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Lansoprazole inhibits adipocyte differentiation via LXR‐independent mechanism
Author(s) -
Benchamana Ameena,
Soodvilai Sunhapas
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.829.11
Subject(s) - adipocyte , adipogenesis , peroxisome proliferator activated receptor , liver x receptor , chemistry , fenofibrate , nuclear receptor , receptor , pharmacology , endocrinology , medicine , transcription factor , biology , adipose tissue , biochemistry , gene
Liver X receptor (LXR), a ligand‐activated transcription factor, belongs to the nuclear receptor superfamily. It is believed to regulate adipocyte differentiation and lipid metabolism. Lansoprazole (LPZ), an effective FDA‐approved drug used in acid relate disorders, recently is known to be LXR agonist. However, the effect of LPZ on adipocyte differentiation is still unknown. In this study, we investigated anti‐adipogenesis effect of LPZ in 3T3‐L1 pre‐adipocyte and elucidated its possible underlying mechanisms. To determine whether LPZ inhibit adipogenesis, 3T3‐L1 pre‐adipocyte was treated with LPZ (10, 50 and 100 μM) for 48 hours during differentiation induction followed by determination of intracellular lipid accumulation by Oil Red O staining. Our findings showed that LPZ significantly reduced intracellular lipid accumulation only at dose 100 μM without cytotoxicity effect. Co‐treatment the cells with LPZ and LXR antagonists (fenofibrate 10 μM and SR9238 1 μM) for 24 hours failed to attenuate the effect of LPZ on adipocyte differentiation. This result indicated that LPZ inhibited adipocyte differentiation via LXR‐independent mechanism. Expressions of adipocyte differentiation related proteins; peroxisome proliferator‐activated receptor‐γ (PPARγ), CCAAT‐enhancer‐binding protein‐α (C/EBPα), and fatty acid synthase (FAS) were significantly reduced following LPZ treatment. Taken together, our results demonstrated that LPZ inhibits adipocyte differentiation through downregulate PPARγ, C/EBPα, and FAS expression and this inhibition was LXR‐independent pathway. Our results point towards the new indication of LPZ as an alternative therapeutic agent for obesity treatment. Support or Funding Information This work was carried out by the support from the Office of the Higher Education Commission of Thailand (Grant to Ameena Benchamana). This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .