大鼠槲皮素灌胃后门脉血浆代谢组学研究

目的:研究槲皮素灌胃后对大鼠门脉血浆代谢组的影响。方法:健康雄性Wistar大鼠按40mg/kgbw剂量灌胃槲皮素,分别于灌胃前后0、0.5、1.0、2.0和4.0h采集门脉血液制备血浆,测定1H核磁共振谱,采用PLS-DA分析法对采集的数据进行分析。结果:灌胃槲皮素后,大鼠门脉血浆中二甲基亚砜水平明显升高,乳酸、葡萄糖含量呈现出先升高后逐渐恢复的趋势,谷氨酸、丙氨酸、琥珀酸、酮体水平也有所上升,柠檬酸、酪氨酸水平略有下降。结论:槲皮素灌胃后对肠道内源性代谢具有显著影响。     

酒精灌胃大鼠血浆中乙醇浓度变化

目的通过实验了解大鼠酒精灌胃后体内乙醇代谢的特点,为建立大鼠乙醇中毒所致慢性酒精性肝病模型提供依据。方法雄性Wistar大鼠30只,随机分成三个剂量组。实验大鼠以50%的酒精按各组剂量给予灌胃,灌胃后分别于第0.5、1、1.5、2、2.5、3、5、10h经眼眶静脉丛采集大鼠血标本,以乙醇脱氢酶法测定血浆中乙醇浓度。结果对各时段点乙醇浓度测定分析,大鼠摄入酒精后乙醇浓度的高峰均出现在灌胃后1~1.5h处,随后开始缓慢下降,代谢曲线与醉酒表现一致。结论酒精灌胃剂量小于8g/kg是比较安全的,灌胃后1~1.5h达到代谢吸收高峰期,10h后醉酒状态基本恢复,这为制备大鼠酒精性肝病模型提供理论依据。     

截肢后大鼠血浆及肝肾组织中硫化氢／胱硫醚-γ-裂解酶含量的变化

目的探讨截肢后大鼠血浆及肝、肾等远隔器官组织中内源性硫化氢(hydrogensulfide,H2S)的含量变化规律,以期找到硫化氢在创伤与修复过程中的作用机制。方法通过手术制备大鼠左后肢截肢模型,将雄性Wistar大鼠按手术时间随机分为9组:正常对照组(7只);手术后1、2、4、6、12、24、48、72h组(各7只)。测定血浆中H2S含量及肝、肾组织中CSE活性,分析其随时间变化规律。光镜观察各组组织形态学变化。结果与正常对照组相比,手术后大鼠血浆H2S含量逐渐降低,6h达最低值39.286±6.526(P<0.01),此后逐渐升高,48h后基本恢复正常。肝、肾组织CSE活性变化大体趋势与血浆相同,但下降幅度及到达最低值时间不同,肝在术后12h最低为166.162±10.878(P<0.01),肾在术后6h最低为60.664±7.574(P<0.01)。肝、肾组织出现一定程度组织损伤。结论H2S是一种新的内源性介质,在体内广泛存在,可能参与了组织损伤与修复的一系列病理生理过程。     

营养因素对大鼠供肝冷保存损伤的影响

探讨供体进食状况及提升肝糖原对大鼠供肝冷保存损伤的影响。将健康的雄性 SD大鼠 32只随机分为四组 ,分别为进食组 (A组 )、禁食组 (B组 )、进食 +强化组 (C组 )、禁食+强化组 (D组 )。切取大鼠肝脏 ,以高渗枸橼酸盐嘌呤液 4℃冷保存 2 4h。分别收集保存前后肝组织标本 ,测定肝组织糖原、蛋白质、丙二醛 (MDA)含量 ,超氧化物歧化酶 (SOD)、ATP酶活性。结果 :1进食及葡萄糖强化能明显提升肝的糖原含量 ,肝冷保存后糖原含量均有显著下降。 2饮食因素及葡萄糖强化在短期内并未明显影响到肝的蛋白质代谢 ,冷保存对肝的蛋白质代谢亦未见明…     

