title: Salacia reticulata inhibits differentiation of 3T3-L1 adipocytes.
abstract: ETHOPARMACOLOGICAL RELEVANCE: Salacia reticulata, a herbal medicine which has been used for the treatment of early diabetes in Ayurvedic medicine, is reported to have an anti-obesity effect and to be useful in the treatment of diabetes mellitus, insulin resistance and other metabolic diseases.
  
  
  OBJECTIVE
  The present study was performed to elucidate the mechanism of action of Salacia reticulata with special attention to the adipocytes as the tissue primarily involved in the pathology of metabolic diseases.
  
  
  METHODS
  Mouse-derived adipocyte precursor 3T3-L1 cells were treated with differentiation inducers in the presence or absence of Salacia reticulata (SRCD). We determined triacylglycerol accumulations, differentiation makers, released glycerol and adiponectin. Mangiferin, the primary component of SRCD, was also treated to 3T3-L1 cells.
  
  
  RESULTS
  Concurrent administration of the extract of SRCD and differentiation inducers resulted in a significant inhibition of differentiation into mature adipocytes. SRCD also exhibited significant inhibitory action on the expression of genes and proteins of peroxisome proliferator-activated receptor (PPAR)γ and CCAAT-enhancer binding protein (C/EBP)α, as well as on the activity of glycerol-3-phosphate dehydrogenase (GPDH), a differentiation marker, and caused a reduction in the concentration of released adiponectin. However, SRCD had no influence on lipolysis as indicated by the release of glycerol into the culture medium. The primary component of SRCD, mangiferin, was investigated for its effect on adipocytes; mangiferin caused no suppression of fat accumulation, suggesting that a component of SRCD other than mangiferin may be involved in the inhibition of adipocyte differentiation.
  
  
  CONCLUSIONS
  The above results suggest that the inhibitory action of SRCD on adipocyte differentiation, and not the promotion of lipolysis, is involved in the suppression of fat accumulation.
authors.affiliation: Research Institute of Pharmaceutical Sciences, Musashino University, 1-1-20 Shinmachi Nishitokyo-shi, Tokyo 202-8585, Japan.
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Shimada
authors.forename: Eiichi
authors.initials: E
authors.lastname: Nagai
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Harasawa
authors.forename: Michiru
authors.initials: M
authors.lastname: Watanabe
authors.forename: Kenichi
authors.initials: K
authors.lastname: Negishi
authors.forename: Tomoko
authors.initials: T
authors.lastname: Akase
authors.forename: Yoshimichi
authors.initials: Y
authors.lastname: Sai
authors.forename: Ken-Ichi
authors.initials: K
authors.lastname: Miyamoto
authors.forename: Masaki
authors.initials: M
authors.lastname: Aburada
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D052242:Adiponectin / Q000378:metabolism; D000818:Animals; D022763:CCAAT-Enhancer-Binding Protein-alpha / Q000235:genetics / Q000378:metabolism; D002454:Cell Differentiation / Q000187:drug effects*; D015870:Gene Expression; D005990:Glycerol / Q000378:metabolism; D005993:Glycerolphosphate Dehydrogenase / Q000378:metabolism; D008066:Lipolysis / Q000187:drug effects; D008659:Metabolic Diseases / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism; D010936:Plant Extracts / Q000494:pharmacology* / Q000627:therapeutic use; D049918:Salacia; D044004:Xanthones / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D052242:Adiponectin; D022763:CCAAT-Enhancer-Binding Protein-alpha; D047495:PPAR gamma; D010936:Plant Extracts; D044004:Xanthones; C013592:mangiferin; D005993:Glycerolphosphate Dehydrogenase; D005990:Glycerol