Wen-pi-tang-Hab-Wu-ling-san, a Polyherbal Medicine, Attenuates ER Stress in 3T3-L1 Preadipocytes by Promoting the Insulin Signaling Pathway

• Published in: Evidence-based complementary and alternative medicine 2013-01, Vol.2013 (2013), p.1-5
• Main Authors: Han, Yunkyung, Jung, Hyo Won, Bae, Hyo Sang, Park, Yong-Ki
• Format: Article
• Language: English
• Subjects: 1-Phosphatidylinositol 3-kinase; Adipocytes; c-Jun protein; CCAAT/enhancer-binding protein; Chemical compounds; Diabetes; Diabetes mellitus; Diabetes mellitus (non-insulin dependent); Endoplasmic reticulum; Enzymes; Glucose; Homology; Initiation factor eIF-2α; Insulin; Insulin receptor substrate 1; Insulin resistance; Investigations; Ischemia; Kinases; Medicine; Obesity; Phosphorylation; Physiology; Preadipocytes; Protein kinase; Proteins; Signal transduction; Stress; Stress response; Terminal protein; Transcription factors; Tunicamycin
• ISSN: 1741-427X; 1741-4288
• DOI: 10.1155/2013/825814

The endoplasmic reticulum (ER) is an organelle that functions to synthesize, fold, and transport proteins. ER stress is a key link between type 2 diabetes (T2D), obesity, and insulin resistance. In this study, we investigated the effect of WHW on the ER stress response and the insulin signaling pathway in 3T3-L1 preadipocytes. 3T3-L1 preadipocytes were differentiated into adipocytes, and ER stress was then induced by treatment with tunicamycin. ER stress-induced adipocytes were treated with different concentrations of WHW for 24 h. The expression of ER stress-related molecules such as X-box-binding protein-1 (XBP-1), glucose-regulated protein 78 (GRP78), C/EBP-homologous protein 10 (CHOP10), and eukaryotic initiation factor 2α (eIF2α) and signaling molecules such as phosphatidylinositol 3-kinase (PI3K), insulin receptor substrates-1 (IRS-1), and c-Jun N-terminal protein kinase (JNK) were investigated. WHW significantly inhibited the expression of XBP-1, GRP78, CHOP10, and eIF2α in ER stress-induced 3T3-L1 adipocytes. WHW also increased the PI3K expression and the IRS-1 phosphorylation but decreased the phosphorylation of JNK in ER stress-induced 3T3-L1 adipocytes. Our results indicate that WHW inhibits ER stress in adipocytes by suppressing the expression of ER stress-mediated molecules and the insulin signaling pathway, suggesting that WHW may be an attractive therapeutic agent for managing T2D.