截肢后大鼠血浆及肝肾组织中硫化氢/胱硫醚-γ-裂解酶含量的变化

目的 探讨截肢后大鼠血浆及肝、肾等远隔器官组织中内源性硫化氢(hydrogen sulfide,H2S)的含量变化规律,以期找到硫化氢在创伤与修复过程中的作用机制.方法 通过手术制备大鼠左后肢截肢模型,将雄性Wistar大鼠按手术时间随机分为9组:正常对照组(7只);手术后1、2、4、6、12、24、48、72 h组(各7只).测定血浆中H2S含量及肝、肾组织中CSE活性,分析其随时间变化规律.光镜观察各组组织形态学变化.结果 与正常对照组相比,手术后大鼠血浆H2S含量逐渐降低,6 h达最低值39.286±6.526(P＜0.01),此后逐渐升高,48h后基本恢复正常.肝、肾组织CSE活性变化大体趋势与血浆相同,但下降幅度及到达最低值时间不同,肝在术后12 h最低为166.162±1 o.878(P＜0.01),肾在术后6 h最低为60.664±7.574(P＜0.01).肝、肾组织出现一定程度组织损伤.结论 H2S是一种新的内源性介质.在体内广泛存在,可能参与了组织损伤与修复的一系列病理生理过程.     

甘油二酯减肥功能及其可能的代谢机制

目的研究甘油二酯的减肥效果及可能机制。方法(1)5wSD大鼠随机分为3组,每组10只,对照组[饲料甘油三酯(TG)含量7%],高甘油三酯组(TG20%),高甘油二酯(DG)组(DG20%)自由进食喂养8w。实验期间记录动物进食量、排泄量、体重变化,分析脂肪消化率。实验结束后检测动物腹部脂肪重量、血清生化指标变化。(2)餐后血浆脂质动态分析实验采用13w雄性Wistar大鼠(n=50),分两组分别灌胃10%DG或10%TG乳化物,灌胃量0.73ml/100gbw。不同时间麻醉,颈静脉、门静脉分别取血,测血浆中游离脂肪酸(FFA)和TG含量(每次5只)。(3)酮体实验采用6w雄性Wistar大鼠,随机均分三组,分别用20%DG和20%TG乳化物灌胃,对照组用等能量葡萄糖水溶液(GS)作安慰剂。代谢笼中饲养6d,灌胃量0.5ml/100gbw,连续收集144h的尿液,测尿中总酮体量。结果DG组腹部脂肪重量、体重增加及血清TG水平均明显低于高TG组。DG组大鼠门静脉FFA水平明显高于TG组,而颈静脉TG水平略低于TG组,而尿酮体量显著高于TG组。结论膳食DG能明显抑制实验大鼠体重增加,降低血清中性TG水平,与TG组相比,其减肥降血脂效果可能源于其代谢途径不同。     

不同营养支持途径对烧伤后肠源性高代谢的影响

目的:探讨不同营养支持途径对烧伤后肠源性高代谢的影响及其发生机制.方法:将88只大鼠随机分为烧伤后静脉营养支持(TPN)组和肠道营养支持(EN)组,观察伤前及伤后第1、3、5、7、10天大鼠静息能量代谢率(REE)的变化,同时检测血浆内毒素(LPS)、肿瘤坏死因子(TNF)和白细胞介素-1(IL-1)的含量.结果:烧伤后两组大鼠的REE、TNF、LPS和IL-1均明显高于伤前(P＜0.01),两组相比,EN组大鼠REE较TPN组明显降低,下降幅度为17%～20%,血浆TNF、LPS及IL-1水平也明显低于TPN组(P＜0.05或0.01).结论:肠道营养可降低烧伤大鼠肠道受损程度,降低炎症介质的释放,从而降低高代谢反应.     

高氧平衡盐溶液对急性一氧化碳中毒性肝损伤的保护作用

目的探索高氧平衡盐溶液(HBS)对急性CO中毒肝损伤的保护作用。方法 SPF级SD大鼠30只随机分为5组,每组6只。N组为正常对照组,C组为CO中毒无治疗对照组,H组为CO中毒HBS治疗组,H组依据静脉输注HBS的剂量分为10(H10组)、15(H15组)和20ml/kg(H20组)。C组与H组均通过腹腔注射CO 120ml/kg建立SD大鼠中毒模型,N组腹腔注射等量的空气。在腹腔注射CO后1.3h,从尾静脉按0.2h恒速输注不同剂量的HBS给各治疗组大鼠,即刻从各组大鼠股动脉取血0.5ml行血气分析,1d后抽取血3ml进行肝损害敏感酶谱的测定,最后取相同部位肝组织行病理学检测。结果腹腔注射CO 120ml/kg后1.5h产生严重的缺氧状态。中毒后天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)和谷氨酰转肽酶(GGT)活力明显升高(P0.01)。CO中毒后24h肝组织放射状分布不清晰,肝细胞索排列不规律,大多数肝细胞水肿或呈空泡样变,可见较多红细胞渗出和中性粒细胞浸润。H组静脉输注不同剂量的HBS后,动脉血氧分压由(45.6±2.4)mm Hg分别上升到(63.9±3.6)、(73.8±3.9)和(78.6±3.8)mm Hg,3种酶均呈现不同幅度的降低,肝组织的病理学变化较C组明显减轻,其中H20组明显降低。结论 HBS用量与结果之间存在一定的量效关系。HBS可明显提高CO急性中毒大鼠的PaO_2和SaO_2,对肝损伤具有很好的保护作用。     

