• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

用20-羟基蜕皮酮进行膳食补充可改善高脂高果糖饮食喂养的去卵巢大鼠的肝脂肪变性并减少白色脂肪组织质量。

Dietary Supplementation with 20-Hydroxyecdysone Ameliorates Hepatic Steatosis and Reduces White Adipose Tissue Mass in Ovariectomized Rats Fed a High-Fat, High-Fructose Diet.

作者信息

Buniam Jariya, Chansela Piyachat, Weerachayaphorn Jittima, Saengsirisuwan Vitoon

机构信息

Princess Srisavangavadhana College of Medicine, Chulabhorn Royal Academy, Bangkok 10210, Thailand.

Department of Anatomy, Phramongkutklao College of Medicine, Bangkok 10400, Thailand.

出版信息

Biomedicines. 2023 Jul 23;11(7):2071. doi: 10.3390/biomedicines11072071.

DOI:10.3390/biomedicines11072071
PMID:37509710
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10377470/
Abstract

Metabolic dysfunction-associated fatty liver disease (MAFLD) is defined as hepatic steatosis in combination with overweight, diabetes, or other metabolic risk factors. MAFLD affects a significant number of the global population and imposes substantial clinical and economic burdens. With no approved pharmacotherapy, current treatment options are limited to diet and exercise. Therefore, the development of medicines for MAFLD treatment or prevention is necessary. 20-Hydroxyecdysone (20E) is a natural steroid found in edible plants and has been shown to improve metabolism and dyslipidemia. Therefore, it may be useful for MAFLD treatment. Here, we aimed to determine how dietary supplementation with 20E affects fat accumulation and lipogenesis in the liver and adipose tissue of ovariectomized rats fed a high-fat, high-fructose diet (OHFFD). We found that 20E reduced hepatic triglyceride content and visceral fat deposition. 20E increased the phosphorylation of AMP-activated protein kinase and acetyl CoA carboxylase while reducing the expression of fatty acid synthase in the liver and adipose tissue. Additionally, 20E increased hepatic expression of carnitine palmitoyltransferase-1 and reduced adipose expression of sterol regulatory element-binding protein-1. In conclusion, 20E demonstrated beneficial effects in rats with OHFFD-induced MAFLD. These findings suggest that 20E may represent a promising option for MAFLD prevention or treatment.

摘要

代谢功能障碍相关脂肪性肝病(MAFLD)被定义为肝脂肪变性合并超重、糖尿病或其他代谢危险因素。MAFLD影响着全球大量人口,并带来了巨大的临床和经济负担。由于尚无获批的药物治疗方法,目前的治疗选择仅限于饮食和运动。因此,开发用于治疗或预防MAFLD的药物是必要的。20-羟基蜕皮激素(20E)是一种存在于可食用植物中的天然类固醇,已被证明可改善新陈代谢和血脂异常。因此,它可能对MAFLD治疗有用。在此,我们旨在确定在喂食高脂高果糖饮食(OHFFD)的去卵巢大鼠的肝脏和脂肪组织中,饮食补充20E如何影响脂肪积累和脂肪生成。我们发现20E降低了肝脏甘油三酯含量和内脏脂肪沉积。20E增加了肝脏和脂肪组织中AMP激活的蛋白激酶和乙酰辅酶A羧化酶的磷酸化,同时降低了脂肪酸合酶的表达。此外,20E增加了肝脏中肉碱棕榈酰转移酶-1的表达,并降低了脂肪组织中固醇调节元件结合蛋白-1的表达。总之,20E在OHFFD诱导的MAFLD大鼠中显示出有益作用。这些发现表明,20E可能是预防或治疗MAFLD的一个有前景的选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bb7/10377470/80cce09fcc63/biomedicines-11-02071-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bb7/10377470/376431cfb60a/biomedicines-11-02071-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bb7/10377470/4d7642f8196d/biomedicines-11-02071-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bb7/10377470/b3c79caa5fa3/biomedicines-11-02071-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bb7/10377470/0d5a7a0e3058/biomedicines-11-02071-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bb7/10377470/9c3a619741e2/biomedicines-11-02071-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bb7/10377470/f74ad86eec6a/biomedicines-11-02071-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bb7/10377470/80cce09fcc63/biomedicines-11-02071-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bb7/10377470/376431cfb60a/biomedicines-11-02071-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bb7/10377470/4d7642f8196d/biomedicines-11-02071-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bb7/10377470/b3c79caa5fa3/biomedicines-11-02071-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bb7/10377470/0d5a7a0e3058/biomedicines-11-02071-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bb7/10377470/9c3a619741e2/biomedicines-11-02071-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bb7/10377470/f74ad86eec6a/biomedicines-11-02071-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bb7/10377470/80cce09fcc63/biomedicines-11-02071-g007.jpg

