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膳食脂肪不能克服反式-10, 顺式-12 共轭亚油酸对泌乳小鼠乳脂合成的抑制作用。

Dietary Fat Does Not Overcome trans-10, cis-12 Conjugated Linoleic Acid Inhibition of Milk Fat Synthesis in Lactating mice.

机构信息

Department of Animal Science, Cornell University, Ithaca, NY, 14853, USA.

Department of Animal Science, Penn State University, University Park, PA, 16802, USA.

出版信息

Lipids. 2020 May;55(3):201-212. doi: 10.1002/lipd.12228. Epub 2020 Feb 24.

DOI:10.1002/lipd.12228
PMID:32092162
Abstract

Trans-10, cis-12 conjugated linoleic acid (CLA) is a potent inhibitor of milk fat synthesis in the cow and similarly reduces milk fat in rodents. The objective of this study was to determine whether dietary fat can overcome CLA inhibition of milk fat concentration in lactating mice. Wild type C57Bl/6J mice (n = 31) were fed semipurified diets containing either low fat (LF; 4% fat) or high fat (HF; 23.6% fat) starting 4-6 days postpartum. Dietary fat was increased by inclusion of high oleic sunflower oil. After 2 days on the experimental diets, lactating dams were orally dosed with either water (control) or trans-10, cis-12 CLA (20 mg/day) for 5 days. CLA treatment decreased pup growth similarly in both HF and LF diets. Milk fat percent was increased over 16% by the HF diet and decreased over 12% by CLA, but there was no interaction of dietary fat and CLA. Both CLA and the HF diet reduced the proportion of short- and medium-chain fatty acids that originate from de novo synthesis, and there was no interaction of diet and CLA. CLA had no effect on the percent of preformed fatty acids, but the HF diet increased their abundance. Dietary fat and CLA both modified mammary expression of lipogenic enzymes and regulators, but no interactions were observed. In conclusion, CLA reduced milk fat concentration and litter growth, but these effects were not overcome by increased dietary fat from high oleic sunflower oil. CLA inhibition of milk fat in the mammary gland is not substrate dependent, and the mechanism is independent from dietary supply of oleic acid.

摘要

反式-10,顺式-12 共轭亚油酸(CLA)是一种有效的奶牛乳脂合成抑制剂,同样可以减少啮齿动物的乳脂。本研究的目的是确定饮食中的脂肪是否可以克服 CLA 对泌乳小鼠乳脂浓度的抑制作用。野生型 C57Bl/6J 小鼠(n = 31)在产后 4-6 天开始接受含有低脂肪(LF;4%脂肪)或高脂肪(HF;23.6%脂肪)的半纯化饮食。通过添加高油酸葵花籽油来增加饮食中的脂肪。在实验饮食上进行 2 天后,泌乳母鼠经口给予水(对照)或 trans-10,cis-12 CLA(20 mg/天)5 天。CLA 处理同样降低了 HF 和 LF 饮食中幼鼠的生长速度。HF 饮食使乳脂百分比增加了 16%以上,CLA 使乳脂百分比降低了 12%以上,但饮食和 CLA 之间没有相互作用。CLA 和 HF 饮食都降低了短链和中链脂肪酸的比例,这些脂肪酸来自从头合成,且饮食和 CLA 之间没有相互作用。CLA 对已形成脂肪酸的比例没有影响,但 HF 饮食增加了它们的丰度。饮食脂肪和 CLA 都改变了乳腺中脂肪生成酶和调节剂的表达,但没有观察到饮食和 CLA 之间的相互作用。总之,CLA 降低了乳脂浓度和窝仔生长,但这些影响并没有被高油酸葵花籽油增加的饮食脂肪所克服。CLA 对乳腺乳脂的抑制作用不是底物依赖性的,其机制与油酸的膳食供应无关。

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