title: Caffeic acid phenethyl ester suppresses the production of adipocytokines, leptin, tumor necrosis factor -alpha and resistin, during differentiation to adipocytes in 3T3-L1 cells.
abstract: We previously reported that caffeic acid phenethyl ester (CAPE) suppresses 3T3-L1 differentiation to adipocytes through the inhibition of peroxisome proliferator-activated receptor (PPAR) gamma, CCAAT/enhancer-binding protein (C/EBP) alpha, fatty acid synthase (Fas) and adipocytes-specific fatty acid binding protein 2 (aP2) expressions (Juman et al., Biol. Pharm. Bull., 33, 1484-1488 (2010)). In the present study, we confirmed that CAPE had inhibitory effects on increased glycerol-3-phosphate dehydrogenase (GPDH) activity and an increased insulin receptor substrate 1 (IRS-1). Our data show that treatment with 50 µM CAPE significantly reduced the levels of leptin (p<0.05), resistin (p<0.05) and tumor necrosis factor (TNF)-alpha (p<0.05) which are known to aid adipocytokines production in adipocytes. In 3T3-L1 cells, treatment of CAPE decreased the triglyceride deposition similar to resveratrol, which is known to have an inhibitory effect on 3T3-L1 differentiation to adipocytes. In conclusion, we found that CAPE suppresses the production and secretion of adipocytokines from mature adipocytes in 3T3-L1 cells.
authors.affiliation: School of Pharmacy and Pharmaceutical Sciences, Mukogawa Women's University, Koshien Kyuban-cho, Nishinomiya, Japan. manju129@mukogawa-u.ac.jp
authors.forename: Sachiko
authors.initials: S
authors.lastname: Juman
authors.forename: Naomi
authors.initials: N
authors.lastname: Yasui
authors.forename: Hiroto
authors.initials: H
authors.lastname: Okuda
authors.forename: Ai
authors.initials: A
authors.lastname: Ueda
authors.forename: Hiroko
authors.initials: H
authors.lastname: Negishi
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Miki
authors.forename: Katsumi
authors.initials: K
authors.lastname: Ikeda
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D054392:Adipokines / Q000096:biosynthesis*; D000818:Animals; D002109:Caffeic Acids / Q000494:pharmacology*; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology; D005993:Glycerolphosphate Dehydrogenase / Q000037:antagonists & inhibitors; D055504:Insulin Receptor Substrate Proteins / Q000037:antagonists & inhibitors; D020738:Leptin / Q000096:biosynthesis*; D051379:Mice; D010626:Phenylethyl Alcohol / Q000031:analogs & derivatives* / Q000494:pharmacology; D011429:Propolis / Q000737:chemistry*; D052243:Resistin / Q000096:biosynthesis*; D000077185:Resveratrol; D013267:Stilbenes / Q000494:pharmacology; D014280:Triglycerides / Q000096:biosynthesis; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*
chemical_list: D054392:Adipokines; D002109:Caffeic Acids; D055504:Insulin Receptor Substrate Proteins; D020738:Leptin; D052243:Resistin; D013267:Stilbenes; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D011429:Propolis; D005993:Glycerolphosphate Dehydrogenase; C055494:caffeic acid phenethyl ester; D010626:Phenylethyl Alcohol; D000077185:Resveratrol