首页> 外文期刊>Ukrainian Biochemical Journal >L-carnitine administration effects on AMPK, APPL1 and PPARγ genes expression in the liver and serum adiponectin levels and HOMA-IR in type 2 diabetes rat model induced by STZ and nicotinamide
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L-carnitine administration effects on AMPK, APPL1 and PPARγ genes expression in the liver and serum adiponectin levels and HOMA-IR in type 2 diabetes rat model induced by STZ and nicotinamide

机译:L-肉碱给药对AMPK,APPL1和PPARγ基因的表达在STZ和烟酰胺诱导的2型糖尿病大鼠模型中的肝脏和血清脂联素水平和HOMA-IR中的表达

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Diabetes is a chronic disease and a public health problem globally. L-Carnitine is synthesized in the liver, promotes fatty acids oxidation and currently is used as a supplement against weight gain. Carnitine level is found to be reduced in diabetic patients and to be beneficial as a supplement at diabetes, but the mechanisms of this effect is not fully understood. Therefore, we evaluated the oral L-carnitine supplementation on expression of AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptor gamma (PPARγ), adaptor protein APPL1 genes in the liver and insulin and adiponectin levels in the serum of diabetic rats. Rats were randomly divided into three groups ( n = 8) as follow: group 1 – control without any treatment, group 2 – diabetic control rats which received STZ (45 mg/kg) and nicotinamide (200 mg/kg) by i.p. injection, group 3 – diabetic rats which received 600 mg/kg/day carnitine orally for 35 days. It was found that L-carnitine supplementation reduced the level of fasting glucose compared to that in control and diabetic groups ( P = 0.001, P = 0.0001 respectively) and increased adiponectin level compared to diabetic nontreated rats ( P = 0.0001). Homeostasis model assessment of insulin resistance (HOMA-IR) was significantly increased in the diabetic group and reduced in the group that received L-carnitine. These promising beneficial effect of L-carnitine on the type 2 diabetes in rats’ model was shown to be conducted through the up-regulation of AMPK , PPARγ and APPL1 genes expression in the liver and elevation of serum adiponectin level.
机译:糖尿病是一种慢性疾病和全球公共卫生问题。 L-肉碱在肝脏中合成,促进脂肪酸氧化,目前用作对重量增益的补充剂。发现肉毒碱水平在糖尿病患者中减少,并有益于糖尿病的补充剂,但这种效果的机制尚不完全明白。因此,我们评估了在糖尿病大鼠血清中表达AMP活化蛋白激酶(AMPK),过氧化物体增殖物激活的受体γ(PPARγ),肝脏蛋白Appl1基因的肝硬化蛋白Appl1基因的口腔左旋肉碱的补充剂。将大鼠随机分为三组(n = 8),如下:第1组 - 无任何处理的控制,第2组 - 糖尿病对照大鼠接受STZ(45mg / kg)和烟酰胺(200mg / kg)的糖尿病对照大鼠I.p.注射,第3组 - 口服600mg / kg /天肉碱的糖尿病大鼠35天。结果发现,与对照和糖尿病群(P = 0.001,P = 0.0001分别)相比,左旋肉碱补充剂减少了空腹葡萄糖水平并与糖尿病非残留大鼠相比增加脂联素水平(P = 0.0001)。糖尿病群体胰腺炎抵抗(HOMA-IR)的稳态模型评估在接受L-肉碱的组中显着增加。 L-肉碱对大鼠模型中2型糖尿病对2型糖尿病的这些有希望的有益效果显示通过在肝脏肝脏和血清脂联素水平的肝脏和升高中进行AMPK,PPARγ和Appl1基因表达进行。

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