酒精对高脂喂养大鼠肝脏胰岛素抵抗的影响

目的探讨长期高脂饮食状态下不同剂量酒精摄入对大鼠胰岛素抵抗的影响及可能机制。方法清洁级Wistar大鼠,随机分为正常对照、高脂对照、高脂+5%、10%、20%、30%、40%酒精共7组。13w后,断头取血,测空腹血糖(FPG)及血胰岛素(FINS)浓度,计算胰岛素抵抗指数(homeostasis model assessment,HOMA-IR)及HOMA-β功能指数(HOMAβ-cellindex,HBCI)。RT-PCR法测定肝脏胰岛素受体底物-1(IRS-1),磷脂酰肌醇3激酶(PI-3K)、葡萄糖转运体-2(GLUT-2)的mRNA表达水平。Westernblotting测定肝脏PI-3K(p85α)、GLUT-2的蛋白表达水平。结果高脂对照组与正常对照组比,血胰岛素、HOMA-IR、HBCI明显升高(P0.05),肝脏胰岛素信号传导关键分子没有显著差异。与高脂对照组比,高脂+酒精组空腹血糖、胰岛素抵抗指数明显升高(P0.05),血胰岛素、胰岛β细胞功能指数明显下降(P0.05);肝脏胰岛素信号传导关键分子mRNA、蛋白表达水平随酒精剂量的增加而逐渐下降。结论长期高脂饮食联合酒精摄入导致胰岛素抵抗;同时抑制肝脏胰岛素信号传导关键分子表达水平,在高剂量酒精组更明显,这可能是其导致胰岛素抵抗的分子机制。     

靶向卵巢癌糖酵解途径治疗的研究进展

既往研究表明即使在充足的氧气条件下,肿瘤代谢依然更加倾向于糖酵解途径,即Warburg 效应.卵巢癌是死亡率最高的妇科恶性肿瘤,糖酵解的关键酶(HK,PFK,PKM)在包括卵巢癌在内的多种肿瘤中表达增加,转变肿瘤的糖酵解途径可以改善化疗药物的耐药,抑制肿瘤的增殖.该文就糖酵解途径中关键酶的生物学特征和以糖酵解酶为靶标治疗卵巢肿瘤的研究进展进行概述.     

长期酒精作用对大鼠骨骼肌PI-3K表达的影响

目的:研究酒精长期作用下对大鼠骨骼肌磷脂酰肌醇3激酶(phosphatidylinositol 3-kinase,PI-3K)调节亚基p85αmRNA及蛋白水平表达的影响,探讨酒精引起胰岛素抵抗的相关分子机制。方法:清洁级Wistar大鼠80只(雌雄各半),按体重随机分为对照组和低、中、高剂量组,分别给予蒸馏水以及10%、20%、33%酒精溶液,灌胃剂量为10ml/(kg·bw·d)。第19周末,断头处死大鼠,测定空腹血糖和血胰岛素,计算HOMA胰岛素抵抗指数(HOMA-IR)。分离骨骼肌,通过RT-PCR和Westernblot方法测定p85αmRNA和蛋白表达水平。结果:雄性大鼠高剂量组空腹血糖,低、中剂量组空腹胰岛素水平升高,各酒精剂量组HOMA-IR指数均升高。p85αmRNA及蛋白表达水平表现为随着酒精剂量的增加先升高后降低;雌性大鼠高剂量组空腹血糖升高、空腹血胰岛素下降,p85αmRNA及蛋白的表达在中、高剂量组降低。各剂量组HOMA-IR指数与对照组比较差异无显著性。结论:长期摄入过量酒精可以造成骨骼肌组织p85α表达的改变,这可能是酒精降低胰岛素敏感性,引起胰岛素抵抗的分子机制。     

