大豆寡肽抗疲劳作用的实验研究

目的探讨大豆寡肽对耐力运动小鼠的抗疲劳作用,为新型抗疲劳营养补剂的开发提供理论依据和实验基础。方法雄性KM小鼠150只,按体重随机分为5个小组,分别为正常对照组(CG)、大豆寡肽低剂量组(LD)、大豆寡肽中剂量组(MD)、大豆寡肽高剂量组(HD)、乳清蛋白组(WPC),每组30只,通过每天60min游泳练习建立耐力运动小鼠模型,连续灌胃30天后处死、取材,测定小鼠力竭游泳时间、肝糖原和肌糖原含量、血乳酸代谢水平和乳酸脱氢酶活性。结果HD、WPC组力竭游泳时间与CG组比较有显著性差异(P0.05),MD组与CG、WPC组比较有极显著性差异(P0.01);MD组小鼠肝糖原、肌糖原含量与CG组比较均有显著性差异(P0.05);MD、HD组小鼠游泳后15min血乳酸与CG组比较有显著性差异(P0.05);MD、HD组小鼠游泳后90min血乳酸与CG组比较有显著性差异(P0.05);MD组小鼠游泳后血乳酸平均清除率与CG组比较有极显著性差异(P0.01);MD、HD组血清中乳酸脱氢酶的活性与CG组比较有显著性差异(P0.05)。结论大豆寡肽能够延长小鼠力竭游泳时间,增加肌糖原和肝糖原含量,减少小鼠运动时的乳酸生成,促进运动后血乳酸的清除,从而起到一定的抗疲劳作用。     

三七皂苷Rg1抗疲劳和耐缺氧作用的研究

目的观察三七皂苷Rg1对小鼠的抗疲劳和耐缺氧作用。方法采用灌胃法,给予小鼠不同剂量的三七皂苷Rg1,分别测定小鼠的负重游泳时间、爬杆时间、肝糖原、外周血血象、血清尿素氮（BUN）、乳酸脱氢酶（LDH）、尿激酶（UK）等含量。结果三七皂苷Rg1能够明显延长小鼠负重游泳时间和爬杆时间（P〈0．01）,能明显增加了运动后小鼠的肝糖原含量（P〈0．01）,能明显的改善小鼠外周血血象,降低小鼠血清中尿素氮、乳酸脱氢酶、尿激酶等指标（P〈0.01）。结论三七皂苷Rg1对小鼠抗疲劳和耐缺氧有明显的效果。     

八角茴香提取液的抗疲劳效应

背景：延缓疲劳或消除疲劳是运动医学的研究热点,利用中药来消除运动性疲劳,提高机体运动能力,具有重要应用前景。目的：观察八角茴香提取液对小鼠的抗疲劳作用。方法：将120只雄性昆明种小鼠按体质量随机分为4组：分别给予21,42,84mL/（kg·d）的八角茴香提取液和蒸馏水,35d后,检测小鼠力竭游泳时间、爬杆时间及运动后血乳酸水平;40d后,检测小鼠运动后肝糖原含量、血清尿素氮和乳酸脱氢酶活力。结果与结论：八角茴香提取液可增加小鼠力竭游泳时间、爬杆时间及运动后肝糖原含量,提高运动后小鼠血乳酸脱氢酶活力,同时降低小鼠运动后血乳酸及尿素氮水平,尤以84mL/（kg·d）八角茴香提取液的效果最明显（P〈0.05或P〈0.01）。说明八角茴香提取液有明显的抗疲劳作用。     

