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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)


Obesity (Silver Spring) 2006 Mar
PMID:Comparison of bioelectrical impedance and BMI in predicting obesity-related medical conditions. 1664 20


Obesity (Silver Spring) 2006 Mar
PMID:Rapid infant weight gain predicts childhood overweight. 1664 21


Obesity (Silver Spring) 2006 Mar
PMID:Lifestyle variables, non-traditional cardiovascular risk factors, and the metabolic syndrome in an Aboriginal Canadian population. 1664 22


Obesity (Silver Spring) 2006 Mar
PMID:Obesity is a risk factor for reporting homebound status among community-dwelling older persons. 1664 23


Obesity (Silver Spring) 2006 Mar
PMID:Neighborhood safety, collective efficacy, and obesity in women with young children. 1664 24


Obesity (Silver Spring) 2006 Mar
PMID:BMI and cervical cancer screening among white, African-American, and Hispanic women in the United States. 1607 99

This paper presents the 12th update of the human obesity gene map, which incorporates published results up to the end of October 2005. Evidence from single-gene mutation obesity cases, Mendelian disorders exhibiting obesity as a clinical feature, transgenic and knockout murine models relevant to obesity, quantitative trait loci (QTL) from animal cross-breeding experiments, association studies with candidate genes, and linkages from genome scans is reviewed. As of October 2005, 176 human obesity cases due to single-gene mutations in 11 different genes have been reported, 50 loci related to Mendelian syndromes relevant to human obesity have been mapped to a genomic region, and causal genes or strong candidates have been identified for most of these syndromes. There are 244 genes that, when mutated or expressed as transgenes in the mouse, result in phenotypes that affect body weight and adiposity. The number of QTLs reported from animal models currently reaches 408. The number of human obesity QTLs derived from genome scans continues to grow, and we now have 253 QTLs for obesity-related phenotypes from 61 genome-wide scans. A total of 52 genomic regions harbor QTLs supported by two or more studies. The number of studies reporting associations between DNA sequence variation in specific genes and obesity phenotypes has also increased considerably, with 426 findings of positive associations with 127 candidate genes. A promising observation is that 22 genes are each supported by at least five positive studies. The obesity gene map shows putative loci on all chromosomes except Y. The electronic version of the map with links to useful publications and relevant sites can be found at http://obesitygene.pbrc.edu.
Obesity (Silver Spring) 2006 Apr
PMID:The human obesity gene map: the 2005 update. 1674 Dec 64

Disease management, a system of coordinated health care interventions and communications for chronically ill populations, relies on patient education and case management to engage individuals in the management of their condition. Disease management also aims to enhance the quality of interactions between doctors and patients and advance evidence-based medicine. Because these programs' interventions frequently include helping individuals who suffer comorbidities associated with obesity to reduce their BMI, adaptation of disease management to populations with obesity seems a viable option. A major barrier for implementing disease management for obesity, however, is the lack of proven return on investment, which limits health plan and disease management organization interest. Purchaser demand may overcome this reluctance. Further research is needed to objectively test whether disease management interventions would be clinically effective for obese populations, produce positive financial outcomes for insurers, and enhance workplace productivity.
Obesity (Silver Spring) 2006 Apr
PMID:Obesity disease management opportunities and barriers. 1674 Dec 65

Three polymorphisms of the glutamate decarboxylase 2 gene, which encodes the glutamic acid decarboxylase enzyme, have been associated with severe obesity in a large French cohort. One of these polymorphisms was shown to have functional consequences on promoter expression. Another polymorphism was associated with insulin levels and secretion. These associations were examined in 855 severely obese Utah subjects (mean BMI = 48 kg/m(2)) and a normal-weight and normoglycemic subset (N = 130, mean BMI = 22 kg/m(2)) of a random sample of the Utah population (N = 462). Comparisons of the normal-weight random group with the severely obese group did not result in significant genotype or allele frequency differences for any of the three polymorphisms, C61450A, T83897A, or A-243G (all p > or = 0.18). Haplotypes were also not related to severe obesity (p = 0.10). None of the polymorphisms was significantly related to fasting glucose, insulin levels, or homeostasis model assessment insulin resistance or secretion indices. This study of normal-weight and severely obese subjects from Utah does not provide evidence for involvement of the three genotyped polymorphisms in the glutamate decarboxylase 2 gene with obesity or with insulin- and glucose-related measures associated with obesity.
Obesity (Silver Spring) 2006 Apr
PMID:Lack of association of glutamate decarboxylase 2 gene polymorphisms with severe obesity in utah. 1674 Dec 66

A polymorphism in the promoter region of uncoupling protein 2 gene -866G/A has been associated with its expression levels in adipose tissue, the risk of obesity, and metabolic abnormalities. Our purpose was to examine the associations of -866G/A with body fat and the risk of metabolic syndrome in a random sample of 4018 Asians (1858 men and 2160 women) from three ethnic groups (Chinese, Malay, and Indian). The minor allele frequency of -866G/A polymorphism in South Asians was similar to that in whites. After adjustment for covariates including age, cigarette smoking, and physical activity, the -866A/A genotype was associated with higher waist-to-hip ratio as compared with the wild-type genotype in Chinese and Indian men (p = 0.018 and p = 0.046, respectively). Moreover, Indian men with -866A/A genotype had a significantly increased risk of metabolic syndrome as compared with those homozygous for the wild-type (odds ratio, 2.66; 95% confidence interval, 1.21 to 5.88; p = 0.015). Such a risk was mainly caused by the excess presence of hypertriglyceridemia and central obesity. Our findings indicate that the uncoupling protein 2 gene -866G/A polymorphism may increase the risks of central obesity and metabolic syndrome, with greater effects on Asian men.
Obesity (Silver Spring) 2006 Apr
PMID:Uncoupling protein 2 promoter polymorphism -866G/A, central adiposity, and metabolic syndrome in Asians. 1674 Dec 67


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