Molecular Genetic Studies of Porcine Genes for ObesitySwine Research Report, 2002
Extension NumberASL R1803
AbstractThe similarities between humans and pigs at the physiological and genomic levels can provide advantages for the use of the pig as a genetic model for human obesity. Several approaches have been used to identify chromosomal regions or genes affecting obesity-related phenotypes in pigs. Current approaches include the use of candidate genes, quantitative trait loci (QTL) scanning, and gene transcript profiling. Many pig populations have been generated from crosses between breeds with different genetic backgrounds, and QTL analyses in these populations have identified several major pig chromosomal regions that influence obesity-related phenotypes. Homologous human chromosomal regions might be potentially important for genetic causes of human obesity. A single nucleotide polymorphism (SNP) causing an amino acid substitution in the porcine melanocortin-4 receptor (MC4R) gene was significantly associated with increased levels of backfat and similar MC4R mutations resulted in several cases of human obesity. In addition, we have identified several polymorphisms (SNPs) in other candidate genes that are associated with obesity phenotypes. Further analyses of these SNPs will be useful for dissecting the genetics of human obesity. Other published research has included the use of human microarrays to study gene expression in various tissues at different growth stages between young pigs with extremes in fat content. Many of these genes may play a significant role in obesity. New research to integrate these QTL studies, candidate gene discovery, and transcript profiling in pigs can provide novel insights into the genetic components of human obesity and their molecular and physiological mechanisms.
Copyright OwnerIowa State University
Citation InformationKwan-Suk Kim, James M. Reecy, Lloyd L. Anderson and Max F. Rothschild. "Molecular Genetic Studies of Porcine Genes for Obesity" (2003)
Available at: http://works.bepress.com/james_reecy/10/