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

Introduction. Increase in body weight is a gradual process that usually begins in childhood and in adolescence as a result of multiple interactions among environmental and genetic factors. This study aimed to analyze the relationship between copy number variants (CNVs) in five genes and four intergenic regions with obesity in Mexican children. Methods. We studied 1423 children aged 6-12 years. Anthropometric measurements and blood levels of biochemical parameters were obtained. Identification of CNVs was performed by real-time PCR. The effect of CNVs on obesity or body composition was assessed using regression models adjusted for age, gender, and family history of obesity. Results. Gains in copy numbers of LEPR and NEGR1 were associated with decreased body mass index (BMI), waist circumference (WC), and risk of abdominal obesity, whereas gain in ARHGEF4 and CPXCR1 and the intergenic regions 12q15c, 15q21.1a, and 22q11.21d and losses in INS were associated with increased BMI and WC. Conclusion. Our results indicate a possible contribution of CNVs in LEPR, NEGR1, ARHGEF4, and CPXCR1 and the intergenic regions 12q15c, 15q21.1a, and 22q11.21d to the development of obesity, particularly abdominal obesity in Mexican children.
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PMID:Copy Number Variations in Candidate Genes and Intergenic Regions Affect Body Mass Index and Abdominal Obesity in Mexican Children. 2842 59

Obesity is a high risk factor for colorectal cancer (CRC). The contribution of underlying epigenetic mechanisms to CRC and the precise targets of epigenetic alterations during cancer development are largely unknown. Several types of epigenetic processes have been described, including DNA methylation, histone modification, and microRNA expression. To investigate the relationship between obesity and CRC, we studied both obese and CRC patients, focusing on genome-wide peripheral blood DNA methylation alterations. Our results show abnormal distributions of overlapping differentially methylated regions (DMRs) such as hypermethylated CpG islands, which may account for epigenetic instability driving cancer initiation in obesity patients. Furthermore, functional analysis suggests that altered DNA methylation of extracellular (e.g., O-glycan processing) and intracellular components contribute to activation of oncogenes (e.g. KRAS and SCL2A1) and suppression of tumor suppressors (e.g. ARHGEF4, EPHB2 and SOCS3), leading to increased oncogenic potency. Our study demonstrates how DNA methylation changes in obesity contribute to CRC development, providing direct evidence of an association between obesity and CRC. It also reveals the diagnostic potential of using DNA methylation as an early risk evaluation to detect patients with high risk for CRC.
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PMID:Genome-wide Analysis Reveals DNA Methylation Alterations in Obesity Associated with High Risk of Colorectal Cancer. 3091 Nov 3