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Theobromine suppresses adipocyte differentiation through the MAPK pathway in 3T3‐L1 preadipocytes (1037.11)
Author(s) -
Jang Yeonjeong,
Kim Jiyun,
Lee Heeweon,
Pyo Suhkneung
Publication year - 2014
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.28.1_supplement.1037.11
Subject(s) - adipogenesis , adipocyte , 3t3 l1 , mapk/erk pathway , chemistry , phosphorylation , ccaat enhancer binding proteins , oil red o , theobromine , adipocyte protein 2 , lipid droplet , microbiology and biotechnology , protein kinase a , transcription factor , runx2 , endocrinology , medicine , biology , biochemistry , adipose tissue , gene , dna binding protein , caffeine , fatty acid
Theobromine (TB) is an alkaloid belonging to the methylxanthines. It is mainly found in cocoa beans. In this study, we show that the inhibitory effect of TB on adipocyte differentiation in 3T3‐L1 cells by reducing adipogenic gene expression. To investigate the effects of TB on adipocyte differentiation, 3T3‐L1 cells were induced to differentiate using 3‐isobutyl‐1‐methylzanthine, dexamethasone, and insulin (MDI) for 8 days in the presence of 50, 100, and 150 μg/ml TB. TB attenuated the accumulation of lipid droplets stained with Oil Red O in dose‐dependent manner. We also found the effect of TB on the inhibition of adipocyte differentiation occurred during early stage of adipogenesis. To elucidate the anti‐adipogenic mechanism of TB, adipogenic transcription factors, the phosphorylation levels of MAPK, and adipogenic gene expression were analyzed by Western blotting. Treatment of cells with TB resulted in a decrease in the protein level of (Peroxisome proliferator‐activated receptor gamma) PPARγ, (CCAAT/enhancer binding protein beta) C/EBPβ, and phosphorylation of ERK and JNK. These results demonstrate that TB inhibits adipogenic differentiation via suppression of the ERK and JNK signaling pathway during the early stages of adipogenesis.