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黄酮木犀草素通过降低 C/EBPδ 表达和抑制脂肪细胞中 PI3K/Akt-FOXO1 信号通路来抑制脂肪酸和甘油三酯的合成。

Suppression of Fatty Acid and Triglyceride Synthesis by the Flavonoid Orientin through Decrease of C/EBPδ Expression and Inhibition of PI3K/Akt-FOXO1 Signaling in Adipocytes.

机构信息

Department of Pathobiochemistry, Osaka University of Pharmaceutical Sciences, 4-20-1 Nasahara, Takatsuki, Osaka 569-1094, Japan.

Department of Pharmacognosy, Osaka University of Pharmaceutical Sciences, 4-20-1 Nasahara, Takatsuki, Osaka 569-1094, Japan.

出版信息

Nutrients. 2018 Jan 26;10(2):130. doi: 10.3390/nu10020130.

DOI:10.3390/nu10020130
PMID:29373533
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5852706/
Abstract

Plant flavonoids have a variety of biological properties. In a previous study, we found that the tea of the Asian dayflower, L., decreased the body weight gain in high-fat diet-fed mice. In this study, we studied the anti-adipogenic ability of a flavonoid orientin that is found in abundance in . Orientin repressed the accumulation of intracellular triglyceride (TG) in mouse adipocyte 3T3-L1 cells. The treatment with orientin also decreased the mRNA levels of the genes involved in adipogenesis, lipogenesis, lipolysis, and TG synthesis, and reduced the release of glycerol. Orientin lowered the expression of CCAAT/enhancer binding protein (C/EBP) δ in the early stage of adipogenesis, leading to a decrease in the expression of the adipogenic master transcription factors such as peroxisome proliferator-activated receptor (PPAR) γ and C/EBPα. Moreover, the anti-adipogenic effect of orientin repressed the phosphorylation of Akt and subsequent phosphorylation of forkhead box protein O1 (FOXO1), which inhibits the transcription of the gene. These results indicate that a plant flavonoid orientin suppressed the expression of the gene through repression of expression and inhibition of the phosphoinositide 3-kinase /Akt-FOXO1 signaling in adipocytes.

摘要

植物类黄酮具有多种生物学特性。在之前的一项研究中,我们发现通泉草属植物 L. 的茶可减少高脂肪饮食喂养的小鼠体重增加。在这项研究中,我们研究了丰度丰富的类黄酮Orientin 的抗脂肪生成能力。Orientin 可抑制小鼠脂肪细胞 3T3-L1 中细胞内甘油三酯 (TG) 的积累。Orientin 的处理还降低了参与脂肪生成、脂肪生成、脂肪分解和 TG 合成的基因的 mRNA 水平,并减少了甘油的释放。Orientin 在脂肪生成的早期阶段降低了 CCAAT/增强子结合蛋白 (C/EBP) δ 的表达,导致脂肪生成主转录因子如过氧化物酶体增殖物激活受体 (PPAR) γ 和 C/EBPα 的表达减少。此外,Orientin 的抗脂肪生成作用抑制了 Akt 的磷酸化以及随后叉头框蛋白 O1 (FOXO1) 的磷酸化,从而抑制了 基因的转录。这些结果表明,植物类黄酮 Orientin 通过抑制 表达和抑制磷酸肌醇 3-激酶/Akt-FOXO1 信号通路在脂肪细胞中抑制 基因的表达,从而抑制脂肪生成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eba0/5852706/2990123146ff/nutrients-10-00130-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eba0/5852706/69db3a9d0927/nutrients-10-00130-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eba0/5852706/27489aa1b2ff/nutrients-10-00130-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eba0/5852706/f79053cea169/nutrients-10-00130-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eba0/5852706/ff788db37b56/nutrients-10-00130-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eba0/5852706/2990123146ff/nutrients-10-00130-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eba0/5852706/69db3a9d0927/nutrients-10-00130-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eba0/5852706/057c9a8637d5/nutrients-10-00130-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eba0/5852706/27489aa1b2ff/nutrients-10-00130-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eba0/5852706/f79053cea169/nutrients-10-00130-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eba0/5852706/a631df5dd963/nutrients-10-00130-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eba0/5852706/ba18f1d7cd11/nutrients-10-00130-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eba0/5852706/4ad4a4fe4bef/nutrients-10-00130-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eba0/5852706/ff788db37b56/nutrients-10-00130-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eba0/5852706/2990123146ff/nutrients-10-00130-g009.jpg

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