长期酒精摄入引起大鼠胰岛素抵抗及其分子机制

目的研究酒精摄入与胰岛素敏感性之间的关系并深入探讨其相关的分子机制。方法清洁级Wistar大鼠80只(雌雄各半),按体重随机分为对照组和低、中、高剂量共4组,每天摄入酒精剂量分别为0、0.8、1.6、2.4g/(kg·bw)。第19w末,断头处死大鼠,测定空腹血糖和血胰岛素,计算HOMA胰岛素抵抗指数(HOMA-IR)。提取肝组织,通过Western blot方法测定磷脂酰肌醇3激酶p85亚单位(p85subunit of phosphoinositide3-kinase,PI-3Kp85),葡萄糖转运体2(Glucose transporter-2)蛋白表达水平。结果与对照组相比,雄性大鼠高剂量组空腹血糖升高,低、中剂量组空腹胰岛素水平升高,各酒精剂量组HOMA-IR指数均升高PI3-K、GLUT-2蛋白在高剂量组表达降低;与对照组比较,雌性大鼠高剂量组空腹血糖升高、空腹血胰岛素下降。各剂量组HOMA-IR指数与对照组比较差异无显著性,PI3-K、GLUT-2蛋白在中,高酒精剂量组的表达均降低。结论长期酒精摄入可以引起胰岛素抵抗,肝脏PI-3K(p85),Glu-4蛋白表达水平的降低,可能是酒精胰岛素抵抗的分子机制之一。     

长期摄入酒精对大鼠血糖和胰岛素的影响

为探讨长期摄入酒精对大鼠血糖，胰岛素及糖耐量（GTT）的影响，以不同学的酒精溶液对大鼠灌胃60天，结果显示：大鼠摄入30％，50％酒精60天后，与对照组比较，空腹血糖明显升高，1h,2h,3h糖耐量异常（P＜0．05），并且雌雄大鼠之间也存在明显差异，随着剂量的增加，各组血胰岛素水平逐渐降低，50％酒精摄入组与对照组存在着明显差异（P＜0．05），结果提示：长期饮酒可导致大鼠空腹血糖升高，糖耐量异常，提示长期饮酒有可能导致糖尿病，并且胰岛素水平降低可能是导致糖尿病的机制之一。     

长期酒精摄入对大鼠骨骼肌组织IR、IRS-1和PI-3K基因表达的影响

目的研究酒精长期作用下对大鼠骨骼肌胰岛素受体(IR)、胰岛素受体底物-1(IRS-1)、磷脂酰肌醇3-激酶p85亚单位(PI-3K)mRNA表达的影响,探讨酒精与胰岛素抵抗的关系及相关分子机制。方法清洁级Wistar大鼠80只(雌雄各半),按体重随机分为对照组和低、中、高剂量组,分别给予蒸馏水以及10%、20%和33%酒精溶液,灌胃剂量为每天10ml/kgbw。第19周末,断头处死大鼠,测定空腹血糖和血胰岛素,计算HOMA胰岛素抵抗指数(HOMA-IR)。提取骨骼肌总RNA,通过RT-PCR测定IR、IRS-1、PI-3K(p85)mRNA表达水平。结果雄性大鼠,与对照组比较高剂量组空腹血糖,低、中剂量组空腹胰岛素水平升高,各酒精剂量组HOMA-IR指数均升高。IRmRNA的表达在中、高剂量组降低,而IRS-1、PI-3K(p85)mRNA表达水平表现为随着酒精剂量的增加先升高后降低,与对照组比较差异有显著性(P<0.05);与对照组比较,雌性大鼠高剂量组空腹血糖升高、空腹血胰岛素下降,IR、IRS-1、PI-3K(p85)mRNA的表达在中、高剂量组降低(P<0.05)。各剂量组HOMA-IR指数与对照组比较差异无显著性。结论长期摄入过量酒精可以造成骨骼肌组织IR、IRS-1、PI-3K(p85)mRNA表达的降低,这可能是酒精降低胰岛素敏感性,引起胰岛素抵抗的分子机制。     

