Dataset Information

Association between the interaction of SMAD3 polymorphisms with body mass index and osteoarthritis susceptibility.

ABSTRACT: This study aimed to investigate the relationship between the interaction of SMAD3 polymorphisms (rs12102171 and rs2289263) with body mass index (BMI) and osteoarthritis (OA) susceptibility.This study involved 112 OA patients and 120 healthy people. The controls were frequency-matched with the cases by age and sex. Hardy-Weinberg equilibrium (HWE) was tested by ?(2) test in the control group. The rs12102171 and rs2289263 polymorphisms were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The relative risk of OA was represented by odds ratio (OR) with 95% confidence interval (CI) calculated by chi-squared test. Gene-environment interaction was analyzed by crossover analysis.The TT genotype and T allele of SMAD3 rs12102171 polymorphism were more frequent in case than control groups (P=0.04 in both of two polymorphisms), which increased the risk of OA (OR=3.39, 95% CI=1.03-11.11 and OR=1.64, 95% CI=1.03-2.59). GG genotype and G allele were also the risk factors for OA (OR=3.22, 95% CI=1.09-9.51 and OR=1.57, 95% CI=1.02-2.42). The BMI had interactions with genotype CC and CT+TT of rs12102171 and TT and TG+GG of rs2289263 (rs12102171: OR=2.15, P=0.02 and OR=3.99, P=1.00×10(-3); rs2289263: OR=2.73, P=4.00×10(-3) and OR=4.67, P=0).CC and CT+TT and TT and TG+GG genotypes of SMAD3 rs12102171 and rs2289263 polymorphisms together with BMI may be susceptible factors to OA, and interactions there between can possibly confer risk to OA.

SUBMITTER: Kang B

PROVIDER: S-EPMC4525971 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature

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Association between the interaction of SMAD3 polymorphisms with body mass index and osteoarthritis susceptibility.

Kang Baolin B Zhao Feng F Zhang Xin X Deng Xiao X He Xijing X

International journal of clinical and experimental pathology 20150601 6

<h4>Purpose</h4>This study aimed to investigate the relationship between the interaction of SMAD3 polymorphisms (rs12102171 and rs2289263) with body mass index (BMI) and osteoarthritis (OA) susceptibility.<h4>Methods</h4>This study involved 112 OA patients and 120 healthy people. The controls were frequency-matched with the cases by age and sex. Hardy-Weinberg equilibrium (HWE) was tested by χ(2) test in the control group. The rs12102171 and rs2289263 polymorphisms were genotyped by polymerase c ...[more]

PMID: 26261637

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Project description:BackgroundDietary fiber reduces body weight and inflammation in clinical trials. It is unclear whether body mass index (BMI) and inflammation might explain the observed association between higher fiber intake and the lower risk of symptomatic knee osteoarthritis (SXKOA).ObjectivesWe quantified the extent to which BMI and inflammation influenced the relation between dietary fiber and SXKOA.MethodsWe used longitudinal data from the Osteoarthritis Initiative (OAI) and the Framingham Offspring Osteoarthritis Study. At baseline of each study, men and women (mean age: 61 y) with or at risk of knee osteoarthritis were followed for 48 mo in the OAI. Adults (mean age: 53 y) were followed for 9.5 y in the Framingham study. Dietary fiber intake was estimated using a validated food-frequency questionnaire. Measured weight and height were used to calculate BMI. Serum high-sensitivity C-reactive protein (CRP) was measured in the Framingham study only. Incident SXKOA was defined as new onset of a combination of knee pain and radiographic osteoarthritis. We applied marginal structural models to quantify the mediation through BMI in the OAI and the sequential mediation through BMI and CRP in the Framingham study.ResultsIncident SXKOA occurred in 861 knees among 2876 persons in the OAI and in 143 knees among 971 persons in the Framingham study. In persons whose fiber intake was ≥21 g/d compared with those with intakes <21 g/d, the OR (95% CI) was 0.70 (0.53, 0.91) for the overall association with SXKOA and was 0.93 (0.92, 0.95) for the mediation via BMI (per kg/m2) in the OAI. In the Framingham study, the overall association was 0.57 (0.30, 1.09), the mediation through BMI (via BMI and the influence of BMI on CRP) was 0.94 (0.85, 1.02), and the mediation through CRP (per milligram per liter) was 0.99 (0.84, 1.19).ConclusionOur findings suggest that the inverse association of fiber intake and the risk of incident symptomatic knee osteoarthritis is partially mediated by BMI.

