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在3T3-L1细胞分化阶段添加花生四烯酸通过降低促脂肪生成前列腺素的作用发挥抗脂肪生成效应。

Arachidonic Acid Added during the Differentiation Phase of 3T3-L1 Cells Exerts Anti-Adipogenic Effect by Reducing the Effects of Pro-Adipogenic Prostaglandins.

作者信息

Nartey Michael N N, Jisaka Mitsuo, Syeda Pinky Karim, Nishimura Kohji, Shimizu Hidehisa, Yokota Kazushige

机构信息

The United Graduate School of Agricultural Sciences, Tottori University, 4-101 Koyama-Minami, Tottori 680-8553, Japan.

Council for Scientific and Industrial Research-Animal Research Institute, Achimota, Accra P.O. Box AH20, Ghana.

出版信息

Life (Basel). 2023 Jan 29;13(2):367. doi: 10.3390/life13020367.

Abstract

A linoleic acid (LA) metabolite arachidonic acid (AA) added to 3T3-L1 cells is reported to suppress adipogenesis. The purpose of the present study aimed to clarify the effects of AA added during the differentiation phase, including adipogenesis, the types of prostaglandins (PG)s produced, and the crosstalk between AA and the PGs produced. Adipogenesis was inhibited by AA added, while LA did not. When AA was added, increased PGE and PGF production, unchanged Δ-PGJ production, and reduced PGI production were observed. Since the decreased PGI production was reflected in decreased CCAAT/enhancer-binding protein-β (C/EBPβ) and C/EBPδ expression, we expected that the coexistence of PGI with AA would suppress the anti-adipogenic effects of AA. However, the coexistence of PGI with AA did not attenuate the anti-adipogenic effects of AA. In addition, the results were similar when Δ-PGJ coexisted with AA. Taken together, these results indicated that the metabolism of ingested LA to AA is necessary to inhibit adipogenesis and that exposure of AA to adipocytes during only the differentiation phase is sufficient. As further mechanisms for suppressing adipogenesis, AA was found not only to increase PGE and PGF and decrease PGI production but also to abrogate the pro-adipogenic effects of PGI and Δ-PGJ.

摘要

据报道,添加到3T3-L1细胞中的亚油酸(LA)代谢物花生四烯酸(AA)可抑制脂肪生成。本研究的目的旨在阐明在分化阶段添加AA的作用,包括脂肪生成、产生的前列腺素(PG)类型以及AA与所产生的PG之间的相互作用。添加AA可抑制脂肪生成,而LA则无此作用。添加AA时,观察到PGE和PGF生成增加,Δ-PGJ生成不变,PGI生成减少。由于PGI生成减少反映在CCAAT/增强子结合蛋白-β(C/EBPβ)和C/EBPδ表达降低,我们预期PGI与AA共存会抑制AA的抗脂肪生成作用。然而,PGI与AA共存并未减弱AA的抗脂肪生成作用。此外,当Δ-PGJ与AA共存时,结果相似。综上所述,这些结果表明,摄入的LA代谢为AA对于抑制脂肪生成是必要的,并且仅在分化阶段使脂肪细胞暴露于AA就足够了。作为抑制脂肪生成的进一步机制,发现AA不仅会增加PGE和PGF并降低PGI生成,还会消除PGI和Δ-PGJ的促脂肪生成作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a393/9962328/9c3209ce4306/life-13-00367-g001.jpg

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