首页> 美国卫生研究院文献>Nutrition Metabolism >Dietary supplementation with long-chain monounsaturated fatty acids attenuates obesity-related metabolic dysfunction and increases expression of PPAR gamma in adipose tissue in type 2 diabetic KK-Ay mice
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Dietary supplementation with long-chain monounsaturated fatty acids attenuates obesity-related metabolic dysfunction and increases expression of PPAR gamma in adipose tissue in type 2 diabetic KK-Ay mice

机译:膳食补充长链单不饱和脂肪酸可减轻2型糖尿病KK-Ay小鼠肥胖相关的代谢功能障碍并增加PPARγ在脂肪组织中的表达

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摘要

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.
机译:本研究的目的是研究链长大于18的长链单不饱和脂肪酸(LC-MUFA)(即C20:1和C22:1异构体的总和)对肥胖相关的代谢功能障碍及其分子的影响机制。将2型糖尿病KK-A y 小鼠(n = 20)随机分配到7%豆油饮食组(对照组)和4%LC-MUFA浓缩饮食组( LC-MUFA组)。在饮食的第8周,结果显示,使用LC-MUFA处理后,血浆,肝脏和脂肪组织中C20:1和C22:1异构体的水平显着增加。补充LC-MUFA可以显着降低小鼠的白色脂肪垫重量以及脂肪细胞的大小。与大豆油饮食对照组相比,LC-MUFA组的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了。饮食中的LC-MUFAs显着增加了过氧化物酶体增殖物激活受体γ(Pparg),脂蛋白脂酶(Lpl),脂肪酸转运蛋白(Fatp),脂肪酸转位酶/ CD36(Cd36)的mRNA表达以及基因的mRNA表达参与肉毒碱棕榈酰转移酶-1A(Cpt1a)和柠檬酸合酶(Cs)等脂质氧化,并降低了糖尿病小鼠脂肪组织中炎症标志物血清淀粉样蛋白A 3(Saa3)的mRNA表达。结果表明,LC-MUFAs可以部分通过增加Pparg及其靶基因的表达以及减少白色脂肪组织中炎性标志物的表达来改善肥胖相关的代谢功能障碍。

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