首页> 美国卫生研究院文献>Nutrients >Anti-TNF-α Agent Tamarind Kunitz Trypsin Inhibitor Improves Lipid Profile of Wistar Rats Presenting Dyslipidemia and Diet-induced Obesity Regardless of PPAR-γ Induction
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Anti-TNF-α Agent Tamarind Kunitz Trypsin Inhibitor Improves Lipid Profile of Wistar Rats Presenting Dyslipidemia and Diet-induced Obesity Regardless of PPAR-γ Induction

机译:无论PPAR-γ诱导如何抗TNF-α剂罗望子Kunitz胰蛋白酶抑制剂均可改善呈现血脂异常和饮食诱导肥胖的Wistar大鼠的脂质谱。

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摘要

The increasing prevalence of obesity and, consequently, chronic inflammation and its complications has increased the search for new treatment methods. The effect of the purified tamarind seed trypsin inhibitor (TTIp) on metabolic alterations in Wistar rats with obesity and dyslipidemia was evaluated. Three groups of animals with obesity and dyslipidemia were formed, consuming a high glycemic index and glycemic load (HGLI) diet, for 10 days: Obese/HGLI diet; Obese/standard diet; Obese/HGLI diet + TTIp (730 μg/kg); and one eutrophic group of animals was fed a standard diet. Rats were evaluated daily for food intake and weight gain. On the 11th day, animals were anesthetized and sacrificed for blood and visceral adipose tissue collection. TTIp treated animals presented significantly lower food intake than the untreated group (p = 0.0065), TG (76.20 ± 18.73 mg/dL) and VLDL-C (15.24 ± 3.75 mg/dL). Plasma concentrations and TNF-α mRNA expression in visceral adipose tissue also decreased in obese animals treated with TTIp (p < 0.05 and p = 0.025, respectively) with a negative immunostaining. We conclude that TTIp presented anti-TNF-α activity and an improved lipid profile of Wistar rats with dyslipidemia and obesity induced by a high glycemic index and load diet regardless of PPAR-γ induction.
机译:肥胖症的流行率增加,因此,慢性炎症及其并发症也增加了对新治疗方法的寻求。评价了纯化的罗望子种子胰蛋白酶抑制剂(TTIp)对肥胖和血脂异常的Wistar大鼠代谢改变的影响。形成了三组具有肥胖和血脂异常的动物,它们食用高血糖指数和高血糖负荷(HGLI)饮食,持续10天:肥胖/ HGLI饮食;肥胖/标准饮食;肥胖/ HGLI饮食+ TTIp(730μg/ kg);给一组富营养化的动物喂食标准饮食。每天评估大鼠的食物摄入量和体重增加。在第11天,将动物麻醉并处死以收集血液和内脏脂肪组织。经TTIp处理的动物的食物摄入量显着低于未经处理的组(p = 0.0065),TG(76.20±18.73 mg / dL)和VLDL-C(15.24±3.75 mg / dL)。免疫染色阴性的TTIp处理的肥胖动物的内脏脂肪组织中的血浆浓度和TNF-αmRNA表达也降低(分别为p <0.05和p = 0.025)。我们得出的结论是,无论PPAR-γ诱导如何,高血糖指数和高负荷饮食所致的高脂血症和肥胖的Wistar大鼠,TTIp均具有抗TNF-α活性和改善的脂质分布。

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