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在顺-9,反-11共轭亚油酸合成过程中,MAC-T细胞对硬脂酰辅酶A去饱和酶1抑制的反应。

Responses of MAC-T Cells to Inhibited Stearoyl-CoA Desaturase 1 during cis-9, trans-11 Conjugated Linoleic Acid Synthesis.

作者信息

Wang Tao, Lee Honggu, Zhen Yuguo

机构信息

College of Animal Science and Technology, Jilin Agricultural University, Xincheng Street no. 2888, Nanguan District, Changchun, 130118, Jilin Province, People' Republic of China.

Key Laboratory of Animal Nutrition and Feed Science of Jilin Province, Jilin Agricultural University, Xincheng Street No. 2888, Nanguan District, Changchun, 130118, Jilin Province, People' Republic of China.

出版信息

Lipids. 2018 Jun;53(6):647-652. doi: 10.1002/lipd.12077.

Abstract

Cis-9-conjugated, trans-11-conjugated linoleic acid (CLA) is known for its positive activities on human health. The synthesis of cis-9, trans-11 CLA in mammary glands is generally thought to be catalyzed by stearoyl-CoA desaturase 1 (SCD1), but this has not been rigorously established. In this study, we hypothesized that the inhibition of SCD1 (by CAY10566) would block the synthesis of cis-9, trans-11 CLA in bovine mammary alveolar cells (MAC-T) cells. Results showed that MAC-T cells incubated with 10 nM CAY10566 for 12 h (CAY) produced less cis-9, trans-11 CLA (p < 0.01), lower 14:1/(14:1 + 14:0)% (p < 0.01), more trans-11 18:1 (TVA) accumulation (p < 0.01), and reduced SCD1 mRNA levels (p < 0.01) compared with the control group (CON). Moreover, the mRNA abundances of sterol regulatory element-binding protein 1 [SREBPF1], acyl-CoA synthetase short-chain family member 2 [ACSS2], and lipin 1 [LPIN1] were significantly elevated when SCD1 was inhibited in the CAY group (p < 0.05). Taken together, CAY10566 inhibition of SCD1 resulted in lower cis-9, trans-11 CLA synthesis ability, and SREBF1, ACSSS2, and LPIN1 were negatively associated with SCD1. These findings not only provide the direct evidence that cis-9, trans-11 CLA synthesis is catalyzed by SCD1, but also help us understand the responses of MAC-T cells to SCD1 inhibition.

摘要

顺-9-共轭、反-11-共轭亚油酸(CLA)因其对人体健康的积极作用而闻名。乳腺中顺-9,反-11 CLA的合成通常被认为是由硬脂酰辅酶A去饱和酶1(SCD1)催化的,但这一点尚未得到严格证实。在本研究中,我们假设抑制SCD1(通过CAY10566)会阻断牛乳腺肺泡细胞(MAC-T)中顺-9,反-11 CLA的合成。结果表明,与对照组(CON)相比,用10 nM CAY10566处理12小时(CAY组)的MAC-T细胞产生的顺-9,反-11 CLA更少(p<0.01),14:1/(14:1 + 14:0)%更低(p<0.01),反-11 18:1(TVA)积累更多(p<0.01),且SCD1 mRNA水平降低(p<0.01)。此外,当CAY组中SCD1被抑制时,固醇调节元件结合蛋白1[SREBPF1]、酰基辅酶A合成酶短链家族成员2[ACSS2]和脂素1[LPIN1]的mRNA丰度显著升高(p<0.05)。综上所述,CAY10566对SCD1的抑制导致顺-9,反-11 CLA合成能力降低,且SREBF1、ACSSS2和LPIN1与SCD1呈负相关。这些发现不仅提供了顺-9,反-11 CLA合成由SCD1催化的直接证据,还帮助我们了解MAC-T细胞对SCD1抑制的反应。

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