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青蒿促进脂肪生成而没有脂肪生成效应物。

Artemisia scoparia promotes adipogenesis in the absence of adipogenic effectors.

机构信息

Department of Adipocyte Biology, Pennington Biomedical Research Center, Baton Rouge, Louisiana, USA.

Department of Biological Sciences, Louisiana State University, Baton Rouge, Louisiana, USA.

出版信息

Obesity (Silver Spring). 2021 Aug;29(8):1309-1319. doi: 10.1002/oby.23199. Epub 2021 Jul 5.

Abstract

OBJECTIVE

Extracts of Artemisia scoparia (SCO) have antidiabetic properties in mice and enhance adipogenesis in vitro, but the underlying mechanisms are unknown. Thiazolidinediones, including rosiglitazone (ROSI), are pharmacological activators of peroxisome proliferator-activated receptor gamma that also promote adipogenesis. The aim of this study was to examine adipogenic pathways responsible for SCO-mediated adipogenesis and identify potential differences between SCO and ROSI in the ability to promote adipocyte development.

METHODS

The ability of SCO or ROSI to promote adipogenesis in 3T3-L1 cells following systematic omission of the common triad of adipogenic effectors dexamethasone, 1-methyl-3-isobutylxanthine (MIX), and insulin was examined. Adipogenesis was assessed by both neutral lipid quantitation and adipocyte marker gene expression.

RESULTS

The results demonstrate that SCO and ROSI promote adipogenesis and increase the expression of several peroxisome proliferator-activated receptor gamma target genes involved in lipid accumulation in the absence of MIX. However, ROSI can enhance adipogenesis in the absence of MIX and insulin and differentially regulates adipogenic and lipid metabolism genes as compared with SCO.

CONCLUSIONS

These data demonstrate the adipogenic capabilities of SCO are similar but not identical to ROSI, thereby warranting further research into SCO as a promising source of therapeutic compounds in the treatment of metabolic disease states.

摘要

目的

青蒿(SCO)提取物在小鼠中具有降血糖作用,并在体外增强脂肪生成,但具体机制尚不清楚。噻唑烷二酮类药物,包括罗格列酮(ROSI),是过氧化物酶体增殖物激活受体γ的药理学激活剂,也可促进脂肪生成。本研究旨在研究负责 SCO 介导的脂肪生成的脂肪生成途径,并确定 SCO 和 ROSI 在促进脂肪细胞发育方面的潜在差异。

方法

系统地排除了脂肪生成效应物地塞米松、1-甲基-3-异丁基黄嘌呤(MIX)和胰岛素的常见三联体后,研究了 SCO 或 ROSI 对 3T3-L1 细胞脂肪生成的促进作用。通过中性脂质定量和脂肪细胞标记基因表达来评估脂肪生成。

结果

结果表明,SCO 和 ROSI 均可促进脂肪生成,并增加参与脂质积累的几个过氧化物酶体增殖物激活受体γ靶基因的表达,而无需 MIX。然而,与 SCO 相比,ROSI 可以在没有 MIX 和胰岛素的情况下增强脂肪生成,并调节脂肪生成和脂质代谢基因。

结论

这些数据表明,SCO 的脂肪生成能力与 ROSI 相似但不完全相同,因此有必要进一步研究 SCO 作为治疗代谢性疾病的有前途的治疗化合物来源。

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