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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2022.7
- 수록면
- 619 - 631 (13page)
- DOI
- 10.3349/ymj.2022.63.7.619
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초록· 키워드
오류제보하기
Purpose: Nonalcoholic fatty liver disease (NAFLD) is closely associated with metabolic diseases, including obesity and diabetes,and has gradually become the most common cause of chronic liver disease. We investigated the effects of sodium glucose cotrans porter 2 (SGLT2) inhibitor canagliflozin on NAFLD in high-fat diet (HFD)-induced obese mice and possible underlying mecha nisms.
Materials and Methods: Male C57BL/6 mice were fed a normal-diet, HFD, or HFD with canagliflozin for 14 weeks. AML-12 hepa tocytes were treated with canagliflozin. Expression of related pathways was assessed.
Results: Canagliflozin administration reduced body weight and fat mass, compared with HFD alone. Canagliflozin improved glu cose and lipid metabolic disorders. Compared with HFD-fed mice, liver weight, serum alanine transaminase (ALT) levels, and he patic lipid accumulation were decreased after canagliflozin administration. Additionally, canagliflozin upregulated lipolysis mark ers (CPT1a, ACOX1, and ACADM), downregulated lipogenesis markers (SREBP-1c and FASN), and suppressed the production ofinflammatory cytokines (TNFα, MCP1, IL-1β, and IL-6), consistent with significantly increased LC3 II/I and Atg7 levels in the liverfollowing canagliflozin treatment. In vitro, canagliflozin increased CPT1a, ACOX1, and ACADM expression, decreased SREBP-1cand FASN protein expression, and reduced TNFα, MCP1, IL-1β, and IL-6 mRNA levels in lipid mixture (LM)-induced hepatocytesin a dose-dependent manner. These changes were reversed by 3-MA, an autophagy inhibitor.
Conclusion: Our findings suggest that canagliflozin ameliorates the pathogenesis of NAFLD by regulating lipid metabolism andinhibiting inflammation, which may be associated with its promotion of autophagy.
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