PTTG沉默通过下调糖酵解相关酶抑制卵巢癌细胞增殖

目的：探讨原癌基因垂体肿瘤转化基因（ PTTG）对卵巢癌细胞增殖的影响及其机制。方法收集西安市第四医院医院2010至2013年有完整病例资料的卵巢癌手术患者病理标本68例。通过免疫组织化学和Western blotting方法,从组织和细胞水平检测PTTG与有氧糖酵解相关酶包括己糖激酶（ HK ）、磷酸果糖激酶（ PFK ）、丙酮酸激酶2（ PKM2）、乳酸脱氢酶 A （LDHA）和葡萄糖转运子1（GLUT-1）表达水平间的关系;利用慢病毒干扰载体下调PTTG表达,建立PTTG沉默的稳定卵巢癌细胞株,通过MTT、软琼脂糖克隆实验检测细胞的增殖能力改变;Western blotting检测PTTG沉默后有氧糖酵解相关酶和葡萄转运子的表达水平变化,并探讨其内在机制。结果通过组织和细胞水平检测发现,PTTG的表达水平与有氧糖酵解相关酶HK、PFK、PKM2、LDHA及GLUT-1表达水平呈正相关性（相关系数r＝0．839～0．987区间,均P＜0．01）,慢病毒干扰载体沉默PTTG后,卵巢癌细胞的增殖能力显著受到抑制,有氧糖酵解相关酶的表达水平也显著下降（干扰前后灰度2．212±0．36 vs 0．782±0．18,t＝2．36,P＜0．01）。 Western blotting检测正常卵巢及卵巢癌组织PTTG、LDHA、PKM2和GLUT－1的表达情况,结果与免疫组化结果相一致,即在正常的卵巢组织中PTTG表达微弱（灰度为0．705±0．13,n＝13）,而在卵巢癌组织中呈现高表达（灰度为2．616±0．33,n＝58）,并与卵巢癌组织的恶性分化呈正相关性（Pearson检验r＝0．908,P＝0．012）。结论 PTTG可能通过降低有氧糖酵解反应过程中的相关调节酶的表达水平,而实现其抑制有氧糖酵解代谢的作用,从而抑制卵巢癌细胞的快速增殖。     

葡萄糖激酶在T2DM大鼠模型不同组织中的表达

目的探讨葡萄糖激酶在2型糖尿病(T2DM)大鼠模型不同组织中的具体调节作用及作用机制。方法使用高糖高脂饲料和一次性腹腔注射链脲佐菌素诱导T2DM动物模型,从60只SD大鼠中挑选10只作为正常组,其余分别为糖尿病组,低剂量治疗组以及高剂量治疗组,每组10只。正常组采用正常饲料喂养,其余3组均采用高脂高糖饲料喂养。正常组用生理盐水灌胃,糖尿病组用溶解葡萄糖激酶激活剂缓冲灌胃,低剂量组和高剂量组分别使用浓度为10mg/kg以及30mg/kg灌胃。1月后通过免疫组织化学染色观察各组的葡萄糖激酶表达量,将新鲜肝组织利用6-磷酸葡萄糖脱氧酶偶联比色法进行肝脏组织葡萄糖激酶Km值测定,同时采用RT-PCR以及Western blotting,从核酸和蛋白水平进行GK表达检测。结果 T2DM大鼠模型构建成功,通过6-磷酸葡萄糖脱氧酶偶联比色法表明相比正常组糖尿病组肝脏葡萄糖激酶Km值增加,治疗组Km降低,并且高剂量治疗组降低明显。通过免疫组化结果发现,相对正常组织糖尿病组肝脏GK表达降低,治疗组GK相比糖尿病组有一定程度升高。通过RT-PCR结果表明,相比正常组,糖尿病组肝组织中GK信使RNA表达降低,与治疗组肝脏中GK信使RNA相比,糖尿病组有一定程度增加,高剂量治疗组增加明显。根据Western blotting结果表明,相比正常组糖尿病组肝脏中GK蛋白含量降低,而治疗组中肝脏GK蛋白相比糖尿病组有一定程度升高,高剂量组升高明显。结论 T2DM大鼠肝脏组织中葡萄糖激酶的活性与其血糖浓度具有一定联系,使用葡萄糖激酶激活剂能够上调大鼠肝脏组织中GK表达量,提高葡萄糖激酶激活剂是通过大鼠肝脏GK浓度和活性来降低血糖浓度的。     

硒对氧化损伤大鼠肝细胞糖代谢关键酶影响

目的 研究硒对氧化损伤大鼠肝细胞糖代谢关键酶表达的影响,并初步探讨其作用机制.方法 采用0.1 mmol/L的H2O2建立氧化损伤细胞模型,并施加不同剂量硒干预,通过实时定量PCR技术检测葡萄糖激酶(glucokinse,GK)、糖原合成酶(glycogen synthase,GS)和蛋白激酶B(protein kinase B,PKB/Akt)的mRNA表达,并采用蛋白免疫印迹(Western-blot)方法检测Akt的蛋白表达水平.结果 补硒各组GK的mRNA表达量为(9.692～16.588)×10-6,均高于H2O2损伤组(P<0.05);高剂量补硒组GS和Akt的mRNA表达量分别为57.618×10-6和0.2398×10-3,均高于H2O2损伤组(P<0.05);补硒各组Akt的蛋白表达量为(0.3343～0.4346)×10-3,均高于H2O2损伤组(P<0.05).结论 补硒可以在一定程度上改善氧化损伤对肝细胞糖代谢关键酶GK、GS的影响,其机制可能与上调胰岛素信号传导通路的关键信号分子Akt的表达有关.     

