β<sub>3</sub>-Adrenergic receptor Trp64Arg polymorphism and increased body mass index in sleep apnoea

Piérola, Javier; Barceló, Antònia; Peña, Mónica de la; Barbé, Ferrán; Soriano, Joan B.; Armengol, Angeles Sánchez; Martı́nez, Carmen; Agustí, Àlvar

doi:10.1183/09031936.00152006

Cited by 20 publications

(12 citation statements)

References 29 publications

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“…This is in accordance with previously reported data from other groups (3,31). Although genetic variants that predispose obesity facilitate the development of OSAS, polymorphisms of several obesity-related genes, including ß 3 -adrenergic receptor (ADRB3) (32), Leptin, and leptin receptor (LEPR) genes (33), are not suggested to associate with OSAS. In the present study, we found that -572G/C polymorphism of IL-6 gene is associated with OSAS susceptibility and severity of sleep-disordered breathing in non-obese subjects, suggested that SNP genotyping of IL-6 gene is a potential strategy for detecting the risk of breathing disordered diseases in non-obese individuals.…”

Section: Discussionsupporting

confidence: 80%

“…In the present study, we found that -572G/C polymorphism of IL-6 gene is associated with OSAS susceptibility and severity of sleep-disordered breathing in non-obese subjects, suggested that SNP genotyping of IL-6 gene is a potential strategy for detecting the risk of breathing disordered diseases in non-obese individuals. Notably, the polymorphisms of the ADRB3 gene favor the development of obesity in patients who already suffer OSAS (32). However, no polymorphisms of IL-6 related to obesity, either in OSAS patients or healthy controls, were found in our investigation.…”

Section: Discussioncontrasting

confidence: 41%

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Genetic variants in interleukin-6 modified risk of obstructive sleep apnea syndrome

Zhang

Liu²,

Li³

et al. 2009

Int J Mol Med

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Abstract. Obesity and inflammation are known to correlate with the pathogenesis of obstructive sleep apnea syndrome (OSAS). Interleukin (IL)-6, an important regulator of obesity and inflammation, was reported to phenotypically increase in patients with OSAS. This study aimed to investigate whether genetic variants in IL-6 confer susceptibility to OSAS. The study population consisted of 151 patients with OSAS and 75 healthy controls from Southeast China. Five haplotype-tagging single nucleotide polymorphisms (tSNPs) were selected across 21 kb of the IL-6 locus using Haploview software V4.1. The tSNPs were amplified by polymerase chain reaction (PCR) and genotyped by restriction enzyme digestion followed by gel electrophoresis. Linkage disequilibrium (LD) and haplotype reconstruction were carried out by means of a SHEsis program. No distribution difference of any of the five tSNPs between OSAS patients and controls was observed. However, in nonobese individuals (n=117), the minor allele G (rs1800796) decreased risk of OSAS compared with the major allele C [odds ratio (OR), 0.48; 95% confidence interval (CI), 0.26-0.86; p=0.014], and the haplotype TG (rs1880242, rs1800796) conferred a significantly decreased risk of OSAS than single allele G (rs1800796) (OR, 0.39; 95% CI, p=0.003). Moreover, the severity of sleep-disordered breathing (measured by apnea hypopnea index) increased linearly in carriers of the C variant of IL-6 -572G/C polymorphism (14.3±5.1, 22.0±3.6 and 34.8±3.5 for GG, CG and CC, respectively; p=0.012). To the best of our knowledge, this is the first study to suggest that genetic variants in IL-6 could modify OSAS susceptibility. SNP genotyping of IL-6 is a potential strategy for detecting the risk of breathing disordered diseases in non-obese individuals.

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Section: Discussionsupporting

confidence: 80%

Section: Discussioncontrasting

confidence: 41%

Genetic variants in interleukin-6 modified risk of obstructive sleep apnea syndrome

Zhang

Liu²,

Li³

et al. 2009

Int J Mol Med

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“…In humans, the beta-3 adrenergic receptor is predominantly expressed in visceral adipose tissue (Krief et al, 1993). Notably, the Arg allele of this SNP has been linked with increased BMI, adiposity and obesity in children (Arashiro et al, 2003;Endo et al, 2000;Erhardt et al, 2005;Ochoa et al, 2004;Park et al, 2005) supporting the evidence in adults Pierola et al, 2007), and the increased risk for obesity at this ADRB3 loci may be driven partly by an interaction effect of the PPARG SNP Pro12Ala Hsueh et al, 2001;Ochoa et al, 2004). Other studies in young children between the ages 4-10 years and in adolescents report no signifi cant effects of Trp64Arg variants on BMI, weight or height when this variant is examined in isolation (Cecil et al, 2007;Haworth et al, 2008a;Hinney et al, 1997;Kurokawa et al, 2003).…”