刺五加皂甙和水飞蓟素提高小鼠运动后即刻肌糖原含量

目的：初步筛选具有促进糖原合成作用的物质。方法：实验于2003—03在国家体育总局运动医学研究所完成。选择SPF／VAF级雌性CD-1小鼠130只。随机分为10组：安静对照组、训练对照组、训练＋烟酸铬组、训练＋五味子素组、训练＋黄芪多糖组、训练＋人参皂甙组、训练＋谷氨酰胺组、训练＋水飞蓟素组、训练＋刺五加甙组、训练＋红景天甙组。每组13只。训练对照和训练＋不同药物组负重2％游泳训练6d，训练＋不同药物组分别灌胃给予烟酸铬0．02g／（kg&;#183;d）、谷氨酰胺4g/（kg&;#183;d）、五味子素、黄芪多糖、人参皂甙、水飞蓟素、刺五加甙或红景天甙[中药提取物的剂量都为0．8g／（kg&;#183;d）]．对照组给予安慰剂。末次训练后20h，负重4％游泳30min后即刻取股四头肌和肝脏，测定糖原。结果：每组实验动物均达到实验目的，全部进入结果分析。①训练或药物对小鼠体质量的影响：实验前各组小鼠体质量差异不显著（F=1．398，P=0．197）；实验后所有训练组（包括训练对照组和训练＋不同药物组）的体质量都显著低于安静对照组（F=3．784，P〈0．01），说明训练降低小鼠体质量。与训练对照相比，人参皂甙或刺五加皂甙组小鼠体质量较高（P〈0．05）。②训练或药物对小鼠一般情况的影响：在实验过程中，所有实验动物的精神状态、摄食活动、毛色、大便等都无异常。③训练或药物对肌糖原的影响：方差分析表明，定量负荷后即刻，股四头肌糖原含量存在组间差异（F=3．154，P=0．002）。训练组与安静组之间无差异；在8个用药组中，刺五加皂甙＋训练组和水飞蓟素＋训练组的肌糖原含量比训练对照组高（P〈0．05）；红景天皂甙＋训练组与训练对照组比有升高趋势，但无统计学意义（P=0．115）；其他用药组与训练对照组间的差异都无统计学意义（P〉0．05）。④训练或药物对肝糖原的影响：多组秩和检验表明，定量负荷后即刻，肝糖原含量在各组间差异无统计学意义（P=0．108）。结论：刺五加皂甙和水飞蓟素具有较明显的促肌糖原合成作用，红景天皂甙可能对肌糖原合成也具有一定的积极意义。     

神经活性物质对小鼠学习记忆能力及耐力的影响

目的：观察神经活性物质（胚脑组织提取物，NAF）对小鼠学习、记忆能力提高的作用，以及对小鼠耐力的影响。方法：采用随机分组法，将51只小鼠按体重等分，分为5个实验组：生理盐水组（A）9只、脑活素组（B）11只和3个不同浓度（C：0．1mg,10只、D：0．2mg，10只、E：0．4mg ,11只）的NAF治疗组.用自制的复杂迷宫检测小鼠的迷宫觅 食时间及行走的错误次数，测定小鼠负重5％体重游泳至淹死的时间。结果：迷宫觅食时间A组治疗前后无明显差异（P＞0．01），B、C、D、E组治疗后缩短或明显缩短（P＜0．05－0．001）；治疗前后小鼠行走的错误次数A组和B组无显著性差异（P＞0．2－0．5），C、D、E组有非常显著性差异（P＜0．02－0．01）；小鼠负重5％体重游泳淹死时间5组间方差分析有显著性差异（P＜0．05）；进一步分析差异来自于C与E组（P＜0．05）和D与E组（P＜0．01）。结论：NAF可提高小鼠的学习、记忆能力，也可增强小鼠的耐力。腹腔注射≥20mg/kg 体重时，小 鼠的耐力反而下降。     

当归多糖抗运动疲劳作用及其机制研究

目的：探讨不同剂量当归多糖(ASP)对小鼠的抗疲劳作用及其机制。方法：选择SPF级雄性昆明小鼠50只,按照随机数字表法分为空白对照组、模型组、ASP高剂量组、ASP中剂量组和ASP低剂量组,每组10只。除空白对照组外,各组小鼠负重游泳至力竭1次/d,持续负重游泳15 d。造模第6天开始,ASP高、中、低剂量组小鼠分别灌胃相应剂量(222.56、111.28、55.64 mg/kg)的药物,空白对照组和模型组仅以等量生理盐水灌胃,连续灌胃10 d。记录最后1次小鼠负重游泳至力竭的时间,评估小鼠运动耐力;而后采集标本,检测血清肌糖原、肝糖原、血乳酸及血尿素氮含量;检测肝脏、肾脏及后肢肌肉中的ATP酶含量。结果：(1)与模型组比较,ASP中、高剂量组小鼠负重游泳时间均有所延长(P<0.05);与低剂量组和中剂量组分别比较,高剂量组小鼠的负重游泳时间均更长(P<0.05)。(2)与空白对照组比较,模型组小鼠血清肌糖原和肝糖原含量均降低(P<0.05);与模型组比较,ASP中剂量组小鼠血清肝糖原含量升高(P<0.05),ASP高剂量组小鼠血清肌糖原和肝糖原含量均升高(P&...     

