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小豆蔻明通过激活蛋白激酶 A 介导的 3T3-L1 细胞棕色化来抑制脂肪生成。

Cardamonin suppresses lipogenesis by activating protein kinase A-mediated browning of 3T3-L1 cells.

机构信息

Department of Food Science and Biotechnology, College of Life Science, CHA University, Seongnam, Kyeonggi 13488, South Korea.

Department of Food Science and Biotechnology, College of Life Science, CHA University, Seongnam, Kyeonggi 13488, South Korea.

出版信息

Phytomedicine. 2019 Dec;65:153064. doi: 10.1016/j.phymed.2019.153064. Epub 2019 Aug 3.

DOI:10.1016/j.phymed.2019.153064
PMID:31645009
Abstract

BACKGROUND

Obesity develops when dietary energy intake exceeds energy expenditure, and can be associated with metabolic syndrome. Recent studies have shown that dietary phytochemicals can promote energy expenditure by inducing the browning of white adipose tissue (WAT).

PURPOSE

This study investigated whether cardamonin induces the browning of 3T3-L1 adipocytes through the activation of protein kinase A (PKA).

METHODS

Anti-obesity potential of cardamonin was evaluated in 3T3-L1 adipocytes. Adipocyte-specific genes were observed using western blot, qPCR analysis and immunocytochemistry.

RESULTS

Cardamonin treatment inhibited lipid droplet accumulation and reduced the expression of the adipogenic proteins C/EBPα and FABP4, and the lipogenic proteins LPAATθ, lipin 1, DGAT1, SREBP1, and FAS. Cardamonin also induced the expression of the browning marker genes PRDM16, PGC1α, and UCP1 at the mRNA and protein levels, and induced mRNA expression of CD137, a key marker of beige adipocytes. It also increased the expression of the β-oxidation genes CPT1 and PPARα at the mRNA and protein levels. In addition, cardamonin increased PKA phosphorylation and the mRNA and protein expression of the downstream lipolytic enzymes adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL).

CONCLUSION

Our findings demonstrate novel effects of cardamonin to stimulate adipocyte browning, suppress lipogenesis, and promote lipolysis, implying it may have potential as an anti-obesity agent.

摘要

背景

当饮食能量摄入超过能量消耗时,就会发生肥胖,并且可能与代谢综合征有关。最近的研究表明,膳食植物化学物质可以通过诱导白色脂肪组织(WAT)褐变来促进能量消耗。

目的

本研究旨在探讨小豆蔻明是否通过激活蛋白激酶 A(PKA)诱导 3T3-L1 脂肪细胞的褐变。

方法

在 3T3-L1 脂肪细胞中评估小豆蔻明的抗肥胖潜力。使用 Western blot、qPCR 分析和免疫细胞化学观察脂肪细胞特异性基因。

结果

小豆蔻明处理抑制了脂滴积累,并降低了脂肪生成蛋白 C/EBPα 和 FABP4 以及脂生成蛋白 LPAATθ、脂酶 1、DGAT1、SREBP1 和 FAS 的表达。小豆蔻明还诱导了褐变标志物基因 PRDM16、PGC1α 和 UCP1 的 mRNA 和蛋白水平表达,并诱导了 beige 脂肪细胞的关键标志物 CD137 的 mRNA 表达。它还增加了 β-氧化基因 CPT1 和 PPARα 的 mRNA 和蛋白水平表达。此外,小豆蔻明增加了 PKA 磷酸化以及下游脂肪酶脂肪甘油三酯脂肪酶(ATGL)和激素敏感脂肪酶(HSL)的 mRNA 和蛋白表达。

结论

我们的研究结果表明小豆蔻明具有刺激脂肪细胞褐变、抑制脂肪生成和促进脂肪分解的新作用,表明它可能具有作为抗肥胖剂的潜力。

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