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首页> 外文期刊>The Journal of Nutritional Biochemistry >Folic acid consumption reduces resistin level and restores blunted acetylcholine-induced aortic relaxation in obese/diabetic mice.
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Folic acid consumption reduces resistin level and restores blunted acetylcholine-induced aortic relaxation in obese/diabetic mice.

机译：叶酸的消耗降低了肥胖/糖尿病小鼠的抵抗素水平并恢复了乙酰胆碱引起的钝性主动脉松弛。

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Folic acid supplementation provides beneficial effects on endothelial functions in patients with hyperhomocysteinemia. However, its effects on vascular functions under diabetic conditions are largely unknown. Therefore, the effect(s) of folic acid (5.7 and 71 mug/kg/day for 4 weeks) on aortic relaxation was investigated using obese/diabetic (+db/+db) mice and lean littermate (+db/+m) mice. Acetylcholine-induced relaxation in +db/+db mice was less than that observed in +db/+m mice. The reduced relaxation in +db/+db mice was restored by consumption of 71 mug/kg folic acid. Acetylcholine-induced relaxation (with and without folic acid treatment) was sensitive to NG-nitro-L-arginine methyl ester, 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one, geldanamycin and triciribine. In addition, acetylcholine-induced relaxation was attenuated by resistin. The plasma level of resistin in +db/+db mice was sevenfold higher than that measured in +db/+m mice, and the elevated plasma level of resistin in +db/+db mice was reduced by 25% after treatment with 71 mug/kg folic acid. Folic acid slightly increased the ratio of reduced glutathione to oxidized glutathione in +db/+db mice. Moreover, folic acid caused a reduction in PTEN (phosphatase and tensin homolog deleted on chromosome 10) expression, an increase in the phosphorylation of endothelial nitric oxide synthase (eNOSSer1177) and AktSer473, and an enhanced interaction of heat shock protein 90 (HSP90) with eNOS in both strains, with greater magnitude observed in +db/+db mice. In conclusion, folic acid consumption improved blunted acetylcholine-induced relaxation in +db/+db mice. The mechanism may be, at least partly, attributed to enhancement of PI3K/HSP90/eNOS/Akt cascade, reduction in plasma resistin level, down-regulation of PTEN and slight modification of oxidative state.
机译：叶酸补充剂对高同型半胱氨酸血症患者的内皮功能具有有益作用。但是，在糖尿病条件下其对血管功能的影响尚不清楚。因此，使用肥胖/糖尿病（+ db / + db）小鼠和瘦同窝婴儿（+ db / + m），研究了叶酸（5.7和71杯/千克/公斤，每天4周）对主动脉松弛的影响。老鼠。乙酰胆碱诱导的+ db / + db小鼠的松弛作用小于在+ db / + m小鼠中观察到的松弛作用。通过消耗71马克/千克叶酸，恢复了+ db / + db小鼠中减少的松弛。乙酰胆碱诱导的松弛（有或没有叶酸处理）对NG-硝基-L-精氨酸甲酯，2-（4-吗啉基）-8-苯基-4H-1-苯并吡喃-4-酮，格尔德霉素和曲西立滨敏感。此外，乙酰胆碱诱导的松弛被抵抗素减弱。 + db / + db小鼠中的抵抗素血浆水平比+ db / + m小鼠中的抵抗素血浆水平高7倍，+ db / + db小鼠中的抵抗素血浆水平升高，经71杯处理后降低了25％ / kg叶酸。在+ db / + db小鼠中，叶酸略微增加了还原型谷胱甘肽与氧化型谷胱甘肽的比例。此外，叶酸引起PTEN（10号染色体上缺失的磷酸酶和张力蛋白同源物）表达降低，内皮型一氧化氮合酶（eNOSSer1177）和AktSer473的磷酸化增加，以及热休克蛋白90（HSP90）与两种品系中的eNOS，在+ db / + db小鼠中观察到的幅度更大。总之，叶酸消耗改善了+ db / + db小鼠的钝性乙酰胆碱诱导的松弛。该机制可能至少部分归因于PI3K / HSP90 / eNOS / Akt级联反应的增强，血浆抵抗素水平的降低，PTEN的下调和氧化态的轻微改变。

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