Harvatine Kevin J, Robblee Megan M, Thorn Stephanie R, Boisclair Yves R, Bauman Dale E
Department of Animal Science, Penn State University, University Park, PA; and.
Department of Animal Science, Cornell University, Ithaca, NY.
J Nutr. 2014 Dec;144(12):1928-34. doi: 10.3945/jn.114.198911. Epub 2014 Oct 15.
Trans-10, cis-12 conjugated linoleic acid (10,12 CLA) is a potent inhibitor of milk fat synthesis in mammals. In the cow, 10 g/d of 10,12 CLA specifically and reversibly inhibits mammary lipogenesis, whereas substantially higher doses are not specific and cause a generalized inhibition of milk synthesis.
The objective of this study was to validate a lactating mouse model by establishing the dose response, specificity, and reversibility of the inhibition of milk fat synthesis by 10,12 CLA.
Lactating mice (C57BL/6J) received daily doses of 0 (control), 7, 20, or 60 mg of 10,12 CLA for 5 d during established lactation. A second group of lactating mice was treated with 20 mg/d of 10,12 CLA for 4 d and followed post-treatment to evaluate reversibility.
CLA decreased pup growth with a 49% decrease occurring with 60 mg/d of CLA. Milk fat percentage was decreased 11% and 20% with the 7 and 20 mg/d dose, respectively, and all CLA treatments had a decreased concentration of de novo synthesized fatty acids (FAs) in milk fat. In agreement, 20 mg/d of 10,12 CLA decreased the lipogenic capacity of mammary tissue by 30% and mammary expression of FA synthase (Fasn), sterol response element binding protein 1 (Srebf1), and thyroid hormone responsive spot 14 (Thrsp) by 30-60%, whereas milk protein percentage and mammary expression of α-lactalbumin (Lalba) were unaltered. This dose of CLA reduced pup growth by nearly 20% and milk de novo synthesized FAs by >35%, and these effects were completely reversed 5 d after 10,12 CLA treatment was terminated.
Inhibition of mammary lipogenesis by 10,12 CLA is dose-dependent in the mouse, with a specific and reversible reduction in milk fat synthesis at the 20 mg/d dose and additional nonspecific effects on milk synthesis at higher CLA doses.
反式-10，顺式-12共轭亚油酸（10,12 CLA）是哺乳动物乳脂肪合成的有效抑制剂。在奶牛中，每天10克10,12 CLA可特异性且可逆地抑制乳腺脂肪生成，而剂量大幅增加则无特异性，并会导致乳汁合成的普遍抑制。
本研究的目的是通过确定10,12 CLA对乳脂肪合成抑制的剂量反应、特异性和可逆性，来验证泌乳小鼠模型。
泌乳小鼠（C57BL/6J）在既定泌乳期内连续5天每天接受0（对照）、7、20或60毫克的10,12 CLA剂量。第二组泌乳小鼠用每天20毫克的10,12 CLA处理4天，并在处理后进行跟踪以评估可逆性。
CLA降低了幼崽生长，60毫克/天的CLA使幼崽生长下降了49%。7毫克/天和20毫克/天剂量的CLA分别使乳脂肪百分比降低了11%和20%，所有CLA处理均使乳脂肪中从头合成脂肪酸（FAs）的浓度降低。同样，每天20毫克的10,12 CLA使乳腺组织的脂肪生成能力降低了30%，脂肪酸合酶（Fasn）、固醇反应元件结合蛋白1（Srebf1）和甲状腺激素反应斑点14（Thrsp）的乳腺表达降低了30 - 60%，而乳蛋白百分比和α-乳白蛋白（Lalba）的乳腺表达未改变。该剂量的CLA使幼崽生长降低了近20%，乳汁中从头合成的FAs降低了>35%，并且在终止10,12 CLA处理5天后，这些影响完全逆转。
10,12 CLA对乳腺脂肪生成的抑制在小鼠中呈剂量依赖性，每天20毫克的剂量可特异性且可逆地降低乳脂肪合成，而更高CLA剂量对乳汁合成有额外的非特异性影响。
