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氯化锂促进牛乳腺上皮细胞内 CLA 的内源性合成。

Lithium Chloride Promotes Endogenous Synthesis of CLA in Bovine Mammary Epithelial Cells.

机构信息

Jilin Provincial Key Laboratory of Livestock and Poultry Feed and Feeding in the Northeastern Frigid Area, College of Animal Sciences, Jilin University, Changchun, 130062, China.

出版信息

Biol Trace Elem Res. 2024 Feb;202(2):513-526. doi: 10.1007/s12011-023-03679-z. Epub 2023 Apr 26.

Abstract

Although conjugated linoleic acid (CLA) can promote human health, its content in milk is insufficient to have a significant impact. The majority of the CLA in milk is produced endogenously by the mammary gland. However, research on improving its content through nutrient-induced endogenous synthesis is relatively scarce. Previous research found that the key enzyme, stearoyl-CoA desaturase (SCD) for the synthesis of CLA, can be expressed more actively in bovine mammary epithelial cells (MAC-T) when lithium chloride (LiCl) is present. This study investigated whether LiCl can encourage CLA synthesis in MAC-T cells. The results showed that LiCl effectively increased SCD and proteasome α5 subunit (PSMA5) protein expression in MAC-T cells as well as the content of CLA and its endogenous synthesis index. LiCl enhanced the expression of proliferator-activated receptor-γ (PPARγ), sterol regulatory element-binding protein 1 (SREBP1), and its downstream enzymes acetyl CoA carboxylase (ACC), fatty acid synthase (FASN), lipoprotein lipase (LPL), and Perilipin 2 (PLIN2). The addition of LiCl significantly enhanced p-GSK-3β, β-catenin, p-β-catenin protein expression, hypoxia-inducible factor-1α (HIF-1α), and downregulation factor genes for mRNA expression (P < 0.05). These findings highlight that LiCl can increase the expression of SCD and PSMA5 by activating the transcription of HIF-1α, Wnt/β-catenin, and the SREBP1 signaling pathways to promote the conversion of trans-vaccenic acid (TVA) to the endogenous synthesis of CLA. This data suggests that the exogenous addition of nutrients can increase CLA content in milk through pertinent signaling pathways.

摘要

虽然共轭亚油酸(CLA)可以促进人体健康,但它在牛奶中的含量不足以产生显著影响。牛奶中的大部分 CLA 是由乳腺内源合成的。然而,通过营养诱导内源性合成来提高其含量的研究相对较少。先前的研究发现,氯化锂(LiCl)存在时,合成 CLA 的关键酶硬脂酰辅酶 A 去饱和酶(SCD)可以在奶牛乳腺上皮细胞(MAC-T)中更活跃地表达。本研究探讨了 LiCl 是否可以促进 MAC-T 细胞中 CLA 的合成。结果表明,LiCl 能有效增加 MAC-T 细胞中 SCD 和蛋白酶体 α5 亚基(PSMA5)的蛋白表达,以及 CLA 的含量及其内源性合成指数。LiCl 增强了过氧化物酶体增殖物激活受体-γ(PPARγ)、固醇调节元件结合蛋白 1(SREBP1)及其下游酶乙酰辅酶 A 羧化酶(ACC)、脂肪酸合成酶(FASN)、脂蛋白脂肪酶(LPL)和 Perilipin 2(PLIN2)的表达。加入 LiCl 显著增强了 p-GSK-3β、β-catenin、p-β-catenin 蛋白表达、缺氧诱导因子-1α(HIF-1α)和下调因子基因的 mRNA 表达(P<0.05)。这些发现表明,LiCl 通过激活 HIF-1α、Wnt/β-catenin 和 SREBP1 信号通路,增加 SCD 和 PSMA5 的表达,促进反式-油酸(TVA)向内源性 CLA 转化,从而增加 SCD 和 PSMA5 的表达。这些数据表明,通过相关信号通路,外源性添加营养物质可以增加牛奶中 CLA 的含量。

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