TargetRx Atlas

MRNA basic information

  • mRNA ID:ENST00000308868
  • Gene Name:LEP
  • mRNA database:Ensembl
  • mRNA expression :down-regulated
  • mRNA Method:qPCR
  • mRNA Pathway:PI3K/Akt pathway
  • Evidence:validated
  • (mRNA-drug)

Drug basic information

  • Drug ID:DB00166
  • Drug Name:Lipoic acid
  • Drug Method:down-regulated the gene expression

Disease basic infommation

  • Disease:diabetes
  • Tissue:cell line 3T3-L1

Other information

  • Title:Lipoic acid inhibits leptin secretion and Sp1 activity in adipocytes
  • Journal:Molecular Nutrition & Food Research
  • Published:2011
  • PubMed ID:21351249
  • Abstract:Scope:Lipoic acid (LA) is an antioxidant with therapeutic potential on several diseases such as diabetes and obesity. Hyperleptinemia and oxidative stress play a major role in the development of obesity-linked diseases. The aim of this study was to examine in vivo and in vitro the effects of LA on leptin production, as well as to elucidate the mechanisms and signalling pathways involved in LA actions. Methods and results:Dietary supplementation with LA decreased both circulating leptin, and adipose tissue leptin mRNA in rats. Treatment of 3T3-L1 adipocytes with LA caused a concentration-dependent inhibition of leptin secretion and gene expression. Moreover, LA stimulated the anaerobic utilization of glucose to lactate, which negatively correlated with leptin secretion. Furthermore, LA enhanced phosphorylation of Sp1 and inhibited Sp1 transcriptional activity in 3T3-L1 adipocytes. Moreover, LA inhibited Akt phosphorylation, a downstream target of phosphatidylinositol 3-kinase (PI3K). Treatment with the PI3K inhibitor LY294002 mimicked LA actions, dramatically inhibiting both leptin secretion and gene expression and stimulating Sp1 phosphorylation. Conclusion:All of these data suggest that the phosphorylation of Sp1 and the accompanying reduced DNA-binding activity are likely to be involved in the inhibition of leptin induced by LA, which could be mediated in part by the abrogation of the PI3K/Akt pathway.
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