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Taurine supplementation prevents endothelial dysfunction and attenuates structural changes in aortas from hypothalamic obese rats

机译:牛磺酸补充剂可防止内皮功能障碍,并从下丘脑肥胖大鼠中衰减主动脉的结构变化

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PurposeObesity predisposes to cardiovascular and metabolic diseases. The amino acid, L-taurine (Tau), regulates glucose and lipid homeostasis and vascular function. Here we investigated whether Tau supplementation prevents endothelial dysfunction in the thoracic aortas of monosodium glutamate-induced obese (MSG) rats.MethodsMale rats received subcutaneous injections of MSG (4mg/kg body weight/day) or saline (control group, CTL) during the first five days of life. From 21 to 150days of age, the rats were distributed into the groups: CTL, MSG, and CTL and MSG supplemented with 2.5% Tau in their drinking water (CTAU and MTAU).ResultsAt 150-days old, MSG rats presented massive abdominal fat deposition, hypertriglyceridemia, hyperinsulinemia, glucose intolerance and high plasma levels of malondialdehyde (MDA), a lipid peroxidation marker. Tau supplementation attenuated fat accumulation in perigonadal adipose tissue and prevented the increase in triglycerides and MDA plasma levels. Aortic rings of MSG rats presented reduced vasodilation in response to acetylcholine (ACh). No modifications in insulin-induced vasodilatation, or Akt and eNOS phosphorylation, were observed in MSG aortas; thoracic aortas from MSG rats presented reduced tunica media thickness, with a lower aortic wall thickness/lumen diameter ratio and decreased total collagen content. Tau supplementation restored ACh-induced vasodilation and collagen content.ConclusionsOur study presents the first evidence that Tau prevents disruptions in vascular reactivity and in extracellular matrix composition in thoracic aortas of MSG-obese rats. The vascular protective actions of Tau may be linked to reduced lipid peroxidation and a reduction in cardiovascular risk factors, such as abdominal fat and hypertriglyceridemia.
机译:缺点性易于心血管和代谢疾病。氨基酸,L-牛磺酸(TAU)调节葡萄糖和脂质稳态和血管功能。在这里,我们调查了TAU补充剂是否可防止谷氨酸氨基甲酸钠诱导的肥胖(MSG)大鼠的胸部主动脉内皮内皮功能障碍。方法在药物(4mg / kg体重/天)或盐水(对照组,CTL)的皮下注射生命前五天。从21至150天的年龄,大鼠分配到组:CTL,MSG和CTL和MSG补充在其饮用水中的2.5%TAU(CTAU和MTAU).Resultsat 150天老,MSG大鼠呈现大规模的腹部脂肪沉积,高甘油肝血症,高胰岛素血症,葡萄糖不耐受性和高血浆水平的丙二醛(MDA),脂质过氧化标记物。 TAU补充衰减Perigonadal脂肪组织中的脂肪积累,预防甘油三酯和MDA血浆水平的增加。响应于乙酰胆碱(ACH),MSG大鼠的主动脉圈呈现较少的血管舒张。在MSG主动脉中,观察到胰岛素诱导的血管舒张或AKT和enos磷酸化的修饰;来自MSG大鼠的胸主动脉呈现出降低的Tunica介质厚度,具有较低的主动脉壁厚/腔直径比并降低总胶原含量。 TAU补充恢复了血管诱导血管舒张和胶原蛋白含量。结论,TAU的第一个证据表明TAU阻止血管反应性和细胞外基质组合物的MSG-OBESE大鼠。 TAU的血管保护作用可能与降低的脂质过氧化和心血管危险因素的降低有关,例如腹部脂肪和高甘油三酯血症。

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