治疗前后酒精灌胃大鼠创伤弧菌脓毒症肝组织Toll样受体等的变化

目的 探讨抗生素对酒精灌胃大鼠创伤弧菌(vibrio vulnificus,VV)脓毒症肝组织Toll样受体(Toll like receptor,TLR)等的影响.方法 大鼠设正常对照组(N组,6只)、酒精灌胃大鼠对照组(A组,6只)、酒精灌胃大鼠抗生素对照组(AA组,6只)、酒精灌胃大鼠VV脓毒症组(AV组,24只;分别于染菌后2、6、12、24 h处死,每时相点动物数均为6只)和酒精灌胃大鼠VV脓毒症抗生素治疗组(AVA组,30只;分别于染菌后6、12、24、36 h和1周时活杀,各时相点动物数均为6只).采用逆转录聚合酶链技术检测各组大鼠不同时点肝组织TLR等的变化.结果 AV-6 h组TLR4 mRNA表达量为0.775±0.101,AVA-6 h组TLR4 mRNA表达量为0.600±0.064;AV-12 h组TLR4 mRNA表达量为0.918±0.133,AVA-12 h组TLR4 mRNA表达量为0.583±0.112;AV-24 h组TLR4 mRNA表达量为0.732±0.110,AVA-24 h组TLR4 mRNA表达量为0.512±0.118.AVA组大鼠染菌后6、12、24h TLR4 mRNA,与同时点AV组相比,TLR4 mRNA表达量明显降低,差异有统计学意义(AVA-6 h组与AV-6 h组比较,t=-3.573,P＜0.01;AVA-12 h组与AV-12 h组比较,t=-4.722,P＜0.01;AVA-24 h组与AV-24 h组比较,t=-3.340,P＜0.01).结论 及早联用抗生素可减低酒精灌胃大鼠VV脓毒症肝组织TLR等的表达,有利于机体促、抗炎平衡恢复,对酒精灌胃大鼠VV脓毒症有明显的治疗作用.     

莲房原花青素对氧自由基和脂质过氧化的作用

目的 :　观察莲房原花青素 ( LSPC)对活性氧自由基 O·-2 、· OH和肝脂质过氧化损伤的作用。方法 :　 ( 1 )应用化学发光法检测 LSPC对 O·-2 和· OH的清除作用 ;( 2 )体外大鼠红细胞、肝线粒体温育引起肝脂质过氧化物 ( LPO)含量变化 ;( 3)体外大鼠肝匀浆温育 ,Fe2 +、H2 O2 诱导引起 LPO含量变化 ;( 4 )小鼠连续口服不同剂量 LSPC 7d后 ,一次性灌胃 5 % CCl4油溶液 1 0 ml/kg bw,2 4 h后检测肝和血浆中超氧化物歧化酶 ( SOD)活性、谷胱甘肽 S-转移酶 ( GST)活性以及脂质过氧化物 ( LPO)含量。结果 :　 LSPC能有效地清除活性氧自由基 O·-2 和· OH,其 IC50 值分别为 1 69.0 mg/L和 1 0 5 .3mg/L;不同剂量 LSPC能明显抑制体外大鼠红细胞、肝线粒体、肝组织LPO产生 ;口服中、低剂量 LSPC能显著降低 CCl4中毒小鼠体内 LPO含量 ,提高 SOD、GST活性。结论 :　适量 LSPC具有抗活性氧自由基和脂质过氧化的作用 ,可能具有护肝功能。     

