Polymorphisms of adiponectin and resistin genes in patients with obesity and anorexia nervosa
Adiponectin and resistin are hormones that may represent a link between obesity and insulin resistance. Genes for these hormones are new candidate genes of insulin resistance and type 2 diabetes mellitus. The aim of our study was to determine the frequency of single nucleotide polymorphisms 45T > G and 276T > G of adiponectin gene and 62G > A and -180C > G of resistin gene in patients with obesity, anorexia nervosa and in lean women and to study the influence of particular genotypes on serum concentrations of these hormones.
Serum adiponectin, resistin, TNF-alfa and insulin levels were measured in 51 patients with obesity, 17 with anorexia nervosa and 17 lean women. DNA analysis was carried out by means of polymerase chain reaction (PCR) with restriction analysis of PCR product (RFLP). Adiponectin levels were lowest in obese women and highest in anorexia nervosa patients. Resistin concentrations were lowest in anorexia nervosa and highest in obese patients. Genotype analysis within respective groups showed no differences in assessed parameters when comparing different adiponectin and resistin polymorphisms. The only difference detected was significantly higher BMI in G/G genotype relative to T allele carries in 276 position of ADP gene in control group (23.48 +/- 0.85 vs. 19,7 +/- 0.95, p < 0.05). In anorexia nervosa patients, frequency of G allele in RETN -180 polymorphism was significantly higher relative to control group (p < 0.05).
Polymorphisms 45T > G a 276T > G of ADP gene and 62G>A and -180C > G RETN gene did not influence serum ADP and RETN concentrations. BMI was influenced by T allele presence in 276 position of ADP gene in control group only. Anorexia nervosa patients had higher frequency of G allele of RETN -180 polymorphism compared to healthy women.
Available from: Swayam Prakash
- "The presence of the adeponectin 276 variant T allele was accompanied by higher adiponectin concentrations in obese patients (Krízová et al., 2008). However, the adeponectin 45 and 276 polymorphisms and the resistin 420 polymorphisms did not influence serum adeponectin and resistin concentrations (Dolinková et al., 2006). "
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ABSTRACT: The adipokines produced from adipose tissues influence energy homeostasis, resulting in alterations of the adipokine concentrations. This process may be associated with fertility impairment, resulting in recurrent miscarriage. The present study investigated whether there was any association between the UCP2 45-bp indel polymorphism and the adipokine gene polymorphisms, namely leptin 2549 (C/A), adeponectin 276 (G/T) and 45 (T/G) and resistin 420 (C/G) in 200 non-obese recurrent miscarriage patients and 300 ethnically matched negative controls. These markers were studied using gene-specific PCR single specific primer and restriction fragment length polymorphism. For leptin 2549 and adeponectin 276, the A allele and G allele showed 3.42-fold (P = 0.0001) and 1.36-fold (P = 0.036) increased risk of recurrent miscarriage, respectively. Combined analysis of UCP2 45-bp indel and leptin 2549 showed U0-L0 and U1-L0 variants to be at 2- and 3-fold increased associative risk, respectively. Combined analysis of leptin 2549 and adeponectin 276 showed L0-D0 and L0-D1 variants to be at 2- and 4-fold increased associative risk, respectively. The combination U1-L0-D1-A1-R1 was 4.39-fold higher (P = 0.0007) among recurrent miscarriage patients. In conclusion, the results highlight the role of the studied adipokine and UCP2 polymorphisms in recurrent miscarriage among the North Indian non-obese population.
Reproductive biomedicine online 07/2012; 25(5). DOI:10.1016/j.rbmo.2012.07.006 · 3.02 Impact Factor
Available from: Yonghua Hu
- ".48 ± 0.85 kg/m 2 vs. 19.7 ± 0.95 kg/m 2 , p < 0.05) (Dolinkova et al., 2006 "
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ABSTRACT: The purpose of this study was to estimate the heritability of obesity-related phenotypes and investigate the association of adiponectin gene polymorphisms +45T>G and +276G>T with these measures in Chinese twins. 1260 twin pairs were recruited from two cities through the Chinese National Twin Registry System from 2001 to 2005. Two SNPs at the adiponectin locus (+45T>G and +276G>T) were genotyped. Structural equation modeling (SEM) was used to estimate heritability and the best-fitting variance component model. The regular association among all twins was analysed with generalised estimating equations (GEE). Sib-transmission/disequilibrium test (TDT) within dizygotic (DZ) twin pairs discordant for their genotype was performed using SEM. Additive genetic, common and unique environmental (ACE) model-based heritability of body mass index (BMI) was 61%, while additive genetic and unique environmental (AE)-model-based heritability of waist circumference (WC) and waist-hip ratio (WHR) were 75% and 61%, respectively. There was no association of adiponectin gene +45T>G and +276G>T genotypes with obesity-related phenotypes in all twins or discordant DZ twins. Our twins data did not support that there was an association between adiponectin gene polymorphisms +45T>G and +276G>T and the obesity-related phenotypes. Further studies are required to better understand the role of adiponectin gene polymorphisms in obesity.
Annals of Human Genetics 03/2010; 74(2):146-54. DOI:10.1111/j.1469-1809.2010.00565.x · 2.21 Impact Factor
Available from: cuni.cz
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ABSTRACT: Anorexia nervosa (AN) is an eating disorder affecting mostly young people which could lead to serious complications and consequences. There are ethnical and gender differences in the incidence and prevalence of AN, but the influence of urbanization has not yet been proved. The relationship of genetic background to the risk of AN is still being investigated. In this review we summarize current knowledge about the relationship between AN and polymorphism of substances known to be regulating eating behaviour or metabolic pathways e.g. serotonin, ghrelin, catechol-O-methyl transferase, neuropeptide Y, brain-derived neurotrophic factor and adipokines.
Prague medical report 02/2007; 108(3):215-25.
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