相似文献

1
Dietary Supplementation with 20-Hydroxyecdysone Ameliorates Hepatic Steatosis and Reduces White Adipose Tissue Mass in Ovariectomized Rats Fed a High-Fat, High-Fructose Diet.用20-羟基蜕皮酮进行膳食补充可改善高脂高果糖饮食喂养的去卵巢大鼠的肝脂肪变性并减少白色脂肪组织质量。
Biomedicines. 2023 Jul 23;11(7):2071. doi: 10.3390/biomedicines11072071.
2
20-Hydroxyecdysone ameliorates metabolic and cardiovascular dysfunction in high-fat-high-fructose-fed ovariectomized rats.20-羟基蜕皮甾酮可改善高脂高果糖喂养去卵巢大鼠的代谢和心血管功能障碍。
BMC Complement Med Ther. 2020 May 6;20(1):140. doi: 10.1186/s12906-020-02936-1.
3
Estrogen and voluntary exercise attenuate cardiometabolic syndrome and hepatic steatosis in ovariectomized rats fed a high-fat high-fructose diet.雌激素和自愿运动可减轻高脂高果糖饮食喂养的去卵巢大鼠的心脏代谢综合征和肝脂肪变性。
Am J Physiol Endocrinol Metab. 2019 May 1;316(5):E908-E921. doi: 10.1152/ajpendo.00466.2018. Epub 2019 Feb 26.
4
Oxymatrine attenuates hepatic steatosis in non-alcoholic fatty liver disease rats fed with high fructose diet through inhibition of sterol regulatory element binding transcription factor 1 (Srebf1) and activation of peroxisome proliferator activated receptor alpha (Pparα).氧化苦参碱通过抑制固醇调节元件结合转录因子 1(Srebf1)和激活过氧化物酶体增殖物激活受体 α(Pparα),减轻高果糖饮食诱导的非酒精性脂肪性肝病大鼠的肝脂肪变性。
Eur J Pharmacol. 2013 Aug 15;714(1-3):89-95. doi: 10.1016/j.ejphar.2013.06.013. Epub 2013 Jun 18.
5
Dietary supplementation with myo-inositol reduces hepatic triglyceride accumulation and expression of both fructolytic and lipogenic genes in rats fed a high-fructose diet.膳食补充肌醇可减少高果糖饮食喂养大鼠肝内甘油三酯的蓄积,并降低果糖分解和脂肪生成基因的表达。
Nutr Res. 2017 Nov;47:21-27. doi: 10.1016/j.nutres.2017.08.005. Epub 2017 Aug 24.
6
Modulation of hepatic sterol regulatory element-binding protein-1c-mediated gene expression contributes to Salacia oblonga root-elicited improvement of fructose-induced fatty liver in rats.调控肝固醇调节元件结合蛋白-1c 介导的基因表达有助于菝葜根提取物改善果糖诱导的大鼠脂肪肝。
J Ethnopharmacol. 2013 Dec 12;150(3):1045-52. doi: 10.1016/j.jep.2013.10.020. Epub 2013 Oct 21.
7
P2Y2R Deficiency Ameliorates Hepatic Steatosis by Reducing Lipogenesis and Enhancing Fatty Acid β-Oxidation through AMPK and PGC-1α Induction in High-Fat Diet-Fed Mice.P2Y2R 缺乏通过诱导 AMPK 和 PGC-1α 减少脂肪生成和增强脂肪酸β氧化来改善高脂肪饮食喂养小鼠的肝脂肪变性。
Int J Mol Sci. 2021 May 24;22(11):5528. doi: 10.3390/ijms22115528.
8
Mitigation of MAFLD in High Fat-High Sucrose-Fructose Fed Mice by a Combination of Genistein Consumption and Exercise Training.通过食用染料木黄酮和运动训练相结合减轻高脂高蔗糖-果糖喂养小鼠的MAFLD
Diabetes Metab Syndr Obes. 2022 Jul 23;15:2157-2172. doi: 10.2147/DMSO.S358256. eCollection 2022.
9
Emodin protects against high-fat diet-induced obesity via regulation of AMP-activated protein kinase pathways in white adipose tissue.大黄素通过调节白色脂肪组织中 AMP 激活的蛋白激酶通路来防止高脂肪饮食诱导的肥胖。
Planta Med. 2012 Jun;78(10):943-50. doi: 10.1055/s-0031-1298626. Epub 2012 Jun 6.
10
Fructose supplementation worsens the deleterious effects of short-term high-fat feeding on hepatic steatosis and lipid metabolism in adult rats.补充果糖会加重短期高脂喂养对成年大鼠肝脏脂肪变性和脂质代谢的有害影响。
Exp Physiol. 2014 Sep;99(9):1203-13. doi: 10.1113/expphysiol.2014.079632. Epub 2014 Jun 27.