银杏叶提取物对酒精所致大鼠睾丸氧化损伤的保护作用的研究

目的研究银杏叶提取物(EGB)对酒精所致大鼠睾丸氧化损伤的预防保护作用。方法雄性SD大鼠30%酒精灌胃(2.37g/kgbw)前,EGB采用分组(低剂量组48μg/gbw和高剂量组96μg/gbw)预防性给药的方法。于实验90d检测大鼠睾丸组织中超氧化物歧化酶(SOD)、谷胱甘肽转移酶(GST)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)、和谷胱甘肽(GSH)、活性氧(ROS)以及丙二醛(MDA)的含量。通过亚细胞分离方法提取大鼠睾丸微粒体,测定微粒体血红素氧化酶-1(HO-1)活性。采用RT-PCR检测睾丸组织中血红素氧化酶-1(HO-1)mRNA表达水平。结果慢性酒精摄入90d后,EGB组睾丸匀浆ROS、MDA较酒精组有明显降低(P<0.05);相反,GST、G-Px、CAT、SOD、HO-1活性以及GSH均有显著性升高(P<0.05);EGB诱导HO-1高表达。结论长期慢性酒精摄入引起大鼠睾丸氧化损伤。EGB可作为一种预防性的抗氧化剂减轻这种氧化损伤;其机制可能与诱导HO-1高表达,清除自由基,抑制脂质过氧化反应有关。     

Effect of urethane, dimethylnitrosamine, paraquat and butylated hydroxytoluene on the activities of glycolytic key enzymes in mouse lung

Effects of carcinogens and noncarcinogenic pulmonary toxicants on the activities of glycolytic key enzymes in the mouse lung were investigated. The carcinogens urethane (URTH) and dimethylnitrosamine (DMN) permanently enhanced, and the noncarcinogenic pulmonary toxicants paraquat (PAR) and butylated hydroxytoluene (BHT) temporarily, enhanced the activities of hexokinase (HK), phosphofructokinase (PFK), and pyruvate kinase (PK) in the lungs of mice.     

α-硫辛酸对高糖诱导GK大鼠肝氧化损伤的影响

[目的]探讨α-硫辛酸（α-LA）对高糖诱导GK大鼠肝氧化损伤的影响。[方法]选用GK大鼠36只,分为6组,阴性对照组普通饮水、阳性对照组及4个干预组分别给予等量30％蔗糖饮水,干预组分别给予不同剂量的α-LA（25、50、75、100mg／kg）灌胃。干预9周后观察不同剂量的α-LA对高糖诱导下GK大鼠肝组织脂质过氧化水平、抗氧化酶活力以及肝线粒体活性氧（ROS）水平的影响。[结果]阳性对照组大鼠丙二醛（MDA）和线粒体ROS水平明显高于阴性对照组（P〈0．05）,而超氧化物歧化酶（SOD）及谷胱甘肽过氧化物酶（GSH-Px）水平明显低于阴性对照组（P〈0．05）,提示高糖饮水明显增加了GK大鼠肝脏的氧化应激水平。在高糖诱导情况下,各α-LA干预组与对照组比较,给予25mg／kg和50mg／kg剂量的α-LA干预可以有效降低肝组织MDA浓度,提高SOD、GSH-P活性以及降低肝线粒体ROS水平（P〈0．05）,其抗氧化损伤的效果好于75mg／kg和100mg／kg两个高剂量干预组。[结论]25mg／kg和50mg／kg剂量的α—LA对高糖诱导的GK大鼠肝组织的氧化损伤具有保护作用,但这种保护作用并未呈现明显的剂量作用关系,高剂量的α-LA（75—100mg／kg）保护作用不如低剂量组。     

Energy production, intracellular amino acid pools, and protein synthesis in chronic renal disease

