Central Research Laboratory, Tokyo Innovation Center, Nippon Suisan Kaisha, Ltd,, 32-3 Nanakuni 1 Chome Hachioji, Tokyo, 192-0991, Japan.
Nutr Metab (Lond). 2013 Jan 30;10(1):16. doi: 10.1186/1743-7075-10-16.
The objective of present study was to examine the effect of long-chain monounsaturated fatty acids (LC-MUFAs) with chain lengths longer than 18 (i.e., C20:1 and C22:1 isomers combined) on obesity-related metabolic dysfunction and its molecular mechanisms. Type-2 diabetic KK-Ay mice (n = 20) were randomly assigned to the 7% soybean oil-diet group (control group) and 4% LC-MUFA concentrate-supplemented-diet group (LC-MUFA group). At 8 weeks on the diet, the results showed that plasma, liver and adipose tissue levels of C20:1 and C22:1 isomers increased significantly with LC-MUFA treatment. Supplementation with LC-MUFAs markedly reduced white fat pad weight as well as adipocyte size in the mice. The levels of plasma free fatty acids, insulin, and leptin concentration in the obese diabetic mice of the LC-MUFA group were also decreased as compared with the mice in the soybean oil-diet control group. Dietary LC-MUFAs significantly increased the mRNA expression of peroxisome proliferator-activated receptor gamma (Pparg), lipoprotein lipase (Lpl), fatty acid transport protein (Fatp), fatty acid translocase/CD36 (Cd36), as well as mRNA expression of genes involved in lipid oxidation such as carnitine palmitoyltransferase-1A (Cpt1a) and citrate synthase (Cs), and decreased the mRNA expression of inflammatory marker serum amyloid A 3 (Saa3) in the adipose tissues of diabetic mice. The results suggest that LC-MUFAs may ameliorate obesity-related metabolic dysfunction partly through increased expression of Pparg as well as its target genes, and decreased inflammatory marker expression in white adipose tissue.
本研究旨在探讨长链单不饱和脂肪酸（LC-MUFA）对肥胖相关代谢功能障碍的影响及其分子机制，这些脂肪酸的碳链长度超过 18 个（即 C20:1 和 C22:1 异构体的组合）。2 型糖尿病 KK-Ay 小鼠（n=20）被随机分为 7%大豆油饮食组（对照组）和 4% LC-MUFA 浓缩物饮食组（LC-MUFA 组）。在饮食 8 周后，结果表明，LC-MUFA 处理后血浆、肝脏和脂肪组织中 C20:1 和 C22:1 异构体的水平显著增加。LC-MUFA 补充显著降低了肥胖糖尿病小鼠的白色脂肪垫重量和脂肪细胞大小。与大豆油饮食对照组相比，LC-MUFA 组肥胖糖尿病小鼠的血浆游离脂肪酸、胰岛素和瘦素浓度也降低。饮食 LC-MUFA 显著增加了过氧化物酶体增殖物激活受体γ（Pparg）、脂蛋白脂肪酶（Lpl）、脂肪酸转运蛋白（Fatp）、脂肪酸转位酶/CD36（Cd36）以及与脂质氧化相关的基因（如肉碱棕榈酰转移酶-1A（Cpt1a）和柠檬酸合酶（Cs）的 mRNA 表达，同时降低了脂肪组织中炎症标志物血清淀粉样蛋白 A3（Saa3）的 mRNA 表达。这些结果表明，LC-MUFA 可能通过增加 Pparg 及其靶基因的表达以及降低白色脂肪组织中炎症标志物的表达来改善肥胖相关的代谢功能障碍。
