Abstract

The obesity epidemic in the United States is a serious concern that has driven researchers to determine genetic mechanisms that may contribute to its development. Previous studies in mice have shown that O‐linked N‐acetylglucosamine transferase (OGT) may serve as a satiety factor responsible for controlling food intake and body weight. OGT appears to signal “fullness” in the brain, and decreased OGT expression leads to massive weight gain and development of an obese phenotype in mice. In channel catfish, genetic selection toward increased growth often leads to the increased accumulation of fats in the abdomen, suggesting that channel catfish can be used as a model organism to study obesity development in humans. Screening of the catfish genome database yielded four highly homologous OGT transcripts. Primers were designed to discriminate two major transcripts containing a fifty base pair insert from the other two transcripts. The nucleotide sequence of amplicon corresponding to OGT transcripts was highly similar (>80%) to those of other fish. Because OGT expression in channel catfish has not been previously studied, the OGT expression was examined in the cDNA of brain, spleen, trunk kidney, liver, Brockman's body, and muscle tissues of “normal” phenotype catfish using RT‐PCR. OGT expression was detected in all tissues and was expressed at various levels. Currently, we are using RT‐PCR to determine quantities of OGT in the tissues. In future research, we will compare OGT expression in obese phenotype catfish to normal phenotype catfish and determine if OGT expression is decreased in obese catfish.Support or Funding InformationSupported by the Kansas IDeA Network of Biomedical Research Excellence (P20GM103418)

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