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Gender and genetic differences in bladder smooth muscle PPAR mRNA in a porcine model of the metabolic syndrome

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Abstract

The metabolic syndrome and diabetes are associated with bladder dysfunction in many people. Peroxisome proliferator-activated receptors (PPARs) may play a role in the effects of the metabolic syndrome on bladder smooth muscle (BSM). The purpose of this study was to determine if there are gender and genetic differences in PPAR levels in BSM. We measured PPAR levels using quantitative PCR in BSM from male Yucatan swine and male and female Ossabaw Island swine, which is a model for the metabolic syndrome. Male Ossabaw swine had 0.732 ± 0.111 the amount of PPAR-α mRNA as male Yucatan swine (P < 0.05), suggesting a genetic difference in PPAR-α levels. This difference may possibly contribute to the incidence of metabolic syndrome in the Ossabaw model compared to the Yucatan model. PPAR-δ mRNA was 2-fold higher in male Ossabaw swine than in female Ossabaw swine, with no significant differences in PPAR-α levels. However, PPAR-γ mRNA was 4.067 ± 0.134 times higher in female Ossabaw swine than in their male counterparts (P < 0.001). Changing the percentage of calories derived from fat did not alter any PPAR mRNA levels. Thus, PPAR-δ and PPAR-γ mRNA levels in male and female Ossabaw swine BSM are not only different, but may also result in gender differences in lipid metabolism in bladder smooth muscle. We conclude that PPAR profiles in BSM may contribute to the susceptibility of BSM to lipotoxicity in the metabolic syndrome.

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Acknowledgments

Additional bladder tissue was graciously provided by Dr. Harold Laughlin’s laboratory. We thank members of the Laughlin lab and Sturek lab, particularly Eric Mokelke, for their help in collecting the bladders. We also thank Dr. Ronald Terjung for allowing us use of his ABI 7000.

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Correspondence to Christopher D. Hardin.

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Mattern, H.M., Lloyd, P.G., Sturek, M. et al. Gender and genetic differences in bladder smooth muscle PPAR mRNA in a porcine model of the metabolic syndrome. Mol Cell Biochem 302, 43–49 (2007). https://doi.org/10.1007/s11010-007-9423-8

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  • DOI: https://doi.org/10.1007/s11010-007-9423-8

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