A PPAR Pan Agonist, MHY2013 Alleviates Age-Related Hepatic Lipid Accumulation by Promoting Fatty Acid Oxidation and Suppressing Inflammation
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- An Hye Jin
- College of Pharmacy, Pusan National University
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- Lee Bonggi
- College of Pharmacy, Pusan National University Korean Medicine (KM)-Application Center, Korea Institute of Oriental Medicine (KIOM)
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- Kim Seong Min
- College of Pharmacy, Pusan National University
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- Kim Dae Hyun
- College of Pharmacy, Pusan National University
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- Chung Ki Wung
- College of Pharmacy, Pusan National University
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- Ha Su Gyeong
- College of Pharmacy, Pusan National University
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- Park Kyung Chul
- College of Pharmacy, Pusan National University
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- Park Yeo Jin
- College of Pharmacy, Pusan National University
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- Kim Seong Jin
- College of Pharmacy, Pusan National University
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- Yun Hwi Young
- College of Pharmacy, Pusan National University
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- Chun Pusoon
- College of Pharmacy, Inje University
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- Yu Byung Pal
- Department of Physiology, The University of Texas Health Science Center at San Antonio
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- Moon Hyung Ryong
- College of Pharmacy, Pusan National University
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- Chung Hae Young
- College of Pharmacy, Pusan National University
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説明
<p>Nonalcoholic fatty liver disease (NAFLD) is frequently observed in obese and aged individuals. Peroxisome proliferator-activated receptors (PPARs) play a role in regulating hepatic lipid accumulation, a hallmark of NAFLD development. A PPAR pan agonist, 2-(4-(5,6-methylenedioxybenzo[d]thiazol-2-yl)-2-methylphenoxy)-2-methylpropanoic acid (MHY2013) has been shown to prevent fatty liver formation and insulin resistance in obese mice (db/db) model. However, the beneficial effects of MHY2013 in aged model remain unknown. In this study, we investigated whether MHY2013 alleviates hepatic lipid accumulation in aged Sprague–Dawley (SD) rats. We confirmed that MHY2013 increased the activities of three PPAR subtypes in HepG2 cells using luciferase assay. When administered orally in aged SD rats, MHY2013 markedly decreased the hepatic triglyceride levels without changes in body weight. Regarding underlying mechanisms, MHY2013 increased the mRNA levels of lipid oxidation-related genes, including carnitine palmitoyltransferase 1 (CPT1) and peroxisomal acyl-CoA oxidase 1 (ACOX1), without apparent change in the mRNA expression of lipogenesis-related genes. Furthermore, MHY2013 significantly increased systemic fibroblast growth factor 21 (FGF21) and adiponectin levels and suppressed inflammatory mRNA expression in the liver. In conclusion, MHY2013 alleviated age-related hepatic lipid accumulation, in part by upregulating β-oxidation signaling and suppressing inflammation in the liver. Therefore, MHY2013 is a potential pharmaceutical agent for treating age-related hepatic lipid accumulation.</p>
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 41 (1), 29-35, 2018
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390001204634272512
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- NII論文ID
- 130006301222
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- NII書誌ID
- AA10885497
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 028739272
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- PubMed
- 29311481
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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