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Year : 2021  |  Volume : 17  |  Issue : 75  |  Page : 505-510

Plant extract-derived betulinic acid chalcone inhibits the development of type 2 diabetes mellitus via targeting peroxisome proliferator-activated receptor-γ-Regulated gene expression

Department of Geriatrics, Nantong First People's Hospital, The Second Affiliated Hospital of Nantong University, Nantong, China

Correspondence Address:
Juehui Ren
Department of Geriatrics, Nantong First People's Hospital, The Second Affiliated Hospital of Nantong University, No. 6 of Haierxiang North Road, Chongchuan District, Nantong-226001
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/pm.pm_321_20

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Aim: Diabetes mellitus is a syndrome related to metabolism having complicated pathogenesis and its morbidity rate is quickly increasing every year. In the present study, the antagonistic effect of betulinic acid chalcone for peroxisome proliferator-activated receptor-γ (PPARγ) was explored with possible implications in diabetic treatment. Materials and Methods: The adipocyte differentiation following betulinic acid chalcone treatment was evaluated using Oil Red O staining. Reverse transcription–polymerase chain reaction was employed for gene expression and Western blot for analysis of differentiation linked protein expression. Results: Betulinic acid chalcone repressed PPARγ-ligand-binding domain level and transcriptional property of retinoid X receptor α-PPARγ in 293T cells. The rosiglitazone suggestively (P < 0.01) augmented grease droplet accumulation in adipocytes in comparison to control adipocytes. The improved grease droplet accumulation by rosiglitazone in adipocytes was suppressed on treatment with betulinic acid chalcone. The surge in grease droplet accumulation by rosiglitazone was lessened completely on treatment with 16-μM betulinic acid chalcone. Treatment of adipocytes with betulinic acid chalcone suppressed rosiglitazone-induced expression of fatty acid synthase (FAS), CCAAT/enhancer-binding protein-α (C/EBPα), adipocyte fatty acid-binding protein 2 (aP2), and HMG-CoA genes pointedly. Treatment of adipocytes with betulinic acid chalcone instigated a marked decrease in rosiglitazone-induced expression of aP2, carboxyl terminus of the Hsc70-interacting protein (CHIP), and C/EBPα. The suppressive effect of rosiglitazone on expression of p-Akt/t-Akt, PPARa, p-FoxO1/t-FoxO1, and p-AMP protein kinase (AMPK)/t-AMPK was expressively (P < 0.01) assuaged in the adipocytes by betulinic acid chalcone. Conclusion: The present study established that betulinic acid chalcone suppressed PPARγ activity and adipocyte differentiation. Moreover, the activation of FoxO1/Akt/AMPK was upregulated and FAS/EBPα/aP2/HMG-CoA expression was subdued by betulinic acid chalcone in the adipocytes. Therefore, betulinic acid chalcone may be appraised further for a possible role in the treatment of diabetes.

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