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Leucine and resistance training improve hyperglycemia, white adipose tissue loss, and inflammatory parameters in an experimental model of type I diabetes

机译:亮氨酸和抗性训练在I型糖尿病的实验模型中改善高血糖,白色脂肪组织丧失和炎症参数

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Background: Loss of white adipose tissue (WAT), associated with type I diabetes (DM I), contributes to increased chronic systemic inflammation. Aim: The aim of this study was to investigate the effects of leucine supplementation and resistance training (RT) in attenuating WAT loss and improving inflammatory parameters and glucose metabolism in DM I rats. Methods: Thirty-two male Wistar rats were distributed into four groups: DA (sedentary and supplemented with non-essential amino acids (NEAA)), DL (sedentary and supplemented with leucine), DTA (submitted to RT and supplemented with NEAA) and DTL (submitted to RT and supplemented with leucine). DM I was induced by streptozotocin (STZ). An 8-week period of RT consisted of climbing a ladder with a progressively increased load, and supplementation was offered in the feed. Results: Glycemia, polyphagia and polydipsia were lower in DL, DTA and DTL groups compared with the DA group by approximately 20% (p<.000l), 28% (p=.004) and 64% (fX.0001), respectively. Weight of total WAT and retroperitoneal adipose tissue (RPAT) were higher by approximately 21% (p=.0l) and 54% (p=.0004), respectively, in DL, DTA and DTL groups compared with DA. However, gene expression of adiponectin and leptin in RPAT was only increased by RT (DTA and DTL) compared with DA and DL by approximately 93% (p<.000l) and 78% (p=.0002), respectively. Similarly, the levels of adiponectin in the serum, tissue IL-10 (RPAT) and serum IL-10 were only increased in DTA and DTL compared with DAand DL by approximately 31% (p=.03), 45% (p=.0009) and 35% (p=.003), respectively. Conclusions: Both interventions, isolated or together, reduced hyperglycemia and excessive loss of WAT, but RT was the main factor responsible for attenuating inflammation.
机译:背景:与I型糖尿病(DM I)相关的白色脂肪组织(Wat)的损失有助于增加慢性全身炎症。目的:本研究的目的是探讨亮氨酸补充和抗性训练(RT)的影响,在DM I鼠中衰减和改善炎症参数和葡萄糖代谢。方法:将32只雄性Wistar大鼠分为四组:DA(久坐不良,补充非必需氨基酸(NEAA)),DL(久坐不应和用亮氨酸补充),DTA(提交至室温并补充NEAA)和DTL(提交至室温并补充亮氨酸)。 DM I由链霉素(STZ)诱导。 RT 8周的RT包括爬上梯子,载重率增加,并在饲料中提供补充。结果:与DA组相比,糖血症,DTA和DTL组中的糖血症,DTA和DTL组分别较为约20%(p <.000),分别为28%(P = .004)和64%(FX.0001) 。与DA相比,总Wat和逆床脂肪组织(RPAT)的重量分别较高约21%(p = .0L)和54%(P = .0004),分别为DL,DTA和DTL组。然而,与DA和DL相比,RPAT中脂联素和瘦蛋白的基因表达仅在RT(DTA和DTL)上分别将约93%(p <.000)和78%(P = .000)增加。类似地,血清,组织IL-10(RPAT)和血清IL-10中的脂联素的水平仅在DTA和DT1中升高,与DAAND D1约31%(P = .03),45%(P =。 0009)和35%(p = .003)。结论:干预措施,孤立或共同,降低高血糖和Wat的过度损失,但RT是负责炎症炎症的主要因素。

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