BMI (de Silva et al 2001) there are some studies proposing additional genes (e.g. APO-E gene, the uncoupling protein 1 gene and the B3-adrenergic receptor gene polymorphisms) as specific regulators of longitudinal increments in adult body weight (Gueguen et al 1989;Sivenius et al 2000;Clement et al 1995).…”

Genetic influences on adult body mass index followed over 29 years and their effects on late-life mobility: a study of twin sisters

“…This is supported as well by several observations at the molecular level. For instance, although the Pro1019Pro Lepr polymorphism is particularly associated with both high adiposity and longitudinal gains in BMI,38 there are some studies proposing additional genes (eg APO-E gene, the uncoupling protein 1 gene and the B3-adrenergic receptor gene polymorphisms) as specific regulators of longitudinal increments in adult body weight 39 – 41. Yet, these specific genes have not been widely replicated as predictors of long-term weight gain.…”