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  • Undergraduate Poster Abstracts
  • THU-367 ANGIOTENSIN RECEPTOR BLOCKADE IMPROVES NON-ESTERIFIED FREE FATTY ACID AND TRIGLYCERIDE ACCUMULATION IN A RAT MODEL OF DIET-INDUCED OBESITY

    • Amy Hang ;
    • Andrew Lee ;
    • Akira Nishiyama ;
    • Rudy Ortiz1 ;

    THU-367

    ANGIOTENSIN RECEPTOR BLOCKADE IMPROVES NON-ESTERIFIED FREE FATTY ACID AND TRIGLYCERIDE ACCUMULATION IN A RAT MODEL OF DIET-INDUCED OBESITY

    Amy Hang1, Andrew Lee1, Akira Nishiyama2, Rudy Ortiz11.

    1University of California, Merced, Merced, CA, 2Kagawa Medical University, Miki-cho, Kita-gun, Kagawa, JP.

    Consumption of a high fat diet (HFD) overburdens the liver’s storage of fatty acids, contributing to non-esterified free fatty acid (NEFA) and triglyceride (TG) accumulation, leading to the development of hepatic steatosis and metabolic syndrome (MetS). Treatment with angiotensin receptor blocker (ARB) was previously shown to decrease hepatic lipid content, possibly improving hepatic steatosis. However, the impact that ARB treatment has on fatty acid storage and the development of hepatic steatosis in a rat model of MetS fed a HFD are unknown. To test the hypothesis that ARB decreases hepatic fatty acid storage in a rat model of MetS fed a HFD, the following groups were studied: Long-Evans Tokushima Otsuka (LETO, control) normal diet (ND), Otsuka Long-Evans Tokushima Fatty (OLETF ND), OLETF HFD (62% fat in food), OLETF ARB (10 mg olmesartan/kg/day), and OLETF HFD + ARB. HFD treatment increased body mass (14%) and liver mass (9%) relative to OLETF. HFD + ARB treatment decreased body mass (48%), liver mass (9%), plasma NEFA (17%), plasma TG (41%), and hepatic TG (44%) compared to HFD. These results demonstrate that ARB decreases hepatic TG accumulation in rats fed a HFD but was unable to completely restore them to control levels, suggesting that other obesity-associated factors are contributing to the impairment.