Dataset Information

Polymorphisms in the neuropeptide Y gene and the risk of obesity: findings from two prospective cohorts.

ABSTRACT: Neuropeptide Y (NPY) increases appetite and food intake in animals. Conflicting evidence has been found for the association between polymorphisms of the NPY gene and obesity in humans.The objective of the investigation was to study four single-nucleotide polymorphisms (SNPs) in the NPY gene [rs17149106 (G>T), rs16147 (C>T), rs16139 (T>C), rs5574 (C>T)] with body adiposity.The study design included a candidate gene association study from two cohorts.Two thousand seventy-one women from the Nurses' Health Study and 1268 men from the Health Professionals Follow-Up study participated in the study.Weight and height were self-reported at baseline and updated every 2 yr to calculate body mass index (BMI).Two SNPs (rs17149106 (G>T) and rs16139 (T>C)), with minor allele frequencies of 4%, were associated with elevated risks of obesity (BMI ? 30 kg/m(2)) in both cohorts. The pooled adjusted odds ratios [95% confidence interval (CI)] were 1.72 (95% CI 1.20-2.47) and 1.79 (95% CI 1.24-2.60), respectively. Haplotype analyses reflected the associations with the individual SNP. TTCC carriers, with the minor allele of both SNPs, had an increased risk of obesity (odds ratio 1.89; 95% CI 1.29-2.75) compared with those carrying the common haplotype GCTT. Carriers of the rs16139 C allele had greater BMI than noncarriers with a pooled mean difference of +0.58 kg/m(2) (95% CI 0.01-1.15) among women and men. Both rs17149106 and rs16139 were associated with weight gain since adolescence/early adulthood but were not associated with abdominal adiposity as measured by waist circumference and waist to hip ratio.NPY gene variants were significantly associated with weight changes from young adulthood to middle age and with risk of obesity.

SUBMITTER: Yeung EH

PROVIDER: S-EPMC3232624 | biostudies-literature | 2011 Dec

REPOSITORIES: biostudies-literature

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Polymorphisms in the neuropeptide Y gene and the risk of obesity: findings from two prospective cohorts.

Yeung Edwina H EH Zhang Cuilin C Chen Jinbo J Bowers Katherine K Hu Frank B FB Kang Guolian G Qi Lu L

The Journal of clinical endocrinology and metabolism 20110921 12

<h4>Context</h4>Neuropeptide Y (NPY) increases appetite and food intake in animals. Conflicting evidence has been found for the association between polymorphisms of the NPY gene and obesity in humans.<h4>Objective</h4>The objective of the investigation was to study four single-nucleotide polymorphisms (SNPs) in the NPY gene [rs17149106 (G>T), rs16147 (C>T), rs16139 (T>C), rs5574 (C>T)] with body adiposity.<h4>Design</h4>The study design included a candidate gene association study from two cohort ...[more]

PMID: 21937627

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Project description:BackgroundPrevious studies indicated that obesity would accelerate frailty progression. However, obesity is heterogeneous by different metabolic status. The associations of metabolic heterogeneity of obesity with frailty progression remain unclear.MethodsA total of 6730 participants from the China Health and Retirement Longitudinal Study (CHARLS) and 4713 from the English Longitudinal Study of Ageing (ELSA) were included at baseline. Metabolic heterogeneity of obesity was evaluated based on four obesity and metabolic phenotypes as metabolically healthy normal weight (MHNW), metabolically unhealthy normal weight (MUNW), metabolically healthy overweight/obesity (MHOO), and metabolically unhealthy overweight/obesity (MUOO). Frailty status was assessed by the frailty index (FI) ranging from 0 to 100 and frailty was defined as FI ≥ 25. Linear mixed-effect models were used to analyse the associations of metabolic heterogeneity of obesity with frailty progression.ResultsIn the CHARLS, MUOO and MUNW presented the accelerated FI progression with additional annual increases of 0.284 (95% CI: 0.155 to 0.413, P < 0.001) and 0.169 (95% CI: 0.035 to 0.303, P = 0.013) as compared with MHNW. MHOO presented no accelerated FI progression (β: -0.011, 95% CI: -0.196 to 0.173, P = 0.904) as compared with MHNW. In the ELSA, the accelerated FI progression was marginally significant for MUOO (β: 0.103, 95% CI: -0.005 to 0.210, P = 0.061) and MUNW (β: 0.157, 95% CI: -0.011 to 0.324, P = 0.066), but not for MHOO (β: -0.047, 95% CI: -0.157 to 0.062, P = 0.396) in comparison with MHNW. The associations of MUOO and MUNW with the accelerated FI progression were stronger after excluding the baseline frail participants in both cohorts. The metabolic status changed over time. When compared with stable MHNW, participants who changed from MHNW to MUNW presented the accelerated FI progression with additional annual increases of 0.356 (95% CI: 0.113 to 0.599, P = 0.004) and 0.255 (95% CI: 0.033 to 0.477, P = 0.024) in the CHARLS and ELSA, respectively. The accelerated FI progression was also found in MHOO participants who transitioned to MUOO (CHARLS, β: 0.358, 95% CI: 0.053 to 0.663, P = 0.022; ELSA, β: 0.210, 95% CI: 0.049 to 0.370, P = 0.011).ConclusionsMetabolically unhealthy overweight/obesity and normal weight, but not metabolically healthy overweight/obesity, accelerated frailty progression as compared with metabolically healthy normal weight. Regardless of obesity status, transitions from healthy metabolic status to unhealthy metabolic status accelerated frailty progression as compared with stable metabolically healthy normal weight. Our findings highlight the important role of metabolic status in frailty progression and recommend the stratified management of obesity based on metabolic status.

Dataset Information

Polymorphisms in the neuropeptide Y gene and the risk of obesity: findings from two prospective cohorts.

Publications

Polymorphisms in the neuropeptide Y gene and the risk of obesity: findings from two prospective cohorts.

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