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首页> 外文期刊>Nutrition Research >Dietary caloric restriction modifies inflammatory responses in the livers of streptozotocin-induced diabetic rats.
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Dietary caloric restriction modifies inflammatory responses in the livers of streptozotocin-induced diabetic rats.

机译:饮食热量限制会改变链脲佐菌素诱导的糖尿病大鼠肝脏的炎症反应。

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Chronic systemic low-grade inflammation plays a key role in the development of insulin resistance, a hallmark of type 2 diabetes. Caloric restriction has been shown to improve glycemic control in diabetes and moderate expression of some markers of inflammation that are up-regulated during aging. Forty male Wistar rats were subjected to 30% caloric restriction (20 animals) and ad libitum feeding (20 animals) for 9 weeks before induction of diabetes by intraperitoneal administration of 35 mg/kg body weight streptozotocin. Caloric restriction significantly increased the concentrations of haptoglobin, interleukin (IL)-1 beta , IL-10, and reduced the tumor necrosis factor- alpha , IL-4, and IL-6 levels in the nondiabetic and diabetic animals when compared with their counterparts. The results presented show that caloric restriction was able to down-regulate the proinflammatory mediators and up-regulate the antiinflammatory cytokines implicated in inflammatory responses during diabetes. These changes are probably attributed to the reduction in deposition of adipose tissues in the liver and concomitant decrease in organ weights..
机译:慢性全身性轻度炎症在2型糖尿病的标志性胰岛素抵抗的发展中起关键作用。热量限制已显示可改善糖尿病患者的血糖控制,并能适度表达某些在衰老过程中上调的炎症标志物。通过腹膜内施用35mg / kg体重的链脲佐菌素,在诱导糖尿病之前,对40只雄性Wistar大鼠进行30%的热量限制(20只动物)和任意喂养(20只动物)9周。与非同类动物相比,热量限制显着增加了非糖尿病和糖尿病动物的触珠蛋白,白介素(IL)-1β,IL-10的浓度,并降低了肿瘤坏死因子-α,IL-4和IL-6的水平。 。提出的结果表明热量限制能够下调促炎介质并上调与糖尿病期间炎症反应有关的抗炎细胞因子。这些变化可能归因于肝脏中脂肪组织沉积的减少以及器官重量的减少。

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