Document Detail

Regulation of adipocyte differentiation by PEGylated all-trans retinoic acid: reduced cytotoxicity and attenuated lipid accumulation.
MedLine Citation:
PMID:  16963253     Owner:  NLM     Status:  MEDLINE    
Obesity is major risk factor for many disorders, including diabetes, hypertension and heart disease. Unfortunately, there is a dearth of therapeutic agents available to clinicians for the treatment of obesity. The principal aim of this study was to investigate whether PEGylated all-trans retinoic acid (PRA) can have favorable stability and biological activity in 3T3-L1 preadipocytes as an antiobesity drug. Here, we found that PRA inhibits the process of adipogenesis, including survival of adipocytes and differentiation to mature adipocytes. The results showed that RA nanoparticles (NPs) were prepared by PEGylation; below 200 nm, PRA-NPs were obtained. Moreover, PRA decreased glycerol-3-phosphate dehydrogenase activity in 3T3-L1 preadipocytes by acting with major adipocyte marker proteins such as PPARgamma2, C/EBPalpha and aP2 modulators. Apoptosis, in addition, increased as the level of RA increased from 10 to 20 microM, whereas PRA reduced apoptosis with increasing concentrations. Our data suggest that PRA-NP has potential as an antiobesity drug carrier due to its small particle size and PEGylated core-shell structure. In addition, our results suggest that PRA inhibits the process of adipogenesis and may be developed to treat obesity. Based on these results, PRA is suitable for adipocyte studies, and an enhanced effect of PRA with adipocyte differentiation offers a challenging approach for pharmaceutical applications.
H S Moon; D D Guo; H H Song; I Y Kim; H L Jiang; H L Jin; Y K Kim; C S Chung; Y J Choi; H K Lee; C S Cho
Related Documents :
15817843 - Mechanisms of insulin-dependent glucose transport into porcine and bovine skeletal muscle.
22374753 - Determinants of evolving metabolic and cardiovascular benefit/risk profiles of rosiglit...
18937363 - Wnt signaling in caudal dysgenesis and diabetic embryopathy.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-09-08
Journal Detail:
Title:  The Journal of nutritional biochemistry     Volume:  18     ISSN:  0955-2863     ISO Abbreviation:  J. Nutr. Biochem.     Publication Date:  2007 May 
Date Detail:
Created Date:  2007-04-23     Completed Date:  2007-07-20     Revised Date:  2008-03-06    
Medline Journal Info:
Nlm Unique ID:  9010081     Medline TA:  J Nutr Biochem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  322-31     Citation Subset:  IM    
School of Agricultural Biotechnology, Seoul National University, Seoul 151-742, South Korea.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
3T3 Cells
Adipocytes / cytology,  drug effects*,  metabolism
Apoptosis / drug effects
CCAAT-Enhancer-Binding Protein-alpha / drug effects,  metabolism
Cell Cycle / drug effects
Cell Differentiation / drug effects*
Dose-Response Relationship, Drug
Lipid Metabolism / drug effects*
PPAR gamma / metabolism
Polyethylene Glycols / chemistry,  pharmacology
Tretinoin / chemistry*,  pharmacology*
Reg. No./Substance:
0/CCAAT-Enhancer-Binding Protein-alpha; 0/PPAR gamma; 0/Polyethylene Glycols; 302-79-4/Tretinoin
Erratum In:
J Nutr Biochem. 2008 Mar;19(3):206
Note: Jin, H L [corrected to Jiang, H L]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Conjugated linoleic acid inhibits Caco-2 cell growth via ERK-MAPK signaling pathway.
Next Document:  Road soil retention of Pb leached from MSWI bottom ash.