Journal
PHYTOMEDICINE
Volume 21, Issue 4, Pages 406-414Publisher
ELSEVIER GMBH, URBAN & FISCHER VERLAG
DOI: 10.1016/j.phymed.2013.10.009
Keywords
Coagulin-L; Withania coagulans; Mitotic clonal expansion; Obesity; 3T3-L1; Adipocytes; Adipogenesis
Categories
Funding
- CSIR-CDRI Network project [BSC0102]
- Department of Biotechnology (DBT) [GAP0079]
- SRF of DBT
- JRF-CSIR
- JRF of University grant commission (UGC), New Delhi
Ask authors/readers for more resources
Obesity is a result of adipocyte hypertrophy followed by hyperplasia. It is a risk factor for several metabolic disorders such as dyslipidemia, type-2 diabetes, hypertension, and cardiovascular diseases. Coagulano-lides, particularly coagulin-L isolated from W. coagulan has earlier been reported for anti-hyperglycemic activity. In this study, we investigated the effect of coagulin-L on in vitro models of adipocyte differentiation including 3T3-L1 pre-adipocyte, mouse stromal mesenchymal C3H10T1/2 cells and bone marrow derived human mesenchymal stem cells (hMSCs). Our results showed that, coagulin-L reduces the expressions of peroxisome proliferator-activated receptor gamma (PPAR gamma) and CCAAT/enhancer-binding protein (C/EBP alpha), the major transcription factors orchestrating adipocyte differentiation. Detailed analysis further proved that early exposure of coagulin-L is sufficient to cause significant inhibition during adipogenesis. Coagulin-L inhibited mitotic clonal expansion (MCE) by delayed entry in G1 to S phase transition and S-phase arrest. This MCE blockade was caused apparently by-decreased phosphorylation of C/EBP beta, modulation in expression of cell cycle regulatory proteins, and upregulation of Wnt/beta-catenin pathway, the early stage regulatory proteins of adipogenic induction. Taken together all evidences, a known anti-hyperglycemic agent coagulin-L has shown potential to inhibit adipogenesis significantly, which can be therapeutically exploited for treatment of obesity and metabolic syndrome. (C) 2013 Elsevier GmbH. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available