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Assessment of Genetic Linkage and Parent-of-Origin Effects on Obesity

Key Laboratory of Biomedical Information Engineering of Ministry of Education and Institute of Molecular Genetics (Y.G., W.W., H.D.), School of Life Science and Technology, Xi’an Jiaotong University, Xi’an 710049, People’s Republic of China; Laboratory of Molecular and Statistical Genetics (Y.G., H.D.), College of Life Sciences, Hunan Normal University, Changsha, Hunan 410081, People’s Republic of China; Osteoporosis Research Center and Department of Biomedical Sciences (Y.G., Yo.L., W.W., D.X., P.X., Ya.L., L.Z., R.R.R.), Creighton University, Omaha, Nebraska 68131; and Departments of Orthopedic Surgery and Basic Medical Sciences (H.S., H.D.), University of Missouri-Kansas City, Kansas City, Missouri 64108

Address all correspondence and requests for reprints to: Hong-Wen Deng, Ph.D., Departments of Orthopedic Surgery and Basic Medical Sciences, University of Missouri-Kansas City, 2411 Holmes Street, Room M3-C03, Kansas City, Missouri 64108-2792. E-mail: dengh{at}umkc.edu.

Context: Obesity is a growing health care problem worldwide and is a major underlying risk factor for common diseases such as diabetes. Parent-of-origin effect has been reported to be involved in the development of obesity. But the genes with imprinting effects related to obesity are largely unknown.

Objective: The objective of the study was to identify obesity-related genetic loci, both with and without imprinting effects.

Design and Subjects: We conducted genome-wide linkage analyses for obesity with and without consideration of imprinting effects in a large sample including more than 4000 individuals. In addition to body mass index (BMI), we also used a more stringent and accurate obesity definition, which simultaneously considers BMI and percentage of fat mass (PFM) in a gender-specific manner. Simulations were performed to identify the genome-wide significant and suggestive significant thresholds.

Results: In nonimprinted linkage analyses, we detected suggestive linkage at 2q31 (LOD = 2.23) and 16q22 (LOD = 1.87) for BMI and 2q37 (LOD = 2.23) for BMI and PFM. Interestingly, 2q37 also achieved a significant maternal linkage with BMI and PFM (LOD=3.34) in imprinted linkage analyses. Imprinted linkage analyses revealed suggestive linkage evidence for BMI at three additional genomic regions, including 3p14 (LOD = 2.20, paternal), 3q24 (LOD = 1.97, maternal), and 19q13 (LOD = 1.81, maternal).

Conclusion: We reported linkage and imprinting effects for obesity on several chromosome regions and suggested the potential importance of parent-of-origin effects and phenotype definition of obesity in delineating the genetic basis of obesity.

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