槲皮素对缺血再灌注损伤肝脏的保护作用

目的 :　探讨槲皮素对大鼠缺血再灌注损伤肝脏的保护作用。方法 :　灌胃给予槲皮素及作为阳性对照的维生素 C,结扎后 3 0 min再开放肝门血管造成肝脏缺血再灌注损伤 ,分别测定血浆谷丙转氨酶 (GPT)、谷草转氨酶 (GOT)活性、丙二醛 (MDA)浓度 ,肝脏槲皮素、MDA、还原型谷胱甘肽 (GSH)含量和黄嘌呤氧化酶 (XO)、谷胱甘肽过氧化物酶 (GSH- Px)、超氧化物歧化酶 (SOD)活性以及肝脏总抗氧化力、活性氧 (ROS)含量、DNA断裂率。结果 :　肝脏缺血再灌注后GPT、GOT活性、MDA水平升高 ,肝脏 XO活性、MDA和 ROS含量以及 DNA断裂率增加 ,而SOD、GSH- Px活性、GSH含量及总抗氧化力降低。槲皮素灌胃后肝脏中槲皮素浓度升高 ,血浆GPT、GOT活性及 MDA浓度降低 ,肝脏 ROS含量降低 ,GSH含量及总抗氧化力升高 ,SOD、GSH- Px活性有所恢复 ,对肝脏 DNA断裂发生无明显影响。维生素 C灌胃后对缺血再灌注损伤肝脏也具有保护作用。结论 :　槲皮素对大鼠缺血再灌注损伤肝脏具有明显的保护作用 ,其机制与增强肝脏抗氧化体系功能有关。     

Quercetin decreases oxidative stress, NF-kappaB activation, and iNOS overexpression in liver of streptozotocin-induced diabetic rats

Increasing evidence in both experimental and clinical studies suggests that oxidative stress is involved in the pathogenesis and progression of diabetic tissue damage. This study investigated the protective effects of quercetin treatment on oxidative stress, nuclear factor (NF)-kappaB activation and expression of inducible nitric oxide synthase (iNOS) in streptozotocin-induced diabetic rats. Male Wistar rats were divided into 4 groups: control rats, control rats treated daily with quercetin (150 micromol/kg, i.p.), untreated diabetic rats, and diabetic rats treated with quercetin. Diabetes was induced by a single i.p. injection of streptozotocin (70 mg/kg). Eight weeks later we measured TBARS and hydroperoxide-initiated chemiluminescence (QL) in liver as markers of oxidative stress, and activities of the antioxidant enzymes catalase, superoxide dismutase (SOD), and glutathione peroxidase, NF-kappaB activation by an electrophoretic mobility shift assay and expression of IkappaB kinases (IKKalpha and IKKbeta), the inhibitor IkappaB (IkappaBalpha and IkappaBbeta), and iNOS by Western blot. The plasma glucose concentration was significantly increased in diabetic rats and was not changed by quercetin. Streptozotocin administration induced significant increases in hepatic TBARS concentration, QL, and SOD and catalase activities that were prevented by quercetin. Activation of NF-kappaB, induction of IKKalpha and iNOS protein levels, and increased degradation of IkappaBalpha were also observed in streptozotocin-treated rats. All of those effects were abolished by quercetin. These findings suggest that quercetin treatment, by abolishing the IKK/NF-kappaB signal transduction pathway, may block the production of noxious mediators involved in the development of early diabetes tissue injury and in the evolution of late complications.     

Effects of commonly consumed fruit juices and carbohydrates on redox status and anticancer biomarkers in female rats

Administration of apple juice, black currant juice, or a 1:1 combination of the two juices significantly decreased the level of the lipid peroxidation biomarker malondialdehyde in plasma of female rats, whereas the protein oxidation biomarker 2-amino-adipic semialdehyde, was significantly increased following administration of orange juice, black currant juice, or the 1:1 combination of apple and black currant juice. A significant increase in 2-amino-adipic semialdehyde was also observed in control rats given sucrose, fructose, and glucose in the drinking water at concentrations approximating the average carbohydrate levels in the employed fruit juices. None of the fruit juices were found to affect the activities of antioxidant enzymes in red blood cells or hepatic glutathione S-transferase. Hepatic quinone reductase activity, on the other hand, was significantly increased by grapefruit juice, apple juice, and black currant juice. The total daily intake of a selected subset of flavonoid aglycones ranged from 0.2 to 4.3 mg, and quercetin was found to be a minor constituent of all the juices investigated. In a parallel study, rats were fed quercetin at doses ranging from 0.001 to 10 g/kg of diet. However, no effects were observed on hepatic glutathione S-transferase or quinone reductase activities, plasma redox status, or the activity of red blood cell antioxidant enzymes. Overall, the results of the present study suggest that commonly consumed fruit juices can alter lipid and protein oxidation biomarkers in the blood as well as hepatic quinone reductase activity, and that quercetin may not be the major active principle. The observation that natural carbohydrates are capable of mediating oxidative stress in vivo warrants further studies due to the central role refined and unrefined carbohydrates play in human nutrition.     