Project description:INTRODUCTION:The role of genetic factors influencing osteoarthritis (OA) susceptibility is well documented and several candidate genes have been identified to be associated with it. Among these genes are Bone Morphogenetic Protein 5 (BMP5) and Smad family member 3 (SMAD3), all involved in Transforming Growth Factor (TGF) signaling pathway. The knee is the commonly affected joint, and knee OA has an especially high prevalence in Asian population. AIM:To investigate associations between Single Nucleotide Polymorphisms (SNPs) rs12901499 in SMAD3 and rs921126 in the BMP5 gene with knee OA susceptibility in and around Lucknow, Uttar Pradesh, India. MATERIALS AND METHODS:SNPs rs12901499 in SMAD3 and rs921126 in BMP5 were genotyped in patients with knee OA and age- sex matched OA-free controls from our population. A total of 450 patients with knee OA and 458 controls were enrolled in the study. Venous blood samples were obtained from all cases as well as controls for PCR-RFLP (Polymerase Chain Reaction- Restriction Fragment Length Polymorphism). Data was collected and entered in excel sheets. Statistical analyses of the data were performed using statistical software package SPSS version 16.0. Chi-square, Student's t-test and logistic regression tests were used to analyse the data. RESULTS:GA and GG genotypes of both SNPs (rs12901499 and rs921126), and variant G, were associated with a significantly increased risk of knee OA. A significantly increased risk of knee OA was associated with the genotype GG and GA of rs12901499 (p < 0.03 and p <0.004 respectively) and rs921126 (p< 0.0001 and p<0.001 respectively) compared with the AA genotype. In addition, those bearing at least one G allele (GG + GA) had a significantly increased risk of knee OA compared with those without the G allele (AA) in rs921126 (p< 0.0001). However, in rs12901499, significant association with the risk of knee OA was not found (p<0.4). On age and gender based stratification, the association between the risk of OA and rs921126 GG mutant compared with AA homozygotes was strong in both gender (adjusted OR= 2.93 for male and 2.25 for female) and in those aged >55 years (adjusted OR= 3.4), similarly in rs12901499, GG mutant compared with AA homozygote was strong in female (adjusted OR= 1.5) and in those aged >55 years (adjusted OR= 1.5). CONCLUSION:The results showed that both in SMAD3 rs12901499 and BMP5 921126, G allele is significantly associated with knee OA. A to G change and variant G genotype may contribute to knee OA risk in our study population of Lucknow.

Project description:BackgroundCircadian rhythms play an important role in the regulation of eating and fasting, and mistimed dietary intakes may be detrimental to metabolic health. Extended overnight fasting has been proposed as a strategy to better align the eating-fasting cycle with the internal circadian clock, and both observational and experimental studies have linked longer overnight fasting with lower body weight. However, it remains unclear if the timing of overnight fasting modifies the relationship between fasting duration and weight outcomes.MethodsThe current study included 495 men and 499 women age 50-74 years. Dietary intake over 12 months was assessed by 24-h dietary recalls every two months, and body-mass index was measured at the beginning, middle and end of the study. Logistic regression was used to estimate the relationship between overnight fasting duration and the likelihood of being overweight or obesity adjusted for multiple confounders, and assessed whether the relationship was modified by the timing of overnight fasting, measured as the midpoint of the fasting period.ResultsAmong participants with early overnight fasting (midpoint < 02:19 am), a longer fasting duration was associated with lower odds of overweight and obesity; while among those with late fasting (≥02:19 am), longer fasting was associated with higher odds of overweight and obesity. Specifically, when compared to the shortest quintile of overnight fasting duration, the longest quintile was associated with a 53% reduction in the odds of overweight and obesity in the early fasting group (OR = 0.47, 95% CI = 0.23, 0.97), but a 2.36-fold increase in the late fasting group (OR = 3.36, 95% CI = 1.48, 7.62). Additionally adjusting for dietary intakes during morning and late evening periods did not affect the observed associations.ConclusionsLonger overnight fasting was associated with a reduced likelihood of being overweight or obese, but only among those with an early timing of fasting.

