Presenter Information

Kacy Richmond, University of Wyoming

Department

Division of Pharmaceutical Sciences, Center for Cardiovascular Research and Alternative Medicine

First Advisor

Subat Turdi

Second Advisor

Jun Ren

Description

Background: Obesity is an independent risk factor for cardiovascular disease. In this study, we observed the effects of tauroursodeoxycholic acid (TUDCA), a known endoplasmic reticulum stress (ER stress) inhibitor, on high-fat diet-induced cardiomyocyte contractile dysfunction in mice. Methods: 3- to 4-month-old C57 mice were fed a low- or high-fat for 20 weeks. High fat-fed mice were subdivided into 2 groups and treated either with TUDCA (300mg/kg.bw.day-1) or natural saline for 15 days prior to the assessment of contractile parameters of isolated ventricular cardiomyocytes including peak cell shortening (PS), time-to-PS (TPS), time-to-90% re-lengthening (TR90) and maximal velocities of shortening and re-lengthening (±dL/dt). Results: High-fat diet depressed PS, ±dL/dt and TR90 compared to the low-fat diet. Interestingly, TUDCA treatment alleviated the depression of PS and ±dL/dt but not TR90. Conclusion: TUDCA may have potential therapeutic implications in treating obesity-induced cardiac dysfunction via a mechanism involving reduced ER stress in the cardiomyocytes, which warrants further studies.

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Tauroursodeoxycholic Acid Alleviates High-Fat Diet-Induced Cardiomyocyte Contractile Dysfunction

Background: Obesity is an independent risk factor for cardiovascular disease. In this study, we observed the effects of tauroursodeoxycholic acid (TUDCA), a known endoplasmic reticulum stress (ER stress) inhibitor, on high-fat diet-induced cardiomyocyte contractile dysfunction in mice. Methods: 3- to 4-month-old C57 mice were fed a low- or high-fat for 20 weeks. High fat-fed mice were subdivided into 2 groups and treated either with TUDCA (300mg/kg.bw.day-1) or natural saline for 15 days prior to the assessment of contractile parameters of isolated ventricular cardiomyocytes including peak cell shortening (PS), time-to-PS (TPS), time-to-90% re-lengthening (TR90) and maximal velocities of shortening and re-lengthening (±dL/dt). Results: High-fat diet depressed PS, ±dL/dt and TR90 compared to the low-fat diet. Interestingly, TUDCA treatment alleviated the depression of PS and ±dL/dt but not TR90. Conclusion: TUDCA may have potential therapeutic implications in treating obesity-induced cardiac dysfunction via a mechanism involving reduced ER stress in the cardiomyocytes, which warrants further studies.