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棕榈酰乳酸诱导 3T3-L1 前脂肪细胞向脂肪生成和棕色脂肪样表型分化。

Palmitoyl lactic acid induces adipogenesis and a brown fat-like phenotype in 3T3-L1 preadipocytes.

机构信息

Department of Microbiology and Immunology, Teikyo University School of Medicine, Tokyo, Japan.

Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan.

出版信息

Biochim Biophys Acta Mol Cell Biol Lipids. 2018 Jul;1863(7):772-782. doi: 10.1016/j.bbalip.2018.04.003. Epub 2018 Apr 12.

DOI:10.1016/j.bbalip.2018.04.003
PMID:29654827
Abstract

Brown adipose tissue is specialized to generate heat by dissipating chemical energy and may provide novel strategies for obesity treatment in humans. Recently, advances in understanding the pharmacological and dietary agents that contribute to the browning of white adipose tissue have been made to alleviate obesity by promoting energy expenditure. Krill oil is widely used as a health supplement in humans. In this study, the components from krill oil that promote adipogenesis of 3T3-L1 cells were screened to reveal palmitoyl lactic acid (PLA) as a promoter of adipogenesis. The PLA-induced adipocytes contained large number of small lipid droplets. Moreover, similar to the peroxisome proliferator-activated receptor (PPAR)γ agonists, pioglitazone and rosiglitazone, PLA significantly enhances adipogenesis in the presence of dexamethasone compared with PLA alone. Treatment with PLA causes a brown fat-like phenotype in 3T3-L1 cells by enhanced expression of various brown/beige cell-specific genes, such as PR domain containing 16 (Prdm16) and peroxisome proliferative activated receptor, gamma, coactivator 1 alpha (Pgc1a), as well as adiponectin gene. The expression profile of the brown/beige cell-specific genes induced by PLA was similar to that of the PPARγ agonist in 3T3-L1 cells. Our findings suggest that PLA induces a brown fat-like phenotype and, thus, likely has therapeutic potential in treating obesity.

摘要

棕色脂肪组织通过消耗化学能来产生热量,这可能为人类肥胖治疗提供新策略。最近,人们在理解促进白色脂肪组织褐变的药理学和饮食因子方面取得了进展,通过促进能量消耗来缓解肥胖。磷虾油在人类中被广泛用作保健品。在这项研究中,筛选了促进 3T3-L1 细胞脂肪生成的磷虾油成分,发现棕榈酸乳酸(PLA)是脂肪生成的促进剂。PLA 诱导的脂肪细胞含有大量小的脂滴。此外,与过氧化物酶体增殖物激活受体(PPAR)γ激动剂吡格列酮和罗格列酮类似,PLA 在与 PLA 单独使用相比,在存在地塞米松的情况下显著增强脂肪生成。PLA 通过增强各种棕色/米色细胞特异性基因的表达,如 PR 结构域包含 16(Prdm16)和过氧化物酶体增殖物激活受体γ共激活因子 1α(Pgc1a),以及脂联素基因,引起 3T3-L1 细胞中的棕色脂肪样表型。PLA 诱导的棕色/米色细胞特异性基因的表达谱与 3T3-L1 细胞中 PPARγ 激动剂的表达谱相似。我们的研究结果表明,PLA 诱导出一种类似棕色脂肪的表型,因此,在治疗肥胖症方面可能具有治疗潜力。

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