Document Detail


Reduction of Food Intake by Fenofibrate is Associated with Cholecystokinin Release in Long-Evans Tokushima Rats.
MedLine Citation:
PMID:  22802699     Owner:  NLM     Status:  PubMed-not-MEDLINE    
Abstract/OtherAbstract:
Fenofibrate is a selective peroxisome proliferator-activated receptor α (PPARα) activator and is prescribed to treat hyperlipidemia. The mechanism through which PPARα agonists reduce food intake, body weight, and adiposity remains unclear. One explanation for the reduction of food intake is that fenofibrate promotes fatty acid oxidation and increases the production of ketone bodies upon a standard experimental dose of the drug (100~300 mg/kg/day). We observed that low-dose treatment of fenofibrate (30 mg/kg/day), which does not cause significant changes in ketone body synthesis, reduced food intake in Long-Evans Tokushima (LETO) rats. LETO rats are the physiologically normal controls for Otsuka Long-Evans Tokushima Fatty (OLETF) rats, which are obese and cholecystokinin (CCK)-A receptor deficient. We hypothesized that the reduced food intake by fenofibrate-treated LETO rats may be associated with CCK production. To investigate the anorexic effects of fenofibrate in vivo and to determine whether CCK production may be involved, we examined the amount of food intake and CCK production. Fenofibrate-treated OLETF rats did not significantly change their food intake while LETO rats decreased their food intake. Treatment of fenofibrate increased CCK synthesis in the duodenal epithelial cells of both LETO and OLETF rats. The absence of a change in the food intake of OLETF rats, despite the increase in CCK production, may be explained by the absence of CCK-A receptors. Contrary to the OLETF rats, LETO rats, which have normal CCK receptors, presented a decrease in food intake and an increase in CCK production. These results suggest that reduced food intake by fenofibrate treatment may be associated with CCK production.
Authors:
Mi-Kyoung Park; Ying Han; Mi Sun Kim; Eunhui Seo; Soojeong Kang; So-Young Park; Hyeongjong Koh; Duk Kyu Kim; Hye-Jeong Lee
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Publication Detail:
Type:  Journal Article     Date:  2012-06-26
Journal Detail:
Title:  The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology     Volume:  16     ISSN:  1226-4512     ISO Abbreviation:  Korean J. Physiol. Pharmacol.     Publication Date:  2012 Jun 
Date Detail:
Created Date:  2012-07-17     Completed Date:  2012-10-02     Revised Date:  2013-05-30    
Medline Journal Info:
Nlm Unique ID:  9709505     Medline TA:  Korean J Physiol Pharmacol     Country:  Korea (South)    
Other Details:
Languages:  eng     Pagination:  181-6     Citation Subset:  -    
Affiliation:
Department of Internal Medicine, Medical Science Research Center, Mitochondria Hub Regulation Center, Dong-A University College of Medicine, Busan 602-714, Korea.
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