Intracellular glycolytic regulating enzyme activities, pyruvate kinase (PK) and phosphofructokinase (PFK), adenylate kinase (AK), energy charge (Ech), free amino acids (ICAA), and protein synthesis (PS) were measured in polymorphonuclear leukocytes--used as a cell model--in 62 adults and 12 children with chronic renal failure, and 66 normal adults and 21 children as comparison controls. In normal subjects, children had significantly lower enzyme activities and cell amino acid levels but similar Ech and higher PS than adults. ICAA concentrations were significantly higher than plasma amino acid concentrations (PAA) in both groups, and the PAA were not correlated with, nor indicative of, the ICAA concentrations. The variance (R2) in PS could be largely accounted for by a combination ("set") of six ICAA, as determined by multivariate analysis. The sets differed in children vs adults, suggesting that different proteins were being synthesized. In the uremic patients, reduced PF, PFK, Ech, most ICAAs and PS were indicative of cellular malnutrition. For the uremic adults, the abnormalities in cell metabolism were modified by therapy--nondialyzed uremics being worst, CAPD patients best and approximately normal, and hemodialyzed intermediate. The uremic CAPD children had reduced, PK, PFK, AK, most ICAA, and PS. Ech was increased. Cellular malnutrition in children with chronic renal failure may contribute to their poor growth.     

荞麦花叶黄酮对糖尿病GK大鼠学习记忆的影响

目的 探讨荞麦花叶黄酮(Flavones of Buckwheat Flower and Leaf,FBFL)对糖尿病GK大鼠学习记忆的影响及其作用机制。 方法 雄性GK大鼠随机分为模型组(MC)和FBFL组(FBFL),各10只;10只同源雄性Wistar大鼠为正常对照组(NC);FBFL给药剂量为100mg/kg,灌胃6w,每周定期测定随机血糖;采用旷场分析与Morris水迷宫测试各组大鼠学习记忆能力;处死后检测血液与海马中的超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量与晚期糖基化终产物(AGEs)含量。 结果 FBFL能降低GK大鼠的血糖(P<0.01);水迷宫测试中FBFL可明显缩短逃避潜伏期、增加穿越平台次数(P<0.05);旷场实验中FBFL组在中央格停留时间明显短于模型组(P<0.01);FBFL可增加SOD活性、降低MDA含量(P<0.05)、抑制海马组织AGEs的产生(P<0.05),但对血液中AGEs的产生无影响。 结论 荞麦花叶黄酮有降血糖作用,改善糖尿病GK大鼠学习记忆障碍,机制可能与增加血液、海马组织SOD活性、降低MDA含量以及抑制海马组织AGEs的产生有关。     

Effects of miglitol, an alpha-glucosidase inhibitor, on glycaemic status and histopathological changes in islets in non-obese, non-insulin-dependent diabetic Goto-Kakizaki rats

Miglitol, a 1-deoxynojirimycin derivative, is an alpha-glucosidase inhibitor. In the present study, the effects of acute (single-dose) and chronic (8-week) oral administration of miglitol in Goto-Kakizaki (GK) rats, an animal model of type 2 diabetes, were investigated. Dose-dependent decreases in incremental blood glucose concentrations integrated over a period of 2 h (deltaAUC0-2 h) for values of blood glucose after sucrose-loading in miglitol-treated GK rats were observed following an acute oral administration of miglitol (1, 3 or 10 mg/kg body weight). At 10 mg/kg, the deltaAUC0-2 h of blood glucose was decreased by 45 % compared with the control group. Following the oral administration of miglitol in a dietary mixture (10 mg, 20 mg or 40 mg miglitol/100 g control diet) for 8 weeks, the ratio of HbA1c at 8 weeks compared with 0 weeks in GK rats treated with 40 mg miglitol/100 g control diet miglitol was significantly decreased compared with control GK rats without changes in body weight. In oral glucose tolerance testing, miglitol caused a slight decrease in the deltaAUC0-2 h of plasma glucose concentration. In addition, miglitol treatment slightly inhibited the reduction in beta-cell mass, and lessened the irregular contours and fibrosis of the islets in GK rats. These results indicate that miglitol ameliorates the hyperglycaemic state of GK rats and the impaired function of the pancreatic islets, as well as preventing the degeneration of islets in GK rats.     

Energy production,intracellular amino acid pools,and protein synthesis in chronic renal disease.

