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Abstract
BackgroundCommon variants rs6232 and rs6235 in the PCSK1 gene have been associated with obesity in European populations. We aimed to evaluate the contribution of these variants to obesity and related traits in Mexican children and adults.Methodology/Principal FindingsRs6232 and rs6235 were genotyped in 2382 individuals, 1206 children and 1176 adults. Minor allele frequencies were 0.78% for rs6232 and 19.99% for rs6235. Rs6232 was significantly associated with childhood obesity and adult class III obesity (OR = 3.01 95%CI 1.64–5.53; P = 4×10−4 in the combined analysis). In addition, this SNP was significantly associated with lower fasting glucose levels (P = 0.01) and with increased insulin levels and HOMA-B (P = 0.05 and 0.01, respectively) only in non-obese children. In contrast, rs6235 showed no significant association with obesity or with glucose homeostasis parameters in any group.Conclusion/SignificanceAlthough rs6232 is rare in the Mexican population, it should be considered as an important risk factor for extreme forms of obesity.
Highlights
The prevalence of obesity has increased worldwide, including Mexico, where more than 70% of the adults and 26% of the children are overweight or obese [1]
SNP rs6232 was significantly associated with obesity in children (OR = 3.78, 95%CI 1.42–9.88; P = 761023) and was significantly associated with class III obesity in adults (OR = 2.61, 95%CI 1.10–6.19; P = 0.02,) showing a trend of association after adjusting for admixture (P = 0.07)
We explored the effect of the rs6232 and rs6235 on glucose homeostasis in non-obese and obese children and in non-diabetic adults
Summary
The prevalence of obesity has increased worldwide, including Mexico, where more than 70% of the adults and 26% of the children are overweight or obese [1]. The discovery of genes causing monogenic forms of obesity such as the prohormone convertase subtilisin/kexin type 1 gene (PCSK1) has greatly improved our understanding of the pathophysiology of obesity [2,3,4]. This gene encodes an enzyme expressed in neuroendocrine cells that converts inactive prohormones into functional key hormones that regulate central and/or peripheral energy metabolism. Loss-of-function mutations in this gene causing childhood obesity and impaired glucose tolerance are rare [5,6,7], two common nonsynonymous variants (rs6232 and rs6235) were recently found to be strongly associated with childhood and adulthood obesity in European population [8]. We aimed to evaluate the contribution of these variants to obesity and related traits in Mexican children and adults
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