Therapeutic effects of açaí seed extract on hepatic steatosis in high‐fat diet‐induced obesity in male mice: a comparative effect with rosuvastatin
Objectives Obesity is considered a risk factor for the development of non‐alcoholic fatty liver disease (NAFLD). The hydroalcoholic extract obtained from the açai seed (ASE), rich in proanthocyanidins, has been shown a potential body weight regulator with antioxidant properties. This study aimed to...
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Published in: | Journal of pharmacy and pharmacology Vol. 72; no. 12; pp. 1921 - 1932 |
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Main Authors: | , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Bognor Regis
Wiley Subscription Services, Inc
01-12-2020
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Subjects: | |
Online Access: | Get full text |
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Summary: | Objectives
Obesity is considered a risk factor for the development of non‐alcoholic fatty liver disease (NAFLD). The hydroalcoholic extract obtained from the açai seed (ASE), rich in proanthocyanidins, has been shown a potential body weight regulator with antioxidant properties. This study aimed to investigate the therapeutic effect of ASE in obesity‐associated NAFLD and compare it with Rosuvastatin.
Methods
Male C57BL/6 mice received a high‐fat diet or standard diet for 12 weeks. The treatments with ASE (300 mg/kg per day) or rosuvastatin (20 mg/kg per day) began in the eighth week until the 12th week.
Key findings
Our data show that the treatments with ASE and rosuvastatin reduced body weight and hyperglycaemia, improved lipid profile and attenuated hepatic steatosis in HFD mice. ASE and Rosuvastatin reduced HMGCoA‐Reductase and SREBP‐1C and increased ABGC8 and pAMPK expressions in the liver. Additionally, ASE, but not Rosuvastatin, reduced NPC1L1 and increased ABCG5 and PPAR‐α expressions. ASE and rosuvastatin increased SIRT‐1 expression and antioxidant defence, although only ASE was able to decrease the oxidative damage in hepatic tissue.
Conclusions
The therapeutic effect of ASE was similar to that of rosuvastatin in reducing dyslipidemia and hepatic steatosis but was better in reducing oxidative damage and hyperglycaemia. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0022-3573 2042-7158 |
DOI: | 10.1111/jphp.13356 |