“灵芝耐力宝”对机体耐疲劳作用的实验应用研究

目的：探讨“灵芝耐力宝”对运动能力的影响和作用。方法：运动员口服灵芝耐力宝，测定定量负荷和最大负荷工作时间。结果：运动员服用后，实验组递增负荷运动时间和做功值明显高于服药前（P＜0．01）；运动时心率负荷及血乳酸的消除（P＜0．05），也显示了服药后训练程度的提高。结论：“灵芝耐力宝”具有一定的提高运动能力及消除疲劳之功效。     

静注高氧液对抗小鼠运动性疲劳

目的：探讨小鼠尾静脉注射高氧液的抗疲劳效果。方法：实验于2003-03／2004—08在第四军医大学基础部病理生理教研室完成。120只小鼠随机分为2组，每组60只。对照组和高氧液组分别静注平衡盐和高氧液。每组再根据给药剂量分为0．1mL／g，0．15mL/g和0．2mL／g3组，每组20只。静注后鼠尾根部负荷5％体质量的铅皮即刻置游泳箱中游泳，静注后即刻和游泳30min检测运动后代谢产物血清乳酸含量评估疲劳程度，检测肌糖原含量（当储量少时可产生疲劳），检测三磷酸腺苷酶活力（活力增高表示机体对疲劳的耐受性强）．检测丙二醛含量和机体的总抗氧化能力。结果：120只小鼠均进入结果分析。①血清乳酸含量：高氧液组明显少于对照组（P〈0．05），高氧液组中0．15mL／g组低于0．1mL／g组和0．2mL／g组[（10．74&;#177;0．90）．（11．62&;#177;1．09），（11．56&;#177;1．19）mmol／L，P〈0．05]。②肌糖原贮备：高氧液组明显多于对照组（P〈0．05），高氧液组中0．15mL／g组高于0．1mL/g组和0．2mL/g组[（1．43&;#177;0．21），（1．08&;#177;0．16），（1．08&;#177;0．21）mg／g，P〈0．05]。③三磷酸腺苷酶活力：高氧液组比对照组增高明显（P〈0．05），高氧液组中0．15mL／g组高于0．1mL／g组和0．2mL／g组（P〈0．05）。④丙二醛含量：高氧液组明显少于对照组（P〈0．05），高氧液组中0．15mL/g组低于0．1mL／g组和0．2mL／g组[（19．10&;#177;1．37）．（22．10&;#177;1．58）．（20．93&;#177;1．18）μmol／g，P〈0．051。⑤总抗氧化能力：高氧液组比对照组增高明显（P〈0．05），高氧液组中0．15mL／g组高于0．1mL／g组和0．2mL/g组[（18．98&;#177;0．71），（10．15&;#177;0．72）．（10．15&;#177;1．44）U／mg，P〈0．05]。结论：静注高氧液有利于小鼠运动耐力的提高，减少无氧代谢产物的生成，从而降低体内能源物资的消耗，延缓疲劳的产生．0．15mL／g高氧液效果优于0．1和0．2mL/g高氧液。     

芦荟多糖的抗疲劳作用研究

目的探讨芦荟多糖的抗疲劳作用。方法160只昆明种雄性小鼠随机均分成4组,用芦荟多糖低、中、高3个剂量给小鼠灌胃,对照组给等剂量蒸馏水,15d后小鼠游泳造成疲劳,测定小鼠力竭时游泳时间、血乳酸（LAC）、血清尿素氮（BUN）及肝糖原。结果芦荟多糖能明显延长小鼠负重游泳时间,明显提高小鼠运动后肝糖原的含量,降低BUN和LAC的含量。结论芦荟多糖对小鼠具有显著抗疲劳作用。     

