Effects of fatty acid treatments on the dexamethasone-induced intramuscular lipid accumulation in chickens.

Effects of fatty acid treatments on the dexamethasone-induced intramuscular lipid accumulation in chickens.
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DOI:
10.1371/journal.pone.0036663
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发表时间:
2012
期刊:
影响因子:
3.7
通讯作者:
Lin H
Lin H
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Wang Xj;Wei Dl;Song Zg;Jiao Hc;Lin H

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糖皮质激素对肌肉中的脂质代谢具有重要影响,而脂肪酸的类型可能会影响线粒体的利用。因此,我们假设不同的脂肪酸类型治疗可能会影响糖皮质激素诱导的肌内脂质积累。研究了地塞米松 (DEX) 对经过和不经过脂肪酸处理的肉鸡 (Gallus gallus Domesticus) 骨骼肌脂肪酸代谢和储存的影响。雄性 Arbor Acres 鸡(31 日龄)用棕榈酸(PA)或油酸(OA)处理 7 天,然后给予 DEX 3 天(35-37 日龄)。 DEX 诱导的脂质摄取和氧化失衡(通过脂肪酸转运蛋白 1 (FATP1) 表达增加和肉碱棕榈酰转移酶 1 活性降低来估计)有助于骨骼肌脂质积累。 DEX 处理鸡的氧化肌比糖酵解肌更敏感,显示 AMP 与 ATP 比率降低,AMP 激活蛋白激酶 (AMPK) α 磷酸化及其活性降低,以及哺乳动物雷帕霉素靶点 (mTOR) 和核糖体 p70S6 激酶的磷酸化增加,但没有 Akt 激活。 DEX 刺激的脂质沉积被 PA 增强,但被 OA 减轻,这是对 AMPK、mTOR 和 FATP1 等不同调节途径的反应。 SFA 加剧了 DEX 诱导的肌内脂质积累,但不饱和脂肪酸则减轻了这种积累。抑制的 AMPK 和增强的 mTOR 信号通路参与了糖皮质激素介导的肌内脂肪积累的增强。
Glucocorticoid has an important effect on lipid metabolism in muscles, and the type of fatty acid likely affects mitochondrial utilization. Therefore, we hypothesize that the different fatty acid types treatment may affect the glucocorticoid induction of intramuscular lipid accumulation. The effect of dexamethasone (DEX) on fatty acid metabolism and storage in skeletal muscle of broiler chickens (Gallus gallus domesticus) was investigated with and without fatty acid treatments. Male Arbor Acres chickens (31 d old) were treated with either palmitic acid (PA) or oleic acid (OA) for 7 days, followed by DEX administration for 3 days (35–37 d old). The DEX-induced lipid uptake and oxidation imbalance, which was estimated by increased fatty acid transport protein 1 (FATP1) expression and decreased carnitine palmitoyl transferase 1 activity, contributed to skeletal muscle lipid accumulation. More sensitive than glycolytic muscle, the oxidative muscle in DEX-treated chickens showed a decrease in the AMP to ATP ratio, a decrease in AMP-activated protein kinase (AMPK) alpha phosphorylation and its activity, as well as an increase in the phosphorylation of mammalian target of rapamycin (mTOR) and ribosomal p70S6 kinase, without Akt activation. DEX-stimulated lipid deposition was augmented by PA, but alleviated by OA, in response to pathways that were regulated differently, including AMPK, mTOR and FATP1. DEX-induced intramuscular lipid accumulation was aggravated by SFA but alleviated by unsaturated fatty acid. The suppressed AMPK and augmented mTOR signaling pathways were involved in glucocortcoid-mediated enhanced intramuscular fat accumulation.
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