| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2024-09-27 |
| タイトル |
|
|
タイトル |
Albumin-fused long-acting FGF21 analogue for the treatment of non-alcoholic fatty liver disease |
|
言語 |
en |
| 言語 |
|
|
言語 |
eng |
| キーワード |
|
|
主題 |
Albumin fusion, FGF21, Non-alcoholic fatty liver disease, Non-alcoholic steatohepatitis, Fatty acid, Insulin resistance |
| 資源タイプ |
|
|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
journal article |
| 著者 |
Mayuko, Chikamatsu
Hiroshi, Watanabe
Yuhi, Shintani
Ryota, Murata
Masako, Miyahisa
Ayano, Nishinoiri
Tadashi, Imafuku
Mei, Takano
Nanaka, Arimura
Kohichi, Yamada
Miya, Kamimura
Baki, Mukai
Takao, Satoh
Hitoshi, Maeda
Toru, Maruyama
|
| 内容記述 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
Non-alcoholic fatty liver disease (NAFLD) currently affects about 25% of the world's population, and the numbers continue to rise as the number of obese patients increases. However, there are currently no approved treatments for NAFLD. This study reports on the evaluation of the therapeutic effect of a recombinant human serum albumin-fibroblast growth factor 21 analogue fusion protein (HSA-FGF21) on the pathology of NAFLD that was induced by using two high-fat diets (HFD), HFD-60 and STHD-01. The HFD-60-induced NAFLD model mice with obesity, insulin resistance, dyslipidemia and hepatic lipid accumulation were treated with HSA-FGF21 three times per week for 4 weeks starting at 12 weeks after the HFD-60 feeding. The administration of HSA-FGF21 suppressed the increased body weight, improved hyperglycemia, hyperinsulinemia, and showed a decreased accumulation of plasma lipid and hepatic lipid levels. The elevation of C16:0, C18:0 and C18:1 fatty acids in the liver that were observed in the HFD-60 group was recovered by the HSA-FGF21 administration. The increased expression levels of the hepatic fatty acid uptake receptor (CD36) and fatty acid synthase (SREBP-1c, FAS, SCD-1, Elovl6) were also suppressed. In adipose tissue, HSA-FGF21 caused an improved adipocyte hypertrophy, a decrease in the levels of inflammatory cytokines and induced the expression of adiponectin and thermogenic factors. The administration of HSA-FGF21 to the STHD-01-induced NAFLD model mice resulted in suppressed plasma ALT and AST levels, oxidative stress, inflammatory cell infiltration and fibrosis. Together, HSA-FGF21 has some potential for use as a therapeutic agent for the treatment of NAFLD. |
| bibliographic_information |
en : Journal of Controlled Release
巻 355,
p. 42-53,
発行年 2023-03-01
|
| item_16_source_id_7 |
|
|
収録物識別子 |
0168-3659 |
| 権利 |
|
|
権利情報 |
(C) 2023 Elsevier B.V. All rights reserved. |
| 権利 |
|
|
権利情報 |
This manuscript version is made available under the CC-BY-NC-ND 4.0 license. https://creativecommons.org/licenses/by-nc-nd/4.0/ |
| 出版タイプ |
|
|
出版タイプ |
AM |
|
出版タイプResource |
http://purl.org/coar/version/c_ab4af688f83e57aa |
| 出版者 |
|
|
出版者 |
Elsevier |
| 関連 |
|
|
関連タイプ |
isVersionOf |
|
|
識別子タイプ |
DOI |
|
|
関連識別子 |
https://doi.org/10.1016/j.jconrel.2023.01.039 |
10.1016_j.jconrel.2023.01.039.pdf (2.3 MB)
.png)