不同剂量力谷源胶囊抗疲劳作用的实验

目的：探讨不同剂量力谷源胶囊缓解体力疲劳功能的差异。方法：实验于2004-06/09在解放军总医院动物实验中心完成。160只昆明雄性小鼠，体质量20～22g,每个实验用40只小鼠，随机分为空白对照组和3个不同剂量组，每组10只，分别为0.36g/kg、0．72g，kg、1．08g，kg 3个剂量组及对照组。各组小鼠每日称体质量后以力谷源胶囊（主要成分为玉米胚芽提取物、葛根提取物、L-精氨酸）灌胃1次，连续30d。进行4个实验：①小鼠负重游泳时间实验：末次给予试验用样品30min后，称体质量，每只鼠尾根部负荷5％体质量铅皮，置于水深（30&;#177;1）cm、水温（25&;#177;1）℃游泳箱中游泳，不时搅动水，使小鼠四肢保持运动，记录自游泳开始至死亡时间（min）。②小鼠肝糖原含量测定实验：末次给予试验用样品30min后处死小鼠，取肝脏，清洗吸干，精确称取100mg，计算肝糖原含量。③血乳酸测定实验：末次给予试验用样品30min后，称体质量，将小鼠置于水深（30&;#177;1）cm、水温（25&;#177;1）℃游泳箱中游泳，不时搅动水，使小鼠四肢保持运动，10min后取出。分别于游泳前、游泳后立即、游泳后休息20min从眼内眦准确采血20μL，用乳酸仪测定血乳酸含量（实测值为测量值3倍），计算血乳酸曲线下面积。④血清尿素氮含量测定实验：末次给予试验用样品30min后，称体质量，将小鼠置于水深（30&;#177;1）cm、水温（25&;#177;1）℃游泳箱中游泳，不时搅动水，使小鼠四肢保持运动，90min后取出，休息60min后，摘眼球采血。用COBAS MIRA全自动生化分析仪测定尿素氮含量。结果：各组小鼠在实验中无意外死亡、丢失及补充，进入结果分析小鼠数量为160只。①各组小鼠体质量的变化：力谷源胶囊对各项实验的小鼠体质量无明显影响，在小鼠游泳时间、肝糖原含量、血清乳酸及血清尿素含量4个实验中，不同剂量组体质量与对照组比较，差异均无显著性（P〉0．05）。②生化代谢指标的变化：各实验组随灌胃力谷源胶囊剂量的增加，小鼠的负重游泳时间延长、血清肝糖原含量增加、血乳酸曲线下面积减少，其中1．08g/kg和0．72g/kg实验组与对照组的差异有显著性（t=3．357～5．625，P〈0．01）；各实验组小鼠的尿素氮含量未见明显变化（P〉0．05）。结论：中剂量（0.72g/kg）、高剂量（1．08g/kg）力谷源胶囊能延长小鼠的负重游泳时间，降低血中乳酸的含量及血清中尿素氮的含量，提高体内肝糖原储备量，从而为机体提供更多的能量来源，延缓疲劳的产生。其效果具有剂量反应关系。     

Assessment of human muscle glycogen synthesis and total glucose content by in vivo 13C MRS

BACKGROUND: Obesity is often accompanied by a decreased ability of insulin to stimulate glucose uptake and glycogenesis in skeletal muscle. The aim of this study was to investigate the rate of glycogen formation and of muscular glucose content in relation to insulin sensitivity under euglycemic conditions. MATERIALS AND METHODS: We applied a hyperinsulinemic (430 pmol m-2 min-1) euglycemic clamp with infusion of 20% glucose (30% enriched with 13C-1-glucose) to 8 subjects with a wide range of insulin sensitivities. Glycogen and glucose levels were monitored simultaneously by in vivo 13C MRS of the calf muscle on a clinical MR system at 1.5T field strength. RESULTS AND CONCLUSIONS: Glycogen synthesis rate showed a strong correlation with whole body glucose uptake during the clamp (r = 0.93, P < 0.01). With the use of 13C MRS, total muscular glucose content could be determined in vivo, and showed a positive, linear correlation with glycogen synthesis rate (r = 0.85, P < 0.01). 13C MRS provides important information regarding in vivo insulin action. Preliminary results indicate that the glycogen synthesis rate improves after treatment with troglitazone.     

The roles of insulin and glucagon in the regulation of hepatic glycogen synthesis and turnover in humans.

