Dietary naringenin increases hepatic peroxisome proliferators-activated receptor α protein expression and decreases plasma triglyceride and adiposity in rats.
BACKGROUND
Naringenin, a flavonoid present in grapefruit, has recently been shown to exert hypolipidemic and hypocholesterolemic effects, which has a particular importance for protecting against chronic diseases. However, the lipid-lowering potential of naringenin at the concentrations in the dietary range and its underlying mechanisms have yet to be fully elucidated.


OBJECTIVE
The aim of the present study was (1) to investigate the effects of dietary naringenin on plasma and hepatic triglyceride and cholesterol levels and on adipose deposition in rat and (2) to determine the contribution of hepatic peroxisome proliferators-activated receptor α (PPARα) expression to fatty acid oxidation.


METHODS
Male Long-Evans hooded rats were fed a diet supplemented with naringenin (0.003, 0.006, and 0.012%) for 6 weeks. We analyzed plasma and hepatic lipid contents and determined the protein expression of PPARα, carnitine-palmitoyl transferase 1L (CPT-1), and uncoupling protein 2 (UCP2), all of which are critical genes for fatty acid oxidation.


RESULTS
Naringenin supplementation caused a significant reduction in the amount of total triglyceride and cholesterol in plasma and liver. In addition, naringenin supplementation lowered adiposity and triglyceride contents in parametrial adipose tissue. Naringenin-fed animals showed a significant increase in PPARα protein expression in the liver. Furthermore, expression of CPT-1 and UCP2, both of which are known to be regulated by PPARα, was markedly enhanced by naringenin treatment.


CONCLUSIONS
Our results indicate that the activation of PPARα transcription factor and upregulation of its fatty acid oxidation target genes by dietary naringenin may contribute to the hypolipidemic and anti-adiposity effects in vivo.
Cho
Kae Won
KW
Department of Nutrition, University of Massachusetts, Amherst, MA 10003, USA.
Kim
Yong Ook
YO
Andrade
Juan E
JE
Burgess
John R
JR
Kim
Young-Cheul
YC
D000273:Adipose Tissue / Q000378:metabolism; D050154:Adiposity; D000818:Animals; D002334:Carnitine O-Palmitoyltransferase / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D032083:Citrus paradisi / Q000737:chemistry; D004032:Diet; D044950:Flavanones / Q000494:pharmacology*; D000960:Hypolipidemic Agents / Q000494:pharmacology*; D007473:Ion Channels / Q000378:metabolism; D050356:Lipid Metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D024101:Mitochondrial Proteins / Q000378:metabolism; D047493:PPAR alpha / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D020318:Rats, Long-Evans; D014157:Transcription Factors / Q000378:metabolism; D014280:Triglycerides / Q000097:blood*; D000071246:Uncoupling Protein 2
D044950:Flavanones; D000960:Hypolipidemic Agents; D007473:Ion Channels; D024101:Mitochondrial Proteins; D047493:PPAR alpha; D014157:Transcription Factors; D014280:Triglycerides; C000604391:Ucp2 protein, rat; D000071246:Uncoupling Protein 2; D002784:Cholesterol; D002334:Carnitine O-Palmitoyltransferase; C005273:naringenin