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Anandamide Increases the Differentiation of Rat Adipocytes and Causes PPARγ and CB1 Receptor Upregulation
Author(s) -
Karaliota Sevasti,
SiafakaKapadai Athanasia,
Gontinou Chrisanthi,
Psarra Katerina,
MavriVavayanni Mary
Publication year - 2009
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1038/oby.2009.177
Subject(s) - anandamide , endocannabinoid system , adipocyte , cannabinoid receptor , endocrinology , medicine , cannabinoid , peroxisome proliferator activated receptor , chemistry , biology , receptor , adipose tissue , agonist
Anandamide ( N ‐arachidonoylethanolamine, AEA) or its metabolites participate in energy balance mainly through feeding modulation. In addition, AEA has been found to increase 3T3–L1 adipocyte differentiation process. In this study, the effect of AEA, R (+)‐methanandamide ( R (+)‐mAEA), URB597, and indomethacin on primary rat adipocyte differentiation was evaluated by a flow cytometry method and by Oil Red‐O staining. Reverse transcription‐PCR and western blotting analysis were performed in order to study the effect of AEA on peroxisome proliferator–activated receptor (PPAR)γ2, cannabinoid receptors (CBRs), fatty acid amidohydrolase (FAAH), and cyclooxygenase‐2 (COX‐2) expression, during the differentiation process. AEA increased adipocyte differentiation in primary cell cultures in a concentration‐ and time‐dependent manner and induced PPARγ2 gene expression, confirming findings with 3T3–L1 cell line. CB1R, FAAH, and COX‐2 expression was also increased while CB2R expression was decreased. Inhibition of FAAH and COX‐2 attenuated the AEA‐induced differentiation. Our findings indicate that AEA regulates energy homeostasis not only by appetite modulation but may also regulate adipocyte differentiation and phenotype.