To determine the respective roles of insulin and glucagon for hepatic glycogen synthesis and turnover, hyperglycemic clamps were performed with somatostatin [0.1 micrograms/(kg.min)] in healthy young men under conditions of: (I) basal fasting) portal vein insulinemia-hypoglucagonemia, (II) basal portal vein insulinemia-basal glucagonemia, and (III) basal peripheral insulinemia-hypoglucagonemia. Synthetic rates, pathway (direct versus indirect) contributions, and percent turnover of hepatic glycogen were assessed by in vivo 13C nuclear magnetic resonance spectroscopy during [1-13C]glucose infusion followed by a natural abundance glucose chase in conjunction with acetaminophen to noninvasively sample the hepatic UDP-glucose pool. In the presence of hyperglycemia (10.4 +/- 0.1 mM) and basal portal vein insulinemia (192 +/- 6 pM), suppression of glucagon secretion (plasma glucagon, I:31 +/- 4, II: 63 +/- 8 pg/ml) doubled the hepatic accumulation of glycogen (Vsyn) compared with conditions of basal glucagonemia [I: 0.40 +/- 0.06, II: 0.19 +/- 0.03 mumol/(liter.min): P < 0.0025]. Glycogen turnover was markedly reduced (I: 19 +/- 7%, II: 69 +/- 12%; P < 0.005), so that net rate of glycogen synthesis increased approximately fivefold (P < 0.001) by inhibition of glucagon secretion. The relative contribution of gluconeogenesis (indirect pathway) to glycogen synthesis was lower during hypoglucagonemia (42 +/- 6%) than during basal glucagonemia (54 +/- 5%; P < 0.005). Under conditions of basal peripheral insulinemia (54 +/- 2 pM) and hypoglucagonemia (III) there was negligible hepatic glycogen synthesis and turnover. In conclusion, small changes in portal vein concentrations of insulin and glucagon independently affect hepatic glycogen synthesis and turnover. Inhibition of glucagon secretion under conditions of hyperglycemia and basal concentrations of insulin results in: (a) twofold increase in rate of hepatic glycogen synthesis, (b) reduction of glycogen turnover by approximately 73%, and (c) augmented percent contribution of the direct pathway to glycogen synthesis compared with conditions of basal glucagonemia.     

Sonographic findings in type I glycogen storage disease.

PURPOSE: The aim of this study was to document the sonographic appearance and dimensions of the liver and spleen in patients affected by type I glycogen storage disease and to correlate those findings with laboratory data to evaluate the potential role of sonography in diagnosing that disease. METHODS: Fourteen patients (age range, 3-26 years; 10 patients younger than 18 years) with type I glycogen storage disease proved by liver biopsy were studied prospectively with gray-scale sonography, color Doppler sonography, and spectral analysis. The liver, kidneys, spleen, portal system, hepatic veins, and hepatic arteries were evaluated. Laboratory data were correlated with sonographic findings. RESULTS: In 13 (93%), of 14 patients, the liver was enlarged, and in 11 patients (79%), hepatic echogenicity was increased. In 9 patients (64%), both kidneys were enlarged, and in 6 cases (43%), the spleen was enlarged. In all patients, flow in the portal, splenic, and superior mesenteric veins was hepatopetal, and flow in the hepatic veins was triphasic. In 5 patients (36%), both triglyceride and total cholesterol levels were higher than normal. No focal hepatic lesions were identified. Analysis found no significant association between sonographic findings and laboratory data. CONCLUSIONS: The most frequent sonographic findings in patients with type I glycogen storage disease were hepatomegaly, increased hepatic echogenicity, and enlarged kidneys. Sonography may help in the diagnosis of type I glycogen storage disease, but a liver biopsy is required for a definitive diagnosis.     