Effects of hysterectomy and semi-starvation on amino-acid gradients across liver, muscle and gut in rats

To study the effects of surgical stress and insufficient food intake on amino-acid exchange of liver, gut, and muscle, blood was sampled in random sequence from the aorta, the inferior caval vein, the portal vein, and the hepatic veins in 3 groups of 20 rats each. Control rats were fed ad libitum, hysterectomised rats were studied on the first and third post-operative day, and semi-starved rats were pair-fed to hysterectomised rats to an intake of 13% of control on the first day. Both groups lost 5-8% of body weight. Surgery increased the concentration gradient (release) of urea across liver by 60%, the glucose gradient (release) by 35%, and doubled the concentration gradients (uptake) across liver of alanine, arginine, glycine, lysine, proline, serine, and threonine, and decreased their plasma concentrations. There was no major change in hepatic amino-acid gradients in semi-starved animals, and there was no appreciable change in gradients of single amino-acids across gut or muscle in animals subjected to surgery or semi-starvation. Post-surgical increases in urea synthesis and hepatic uptake of uragenic and gluconeogenic amino-acids are due to the surgical stress and not to the post-operative semi-starvation.     

大鼠灌胃槲皮素后门静脉槲皮素及其代谢产物的液质分析

目的分析经口给予槲皮素后大鼠门静脉血槲皮素及其代谢产物。方法健康雄性Wistar大鼠按40mg/kg剂量经口给予槲皮素1.0小时后采集门静脉血液制备血浆,采用高效液相-质谱联用的方法进行分析。结果槲皮素处理大鼠门静脉血中可以检测到一定浓度的槲皮素以及异鼠李素、怪柳黄素、槲皮素硫酸酯、槲皮素-3-葡萄糖醛酸、槲皮素葡萄糖醛酸化硫酸酯。结论经口给予槲皮素经肠吸收代谢后以多种形式进入体内。     

Quercetin dihydrate and gallate supplements lower plasma and hepatic lipids and change activities of hepatic antioxidant enzymes in high cholesterol-fed rats

This study was designed to test the lipid-lowering and antioxidant activity of two bioflavonoids, quercetin dihydrate and gallate. Four groups of rats were given a semisynthetic diet containing 10 g cholesterol/kg for six weeks. The control group received only a high-cholesterol diet, whereas the other three groups received a diet including 1 g lovastatin, 1 g quercetin dihydrate, or 1 g gallate/kg. The quercetin dihydrate and gallate supplements both significantly lowered the plasma lipid and hepatic cholesterol levels compared to those of the control. The hepatic 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase activity was significantly lowered by the quercetin dihydrate when compared to the other groups, while the hepatic acyl CoA: cholesterol acyltransferase (ACAT) activity was only significantly higher in the control group. The overall potential for antioxidant protection was significantly enhanced by the quercetin dihydrate and gallate supplements through lowering the plasma and hepatic thiobarbituric acid reactive substances (TBARS) levels and increasing the hepatic superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in high-cholesterol-fed rats. These results suggest that the supplementation of quercetin dihydrate and gallate promotes an increase in fecal sterols, which in turn leads to a decreased absorption of dietary cholesterol as well as lower plasma and hepatic cholesterol.     

Increase of ceramide in the liver and plasma after carbon tetrachloride intoxication in the rat

In fulminant hepatic failure, various toxins causing multi-organ failure increase in plasma. As a novel toxin, levels of ceramide, a well-studied lipid mediator of apoptosis, were determined by LC-MS/MS in the liver and plasma of carbon tetrachloride (CCl4)-intoxicated rats. After 6 h of oral administration of CCl4 (4 mL/kg body weight as a 1:1 mixture of CCl4 and mineral oil) to rats, extensive hepatic failure occurred as evidenced by a severe elevation in plasma AST and ALT. The liver concentration of major ceramide components (C16:0, C24:0, C24:1, C18:0, C22:0, and C24:2 in decreasing order), and the sum of these ceramides increased significantly 2 h after CCl4 intoxication compared to that in the control group given mineral oil. The total ceramide concentration in the plasma was also increased to 4.1 times that in the control 24 h after administration of CCl4. In conclusion, the early increase in liver ceramides may contribute to hepatic cell death and the increase in plasma ceramides during fulminant hepatic failure may cause damage in other organs including the brain and kidney.     