Project description:To evaluate the associations between six single-nucleotide polymorphisms (SNPs) in intron 1 of FTO and body mass index (BMI), a case-control association study of 2314 unrelated Mexican-Mestizo adult subjects was performed. The association between each SNP and BMI was tested using logistic and linear regression adjusted for age, gender, and ancestry and assuming additive, recessive, and dominant effects of the minor allele. Association analysis after BMI stratification showed that all five FTO SNPs (rs1121980, rs17817449, rs3751812, rs9930506, and rs17817449), were significantly associated with obesity class II/III under an additive model (P<0.05). Interestingly, we also documented a genetic model-dependent influence of gender on the effect of FTO variants on increased BMI. Two SNPs were specifically associated in males under a dominant model, while the remainder were associated with females under additive and recessive models (P<0.05). The SNP rs9930506 showed the highest increased in obesity risk in females (odds ratio = 4.4). Linear regression using BMI as a continuous trait also revealed differential FTO SNP contributions. Homozygous individuals for the risk alleles of rs17817449, rs3751812, and rs9930506 were on average 2.18 kg/m(2) heavier than homozygous for the wild-type alleles; rs1121980 and rs8044769 showed significant but less-strong effects on BMI (1.54 kg/m(2) and 0.9 kg/m(2), respectively). Remarkably, rs9930506 also exhibited positive interactions with age and BMI in a gender-dependent manner. Women carrying the minor allele of this variant have a significant increase in BMI by year (0.42 kg/m(2), P = 1.17 x 10(-10)). Linear regression haplotype analysis under an additive model, confirmed that the TGTGC haplotype harboring all five minor alleles, increased the BMI of carriers by 2.36 kg/m(2) (P = 1.15 x 10(-5)). Our data suggest that FTO SNPs make differential contributions to obesity risk and support the hypothesis that gender differences in the mechanisms involving these variants may contribute to disease development.

Project description:ImportanceAlthough high body mass index (BMI) is associated with adverse birth outcomes, the association with severe maternal morbidity is unclear.ObjectiveTo examine the association between prepregnancy BMI and severe maternal morbidity.Design, setting, and participantsRetrospective population-based cohort study including all singleton hospital births in Washington State, 2004-2013. Demographic data and morbidity diagnoses were obtained from linked birth certificates and hospitalization files.ExposuresPrepregnancy BMI (weight in kilograms divided by height in meters squared) categories included underweight (<18.5), normal BMI (18.5-24.9), overweight (25.0-29.9), obesity class 1 (30.0-34.9), obesity class 2 (35.0-39.9), and obesity class 3 (≥40).Main outcomes and measuresComposite severe maternal morbidity or mortality included life-threatening conditions and conditions leading to serious sequelae (eg, amniotic fluid embolism, hysterectomy), complications requiring intensive care unit admission, and maternal death. Logistic regression was used to obtain adjusted odds ratios (ORs) and adjusted rate differences with 95% confidence intervals, adjusted for confounders (eg, maternal age and parity).ResultsOverall, 743 630 women were included in the study (mean age, 28.1 [SD, 6.0] years; 41.4% nulliparous). Prepregnancy BMI was distributed as follows: underweight, 3.2%; normal weight, 47.5%; overweight, 25.8%; obesity class 1, 13.1%; obesity class 2, 6.2%; and obesity class 3, 4.2%. Rates of severe maternal morbidity or mortality were 171.5, 143.2, 160.4, 167.9, 178.3 and 202.9 per 10 000 women, respectively. Adjusted ORs were 1.2 (95% CI, 1.0-1.3) for underweight women; 1.1 (95% CI, 1.1-1.2) for overweight women; 1.1 (95% CI, 1.1-1.2) for women with class 1 obesity; 1.2 (95% CI, 1.1-1.3) for women with class 2 obesity; and 1.4 (95% CI, 1.3-1.5) for women with class 3 obesity compared with women with normal BMI. Absolute risk increases (adjusted rate differences per 10 000 women, compared with women with normal BMI) were 28.8 (95% CI, 12.2-47.2) for underweight women, 17.6 (95% CI, 10.5-25.1) for overweight women, 24.9 (95% CI, 15.7-34.6) for women with class 1 obesity, 35.8 (95% CI, 23.1-49.5) for women with class 2 obesity, and 61.1 (95% CI, 44.8-78.9) for women with class 3 obesity.Conclusions and relevanceAmong pregnant women in Washington State, low and high prepregnancy BMI, compared with normal BMI, were associated with a statistically significant but small absolute increase in severe maternal morbidity or mortality.

Dataset Information

Association between the interaction of SMAD3 polymorphisms with body mass index and osteoarthritis susceptibility.

Publications

Association between the interaction of SMAD3 polymorphisms with body mass index and osteoarthritis susceptibility.

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