Intracellular glycolytic regulating enzyme activities, pyruvate kinase (PK) and phosphofructokinase (PFK), adenylate kinase (AK), energy charge (Ech), free amino acids (ICAA), and protein synthesis (PS) were measured in polymorphonuclear leukocytes–used as a cell model–in 62 adults and 12 children with chronic renal failure, and 66 normal adults and 21 children as comparison controls. In normal subjects, children had significantly lower enzyme activities and cell amino acid levels but similar Ech and higher PS than adults. ICAA concentrations were significantly higher than plasma amino acid concentrations (PAA) in both groups, and the PAA were not correlated with, nor indicative of, the ICAA concentrations. The variance (R2) in PS could be largely accounted for by a combination (“set”) of six ICAA, as determined by multivariate analysis. The sets differed in children vs adults, suggesting that different proteins were being synthesized. In the uremic patients, reduced PF, PFK, Ech, most ICAAs and PS were indicative of cellular malnutrition. For the uremic adults, the abnormalities in cell metabolism were modified by therapy–nondialyzed uremics being worst, CAPD patients best and approximately normal, and hemodialyzed intermediate. The uremic CAPD children had reduced, PK, PFK, AK, most ICAA, and PS. Ech was increased. Cellular malnutrition in children with chronic renal failure may contribute to their poor growth.     

Effects of quantity and quality of dietary protein on certain enzyme activities in rainbow trout

The effects of variation in quality and quantity of dietary protein on certain tissue enzymes in rainbow trout (Salmo gairdneri) were examined. Trout were given for 9 weeks diets containing proteins of different quality (fish-meal, casein and corn gluten) and with protein energy levels ranging from 26 to 74% of total metabolizable energy. In the first experiment, activities of a number of enzymes were monitored by only hepatic serine pyruvate transaminase (SPT) activity changed in response to the dietary treatments--increasing as protein energy level was raised. In the second experiment, opposing glycolytic an gluconeogenic enzyme activities [pyruvate kinase (PK) and phosphoenolpyruvate carboxykinase (PEPCK); phosphofructokinase (PFK) and fructose diphosphatase (FDP)] were measured. Gluconeogenic enzyme activities correlated positively and significantly with dietary protein energy level; glycolytic enzymes correlated negatively and significantly with this parameter for all three proteins. There was no consistent relationship between presumed equilibrium point of opposing enzyme activities and maximum weight gain for the three proteins. It is suggested that hepatic activities of SPT, PFK, PK, FDP and PEPCK will provide useful indices of protein status in trout.     

中学生二,三节课间血糖水平与早餐现状的关系

对杭州市某中学332名学生上午二、三节课间血糖水平的调查，评估了目前中学生早餐的现状，分析了课间血糖水平与早餐质量的关系。结果显示．课间血糖达标率为81．93％，其中34．93％处于正常值的低限。早餐摄入的总热量、碳水化合物和蛋白质量的达标率均较低。上午二、三节课间血糖水平与早餐摄入的总热量（P＜0．05）、碳水化合物量（P＜0．05）有关。本资料提示，目前中学生早餐质量问题应引起重视。     

Effect of a vitamin D3-based nutritional supplement ('Videchol') on carbohydrate metabolism of rats following chronic low dose-rate irradiation.

In this study we evaluated the effects of the administration of a vitamin D3 preparation 'Videchol' to chronically irradiated rats (1 cGy day(-1)) by the assessment of the activities of several glycolytic enzymes: lactic dehydrogenase (LDH) (EC 1.1.1.28), pyruvate kinase (PK) (EC 2.7.1.40) and hexokinase (HK) (EC 2.7.1.1), in populations of erythroid and myeloid bone marrow cells. Videchol treatment of irradiated rats led to the normalisation of HK and LDH activity at cumulative doses of around 30 cGy in granulocyte-monocyte cells and to normalisation of LDH and PK activities in erythroid cells starting at 20 cGy in comparison with irradiated rats who did not receive Videchol. The reaction kinetic parameters of LDH in erythrocytes changed according to the redistribution pattern of the isozymes throughout the different stages of the experiment. The administration of Videchol to irradiated rats led to a rearrangement of the LDH isozymes ratio characterised by kinetic properties more comparable to those of the controls. Thus, vitamin D3 appears to induce a normalisation of carbohydrate metabolism in rats chronically irradiated with low dose-rate ionising radiation.