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苏克斯多芬通过激活过氧化物酶体增殖物激活受体γ(PPARγ)促进脂肪细胞分化并改善葡萄糖代谢异常。

Suksdorfin Promotes Adipocyte Differentiation and Improves Abnormalities in Glucose Metabolism via PPARγ Activation.

作者信息

Iwase Mari, Yamamoto Takayuki, Nishimura Kanako, Takahashi Haruya, Mohri Shinsuke, Li Yongjia, Jheng Huei-Fen, Nomura Wataru, Takahashi Nobuyuki, Kim Chu-Sook, Yu Rina, Taniguchi Masahiko, Baba Kimiye, Murakami Shigeru, Kawada Teruo, Goto Tsuyoshi

机构信息

Laboratory of Molecular Functions of Food, Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Uji, Kyoto, 611-0011, Japan.

Research Unit for Physiological Chemistry, Center for the Promotion of Interdisciplinary Education and Research, Kyoto University, Kyoto, 611-0011, Japan.

出版信息

Lipids. 2017 Jul;52(7):657-664. doi: 10.1007/s11745-017-4269-7. Epub 2017 Jun 10.

Abstract

Although the Apiaceae herb family has been traditionally used for the management of type 2 diabetes, its molecular mechanism has not been clarified. Coumarin derivatives, which are abundant in plants of the Apiaceae family, were evaluated for their effects on adipogenesis. We found that suksdorfin significantly promoted adipocyte differentiation and enhanced production of adiponectin, an anti-diabetic adipokine. We also demonstrated that suksdorfin activates peroxisome proliferator-activated receptor gamma (PPARγ), a master regulator of adipogenesis. Furthermore, we showed metabolic disorders in obese diabetic KK-A mice were attenuated by suksdorfin feeding. Suksdorfin intake induced adipocyte miniaturization and increased expression levels of PPARγ target genes related to adipocyte differentiation. These results indicated that suksdorfin induces adipogenesis in white adipose tissue (WAT) via the activation of PPARγ, leading to improvement of obesity-induced metabolic disorders. Therefore, suksdorfin-mediated amelioration of WAT dysfunctions might be responsible for the anti-diabetic effects of traditional herbal medicine therapy with Apiaceae.

摘要

虽然传统上伞形科草本植物家族被用于治疗2型糖尿病,但其分子机制尚未阐明。对伞形科植物中丰富的香豆素衍生物进行了脂肪生成作用评估。我们发现苏克多芬显著促进脂肪细胞分化并增强脂联素(一种抗糖尿病脂肪因子)的产生。我们还证明苏克多芬激活过氧化物酶体增殖物激活受体γ(PPARγ),这是脂肪生成的主要调节因子。此外,我们表明通过喂食苏克多芬可减轻肥胖糖尿病KK-A小鼠的代谢紊乱。摄入苏克多芬可诱导脂肪细胞小型化并增加与脂肪细胞分化相关的PPARγ靶基因的表达水平。这些结果表明,苏克多芬通过激活PPARγ诱导白色脂肪组织(WAT)中的脂肪生成,从而改善肥胖诱导的代谢紊乱。因此,苏克多芬介导的WAT功能障碍改善可能是伞形科传统草药疗法抗糖尿病作用的原因。

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