Section: Adrenergic Receptor Gene Variants -A Role In Polygenic Obesisupporting

confidence: 51%

Obesity and eating behaviour in children and adolescents: Contribution of common gene polymorphisms

Cecil

Dalton

Finlayson

et al. 2012

International Review of Psychiatry

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The prevalence of childhood obesity is increasing in many countries and confers risks for early type 2 diabetes, cardiovascular disease and metabolic syndrome. In the presence of potent ' obesogenic ' environments not all children become obese, indicating the presence of susceptibility and resistance. Taking an energy balance approach, susceptibility could be mediated through a failure of appetite regulation leading to increased energy intake or via diminished energy expenditure. Evidence shows that heritability estimates for BMI and body fat are paralleled by similar coeffi cients for energy intake and preferences for dietary fat. Twin studies implicate weak satiety and enhanced food responsiveness as factors determining an increase in BMI. Single gene mutations, for example in the leptin receptor gene, that lead to extreme obesity appear to operate through appetite regulating mechanisms and the phenotypic response involves overconsumption and a failure to inhibit eating. Investigations of robustly characterized common gene variants of fat mass and obesity associated ( FTO ), peroxisome proliferator-activated receptor ( PPARG ) and melanocortin 4 receptor ( MC4R ) which contribute to variance in BMI also infl uence the variance in appetite factors such as measured energy intake, satiety responsiveness and the intake of palatable energy-dense food. A review of the evidence suggests that susceptibility to childhood obesity involving specifi c allelic variants of certain genes is mediated primarily through food consumption (appetite regulation) rather than through a decrease in activity-related energy expenditure. This conclusion has implications for early detection of susceptibility, and for prevention and management of childhood obesity.

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“…The BMI of the OSAS group was higher when compared with the individuals in the control group. The BMI results for OSAS patients showed similarity with those of other polymorphism studies (Barceló et al, 2001;Rubinsztajn et al, 2004;Sakai et al, 2005;Piérola et al, 2007).…”

Section: Discussionsupporting

confidence: 75%

Lack of association of ACE gene I/D polymorphism with obstructive sleep apnea syndrome in Turkish patients

Yakut

Karkucak²,

Ursavaş³

et al. 2010

Genet. Mol. Res.

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ABSTRACT. Angiotensin-converting enzyme (ACE) is a vital enzyme in the renin-angiotensin-aldosterone system, and there are reports in the literature describing its role in the development of cardiovascular system diseases, with I/D polymorphism of the ACE gene. We examined the relationship between a patient group with obstructive sleep apnea syndrome (OSAS) and a control group in terms of I/D polymorphism of the ACE gene. We examined 64 patients, with 37 individuals serving as the control group. PCR was used to detect ACE I/D gene polymorphism. Genotype was determined according to the bands that formed on agarose gel electrophoresis. Among the 64 OSAS patients, 27 were identified with the ID genotype, 27 with the DD genotype and 10 with the II genotype; among the 37 control subjects, 19 were identified with the ID genotype, 11 with the DD genotype and 7 with the II genotype. When the case group and controls were compared in terms of ID, II and DD genotypes, no significant difference was observed. On the other hand, when the two groups were compared with respect to mean body 735 ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 9 (2): 734-738 (2010) ACE gene I/D polymorphism in obstructive sleep apnea syndrome mass index, the OSAS group was found to be significantly different from the control group (P = 0.009). We conclude that ACE I/D gene polymorphism is not a genetic risk factor for OSAS in Turkish patients.

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β₃-Adrenergic receptor Trp64Arg polymorphism and increased body mass index in sleep apnoea

Cited by 20 publications

References 29 publications

Genetic variants in interleukin-6 modified risk of obstructive sleep apnea syndrome

Genetic variants in interleukin-6 modified risk of obstructive sleep apnea syndrome

Obesity and eating behaviour in children and adolescents: Contribution of common gene polymorphisms

Lack of association of ACE gene I/D polymorphism with obstructive sleep apnea syndrome in Turkish patients

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β3-Adrenergic receptor Trp64Arg polymorphism and increased body mass index in sleep apnoea

Cited by 20 publications

References 29 publications

Genetic variants in interleukin-6 modified risk of obstructive sleep apnea syndrome

Genetic variants in interleukin-6 modified risk of obstructive sleep apnea syndrome

Obesity and eating behaviour in children and adolescents: Contribution of common gene polymorphisms

Lack of association of ACE gene I/D polymorphism with obstructive sleep apnea syndrome in Turkish patients

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Product

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β₃-Adrenergic receptor Trp64Arg polymorphism and increased body mass index in sleep apnoea