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Naringenin, a citrus flavanone, enhances isoproterenol‐stimulated thermogenic activation of 3T3‐L1 adipocytes
Author(s) -
Zhao Ling,
Bae Jiyoung,
Chen Jiangang
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.691.5
Subject(s) - naringenin , chemistry , thermogenesis , downregulation and upregulation , endocrinology , 3t3 l1 , medicine , stimulation , mapk/erk pathway , adipogenesis , adipocyte , pharmacology , adipose tissue , phosphorylation , biochemistry , biology , flavonoid , antioxidant , gene
Promoting thermogenesis through increasing the activities of functional brown adipocytes has promised new hope for obesity treatment and prevention. Recent evidence has suggested that naringenin, a citrus flavanone, is beneficial for preventing obesity and obesity associated chronic diseases and naringenin is capable of activating nuclear receptors, including PPARγ; however, it has not been reported whether naringenin promotes activities of functional brown adipocytes, similar to what has been reported for rosiglitazone, a synthetic ligand for PPARγ. Here, we investigated the effects of naringenin on browning and isoproterenol (ISO)‐stimulated thermogenic activation of 3T3‐L1 adipocytes. 3T3‐L1 cells were induced to differentiate in the presence or absence of naringenin, followed by stimulation with ISO. We report that naringenin did not increase UCP‐1 expression at basal state; however, it significantly increased the ISO‐stimulated upregulation of UCP‐1 and PGC‐1α and enhanced ISO‐stimulated thermogenesis. Moreover, naringenin enhanced PKA activation and phosphorylation of p38 MAPK downstream of ISO stimulation; and inhibition of either PKA or p38 by their respective pharmacological inhibitors blocked naringenin‐induced upregulation of UCP‐1 mRNA. Our results demonstrate that naringenin enhances ISO‐induced thermogenic activation of 3T3‐L1 adipocytes via PKA/p38 pathways. Support or Funding Information The work was supported in part by UT professional development award to LZ.