L-leucine promotes the synthesis of milk protein and milk fat in bovine mammary epithelial cells through the AKT/mTOR signaling pathway under hypoxic conditions

IF 4.8 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Nutritional Biochemistry Pub Date : 2024-08-08 DOI:10.1016/j.jnutbio.2024.109732
Yuan Liu, Huixia Li
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Abstract

Hypoxia stress has been demonstrated to impede animal embryonic development, spermatogenesis, and lactation, leading to decreased animal production performance. However, the impact of hypoxia-induced activation of hypoxia inducible factor-1 (HIF-1) signaling on milk protein and fat synthesis remains unclear. L-leucine, a branched-chain amino acid, is known to modulate milk protein and fat synthesis. Therefore, our study aimed to evaluate the effect of L-leucine on milk protein and fat synthesis under hypoxic conditions and shed light on the molecular mechanism using an in vitro model. The results indicated that hypoxia treatment significantly decreased the synthesis of α-casein and β-casein, as well as inhibited factors related to milk fat synthesis in bovine mammary epithelial cells (MAC-T). Additionally, hypoxia stress suppressed the activities of the mammalian target of rapamycin (mTOR) and protein kinase B (AKT). Interfering with HIF-1α significantly reversed the expression of AKT, mTOR and factors related to milk synthesis. Importantly, supplementation with L-leucine activated AKT/mTOR signaling, thereby enhancing milk protein and fat synthesis in MAC-T cells to some extent. In conclusion, these findings suggest that HIF-1 signaling plays an important role in milk synthesis and that L-leucine may stimulate the synthesis of milk protein and fat by activating the AKT/mTOR signaling pathway under hypoxic conditions, making it a potential additive for promoting milk synthesis inhibited by hypoxia.

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在缺氧条件下,L-亮氨酸通过 AKT/mTOR 信号通路促进牛乳腺上皮细胞合成乳蛋白和乳脂肪。
低氧应激已被证明会阻碍动物胚胎发育、精子发生和泌乳,导致动物生产性能下降。然而,低氧诱导因子-1(HIF-1)信号的激活对牛奶蛋白质和脂肪合成的影响仍不清楚。众所周知,L-亮氨酸是一种支链氨基酸,可调节牛奶蛋白质和脂肪的合成。因此,我们的研究旨在评估缺氧条件下L-亮氨酸对牛奶蛋白质和脂肪合成的影响,并利用体外模型阐明其分子机制。结果表明,缺氧处理会显著降低牛乳腺上皮细胞(MAC-T)中α-酪蛋白和β-酪蛋白的合成,并抑制乳脂合成的相关因子。此外,低氧应激抑制了哺乳动物雷帕霉素靶标(mTOR)和蛋白激酶 B(AKT)的活性。干扰 HIF-1α 能明显逆转 AKT、mTOR 和与牛奶合成有关的因子的表达。重要的是,补充左旋亮氨酸可激活AKT/mTOR信号转导,从而在一定程度上提高MAC-T细胞的乳蛋白和脂肪合成。总之,这些研究结果表明,HIF-1 信号在乳汁合成中起着重要作用,而在缺氧条件下,L-亮氨酸可通过激活 AKT/mTOR 信号通路来刺激乳蛋白和脂肪的合成,使其成为促进受缺氧抑制的乳汁合成的潜在添加剂。
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来源期刊
Journal of Nutritional Biochemistry
Journal of Nutritional Biochemistry 医学-生化与分子生物学
CiteScore
9.50
自引率
3.60%
发文量
237
审稿时长
68 days
期刊介绍: Devoted to advancements in nutritional sciences, The Journal of Nutritional Biochemistry presents experimental nutrition research as it relates to: biochemistry, molecular biology, toxicology, or physiology. Rigorous reviews by an international editorial board of distinguished scientists ensure publication of the most current and key research being conducted in nutrition at the cellular, animal and human level. In addition to its monthly features of critical reviews and research articles, The Journal of Nutritional Biochemistry also periodically publishes emerging issues, experimental methods, and other types of articles.
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