引用本文的文献

1
Molecular Targets of 20-Hydroxyecdysone in Mammals, Mechanism of Action: Is It a Calorie Restriction Mimetic and Anti-Aging Compound?20-羟基蜕皮酮在哺乳动物中的分子靶点、作用机制:它是一种模拟热量限制和抗衰老的化合物吗?
Cells. 2025 Mar 13;14(6):431. doi: 10.3390/cells14060431.
2
Possible protective effect of natural flavanone naringenin-reduced graphene oxide nanosheets on nonalcoholic fatty liver disease.天然黄酮柚皮素还原氧化石墨烯纳米片对非酒精性脂肪性肝病可能的保护作用
Naunyn Schmiedebergs Arch Pharmacol. 2025 Apr;398(4):4071-4086. doi: 10.1007/s00210-024-03495-9. Epub 2024 Oct 16.

本文引用的文献

1
Nonalcoholic Fatty Liver Disease in Lean/Nonobese and Obese Individuals: A Comprehensive Review on Prevalence, Pathogenesis, Clinical Outcomes, and Treatment.瘦/非肥胖和肥胖个体中的非酒精性脂肪性肝病:关于患病率、发病机制、临床结局及治疗的综合综述
J Clin Transl Hepatol. 2023 Apr 28;11(2):502-515. doi: 10.14218/JCTH.2022.00204. Epub 2022 Dec 23.
2
Molecular mechanisms of metabolic associated fatty liver disease (MAFLD): functional analysis of lipid metabolism pathways.代谢相关性脂肪性肝病(MAFLD)的分子机制:脂质代谢途径的功能分析。
Clin Sci (Lond). 2022 Sep 30;136(18):1347-1366. doi: 10.1042/CS20220572.
3
Enhanced 3T3-L1 Differentiation into Adipocytes by Pioglitazone Pharmacological Activation of Peroxisome Proliferator Activated Receptor-Gamma (PPAR-γ).
吡格列酮通过药理激活过氧化物酶体增殖物激活受体γ(PPAR-γ)增强3T3-L1细胞向脂肪细胞的分化。
Biology (Basel). 2022 May 24;11(6):806. doi: 10.3390/biology11060806.
4
Acetyl-CoA Carboxylases and Diseases.乙酰辅酶A羧化酶与疾病
Front Oncol. 2022 Mar 11;12:836058. doi: 10.3389/fonc.2022.836058. eCollection 2022.
5
Weighing in on Adipogenesis.关于脂肪生成的探讨
Front Physiol. 2022 Feb 25;13:821278. doi: 10.3389/fphys.2022.821278. eCollection 2022.
6
9. Pharmacologic Approaches to Glycemic Treatment: Standards of Medical Care in Diabetes-2022.9. 血糖治疗的药物学方法:《2022 年糖尿病医学诊疗标准》。
Diabetes Care. 2022 Jan 1;45(Suppl 1):S125-S143. doi: 10.2337/dc22-S009.
7
Recent Advances in Adipose Tissue Dysfunction and Its Role in the Pathogenesis of Non-Alcoholic Fatty Liver Disease.脂肪组织功能障碍及其在非酒精性脂肪性肝病发病机制中的作用的最新进展。
Cells. 2021 Nov 25;10(12):3300. doi: 10.3390/cells10123300.
8
Fat Cell Size: Measurement Methods, Pathophysiological Origins, and Relationships With Metabolic Dysregulations.脂肪细胞大小:测量方法、病理生理起源及与代谢紊乱的关系。
Endocr Rev. 2022 Jan 12;43(1):35-60. doi: 10.1210/endrev/bnab018.
9
20-Hydroxyecdysone, from Plant Extracts to Clinical Use: Therapeutic Potential for the Treatment of Neuromuscular, Cardio-Metabolic and Respiratory Diseases.20-羟基蜕皮激素:从植物提取物到临床应用——治疗神经肌肉、心血管代谢及呼吸系统疾病的治疗潜力
Biomedicines. 2021 Apr 29;9(5):492. doi: 10.3390/biomedicines9050492.
10
Liver fat storage pathways: methodologies and dietary effects.肝脏脂肪存储途径:方法学和饮食影响。
Curr Opin Lipidol. 2021 Feb 1;32(1):9-15. doi: 10.1097/MOL.0000000000000720.