Effects of a single exposure to carbon disulphide on the rate of urea production and on plasma free fatty acid and glucose concentrations in the rat.

The concentration of plasma free fatty acids in rats was significantly increased after a short period of exposure to inhalation of carbon disulphide (4 h, 2 mg/1). In contrast, after a longer period of exposure (15 h overnight, 2 mg/1) the concentration of plasma free fatty acid was significantly decreased despite a small hypoglycaemia. At the same time plasma urea concentration was significantly higher in CS2-treated rats. The total esterified fatty acid content of plasma was lower after exposure, but there was no change in plasma glycerol. Following an intragastric water load, no differences were observed in urine flow rate nor in renal clearances of urea and inulin between control and treated rats. It is concluded that the rate of urea production is significantly increased during acute CS2-intoxication, and it is suggested that two factors contribute to this effect: first, an increased breakdown of proteins with which CS2 or its metabolic products have reacted; and secondly an increased rate of utilization of plasma glucose associated with increased gluconeogenesis from amino acid precursors. It is further suggested that the stress effects of CS2 dominate in the short term before being overcome by a diminished sympathetic response. When rats were exposed to CS2 overnight without free access to water, the great vessel haematocrit was significantly lower than in corresponding controls. This was shown to be accounted for by differences in plasma volume. No such difference was observed when rats had free access to water during exposure. These effects probably reflect differing rates of water loss under mildly dehydrating conditions, but a direct effect of CS2 on the cardiovascular system is not excluded.     

Onion peel extracts ameliorate hyperglycemia and insulin resistance in high fat diet/streptozotocin-induced diabetic rats

Background

Quercetin derivatives in onions have been regarded as the most important flavonoids to improve diabetic status in cells and animal models. The present study was aimed to examine the hypoglycemic and insulin-sensitizing capacity of onion peel extract (OPE) containing high quercetin in high fat diet/streptozotocin-induced diabetic rats and to elucidate the mechanism of its insulin-sensitizing effect.

Methods

Male Sprague-Dawley rats were fed the AIN-93G diet modified to contain 41.2% fat and intraperitoneally injected with a single dose of streptozotocin (40 mg/kg body weight). One week after injection, the rats with fasting blood glucose levels above 126 mg/dL were randomly divided into 4 groups to treat with high fat diet containing 0 (diabetic control), 0.5, or 1% of OPE or 0.1% quercetin (quercetin equivalent to 1% of OPE) for 8 weeks. To investigate the mechanism for the effects of OPE, we examined biochemical parameters (insulin sensitivity and oxidative stresses) and protein and gene expressions (pro-inflammatory cytokines and receptors).

Results

Compared to the diabetic control, hypoglycemic and insulin-sensitizing capability of 1% OPE were demonstrated by significant improvement of glucose tolerance as expressed in incremental area under the curve (P = 0.0148). The insulin-sensitizing effect of OPE was further supported by increased glycogen levels in liver and skeletal muscle (P < 0.0001 and P = 0.0089, respectively). Quantitative RT-PCR analysis showed increased expression of insulin receptor (P = 0.0408) and GLUT4 (P = 0.0346) in muscle tissues. The oxidative stress, as assessed by superoxide dismutase activity and malondialdehyde formation, plasma free fatty acids, and hepatic protein expressions of IL-6 were significantly reduced by 1% OPE administration (P = 0.0393, 0.0237, 0.0148 and 0.0025, respectively).

Conclusion

OPE might improve glucose response and insulin resistance associated with type 2 diabetes by alleviating metabolic dysregulation of free fatty acids, suppressing oxidative stress, up-regulating glucose uptake at peripheral tissues, and/or down-regulating inflammatory gene expression in liver. Moreover, in most cases, OPE showed greater potency than pure quercetin equivalent. These findings provide a basis for the use of onion peel to improve insulin insensitivity in type 2 diabetes.