Nobiletin promotes lipolysis of white adipose tissue in a circadian clock-dependent manner

诺比林 脂解 白色脂肪组织 昼夜节律 内科学 内分泌学 脂肪组织 生物钟 化学 细胞生物学 生物 医学 生物化学 类黄酮 抗氧化剂
作者
Xudong Li,Runxuan Zhuang,Zhitian Lu,Fan Wu,Xiaoli Wu,Ke Zhang,Min Wang,Wenxue Li,Huijie Zhang,Wei Zhu,Bo Zhang
出处
期刊:Journal of Nutritional Biochemistry [Elsevier BV]
卷期号:132: 109696-109696 被引量:9
标识
DOI:10.1016/j.jnutbio.2024.109696
摘要

Nobiletin has been reported to protect against obesity-related metabolic disorders by enhancing the circadian rhythm; however its effects on lipid metabolism in adipose tissue are unclear. In this study, mice were fed with high-fat diet (HFD) for four weeks firstly and gavaged with 50 or 200 mg/kg bodyweight/day nobiletin at Zeitgeber time (ZT) 4 for another four weeks while still receiving HFD. At the end of the 8-week experimental period, the mice were sacrificed at ZT4 or ZT8 on the same day. Mature 3T3-L1 adipocytes were treated with nobiletin in the presence or absence of siBmal1, siRora, siRorc, SR8278 or SR9009. Nobiletin reduced the weight of white adipose tissue (WAT) and the size of adipocytes in WAT. At ZT4, nobiletin decreased the TG, TC and LDL-c levels and increased serum FFA level and glucose tolerance. Nobiletin triggered the lipolysis of mesenteric and epididymal WAT at both ZT4 and ZT16. Nobiletin increased the level of RORγ at ZT16, that of BMAL1 and PPARγ at ZT4, and that of ATGL at both ZT4 and ZT16. Nobiletin increased lipolysis and ATGL levels in 3T3-L1 adipocytes in Bmal1- or Rora/c- dependent manner. Dual luciferase assay indicated that nobiletin enhanced the transcriptional activation of RORα/γ on Atgl promoter and decreased the repression of RORα/γ on PPARγ-binding PPRE. Promoter deletion analysis indicated that nobiletin inhibited the suppression of PPARγ-mediated Atgl transcription by RORα/γ. Taken together, nobiletin elevated lipolysis in WAT by increasing ATGL levels through activating the transcriptional activity of RORα/γ and decreasing the repression of RORα/γ on PPARγ-binding PPRE.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
小王完成签到,获得积分20
1秒前
黄小皮发布了新的文献求助10
1秒前
豆豆发布了新的文献求助10
1秒前
shiyi发布了新的文献求助10
1秒前
科研通AI2S应助刘承昭采纳,获得10
2秒前
wz1636完成签到 ,获得积分10
2秒前
xzm发布了新的文献求助10
2秒前
领导范儿应助啦啦啦啦啦采纳,获得10
2秒前
十八岁不想说话完成签到,获得积分10
3秒前
3秒前
杨三多发布了新的文献求助10
3秒前
devil发布了新的文献求助10
3秒前
hzz发布了新的文献求助10
3秒前
totpto发布了新的文献求助10
4秒前
今后应助哈哈李采纳,获得10
4秒前
怕黑的丹翠完成签到,获得积分10
4秒前
李健应助山野有雾都采纳,获得10
4秒前
5秒前
5秒前
6秒前
daemon850121完成签到,获得积分10
6秒前
7秒前
7秒前
小王发布了新的文献求助10
7秒前
刘承昭完成签到,获得积分10
8秒前
8秒前
86发布了新的文献求助10
8秒前
9秒前
太阳完成签到,获得积分10
9秒前
科研通AI6.2应助totpto采纳,获得10
9秒前
yy发布了新的文献求助10
9秒前
田様应助devil采纳,获得10
10秒前
10秒前
共享精神应助自觉的冬云采纳,获得10
11秒前
执念发布了新的文献求助10
11秒前
落寞以寒完成签到,获得积分10
11秒前
东山小红发布了新的文献求助10
11秒前
11秒前
小天使完成签到,获得积分10
12秒前
12秒前
高分求助中
Principles of Economics, 11th Edition 10000
University Physics with Modern Physics, 16th edition 10000
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Arthritis and Related Conditions, An Issue of Orthopedic Clinics 1000
Development of a Bridge Weigh-In-Motion System: A technology to convert the bridge response to the passage of traffic into data on vehicle configurations, speeds, times of travel and weights 1000
ズームレンズの光学設計に関する研究 800
Fundamentals of Pharmaceutical and Biologics Regulations: A Global Perspective, Second Edition 700
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 内科学 物理 复合材料 催化作用 细胞生物学 无机化学 光电子学 物理化学 电极 基因
热门帖子
关注 科研通微信公众号,转发送积分 7293123
求助须知:如何正确求助?哪些是违规求助? 8911877
关于积分的说明 18866546
捐赠科研通 6959942
什么是DOI,文献DOI怎么找? 3209734
关于科研通互助平台的介绍 2379220
邀请新用户注册赠送积分活动 2185758