八角茴香提取液的抗疲劳效应

背景:延缓疲劳或消除疲劳是运动医学的研究热点,利用中药来消除运动性疲劳,提高机体运动能力,具有重要应用前景。目的:观察八角茴香提取液对小鼠的抗疲劳作用。方法:将120只雄性昆明种小鼠按体质量随机分为4组:分别给予21,42,84mL/(kgd)的八角茴香提取液和蒸馏水,35d后,检测小鼠力竭游泳时间、爬杆时间及运动后血乳酸水平;40d后,检测小鼠运动后肝糖原含量、血清尿素氮和乳酸脱氢酶活力。结果与结论:八角茴香提取液可增加小鼠力竭游泳时间、爬杆时间及运动后肝糖原含量,提高运动后小鼠血乳酸脱氢酶活力,同时降低小鼠运动后血乳酸及尿素氮水平,尤以84mL/(kgd)八角茴香提取液的效果最明显(P<0.05或P<0.01)。说明八角茴香提取液有明显的抗疲劳作用。     

Correction of chronic hyperglycemia with vanadate, but not with phlorizin, normalizes in vivo glycogen repletion and in vitro glycogen synthase activity in diabetic skeletal muscle.

Vanadate has insulin-like activity in vitro and in vivo. To characterize the in vivo mechanism of action of vanadate, we examined meal tolerance, insulin-mediated glucose disposal, in vivo liver and muscle glycogen synthesis, and in vitro glycogen synthase activity in 90% partially pancreatectomized rats. Four groups were studied: group I, sham-operated controls; group II, diabetic rats; group III, diabetic rats treated with vanadate; and group IV, diabetic rats treated with phlorizin. Insulin sensitivity, assessed with the euglycemic hyperinsulinemic clamp technique in awake, unstressed rats, was reduced by approximately 28% in diabetic rats. Both vanadate and phlorizin treatment completely normalized meal tolerance and insulin-mediated glucose disposal. Muscle glycogen synthesis was reduced by approximately 80% in diabetic rats (P less than 0.01) and was completely restored to normal by vanadate, but not by phlorizin treatment. Glycogen synthase activity was reduced in skeletal muscle of diabetic rats (P less than 0.05) compared with controls and was increased to supranormal levels by vanadate treatment (P less than 0.01). Phlorizin therapy did not reverse the defect in muscle glycogen synthase. These results suggest that (a) the defect in muscle glycogen synthesis is the major determinant of insulin resistance in diabetic rats; (b) both vanadate and phlorizin treatment normalize meal tolerance and insulin sensitivity in diabetic rats; (c) vanadate treatment specifically reverses the defect in muscle glycogen synthesis in diabetic rats. This effect cannot be attributed to the correction of hyperglycemia because phlorizin therapy had no direct influence on the glycogenic pathway.     

Mechanism by which glucose and insulin inhibit net hepatic glycogenolysis in humans.

13C NMR spectroscopy was used to assess flux rates of hepatic glycogen synthase and phosphorylase in overnight-fasted subjects under one of four hypoglucagonemic conditions: protocol I, hyperglycemic (approximately 10 mM) -hypoinsulinemia (approximately 40 pM); protocol II, euglycemic (approximately 5 mM) -hyperinsulinemia (approximately 400 pM); protocol III, hyperglycemic (approximately 10 mM) -hyperinsulinemia (approximately 400 pM); and protocol IV; euglycemic (approximately 5 mM) -hypoinsulinemia (approximately 40 pM). Inhibition of net hepatic glycogenolysis occurred in both protocols I and II compared to protocol IV but via a different mechanism. Inhibition of net hepatic glycogenolysis occurred in protocol I mostly due to decreased glycogen phosphorylase flux, whereas in protocol II inhibition of net hepatic glycogenolysis occurred exclusively through the activation of glycogen synthase flux. Phosphorylase flux was unaltered, resulting in extensive glycogen cycling. Relatively high rates of net hepatic glycogen synthesis were observed in protocol III due to combined stimulation of glycogen synthase flux and inhibition of glycogen phosphorylase flux. In conclusion, under hypoglucagonemic conditions: (a) hyperglycemia, per se, inhibits net hepatic glycogenolysis primarily through inhibition of glycogen phosphorylase flux; (b) hyperinsulinemia, per se, inhibits net hepatic glycogenolysis primarily through stimulation of glycogen synthase flux; (c) inhibition of glycogen phosphorylase and the activation of glycogen synthase are not necessarily coupled and coordinated in a reciprocal fashion; and (d) promotion of hepatic glycogen cycling may be the principal mechanism by which insulin inhibits net hepatic glycogenolysis and endogenous glucose production in humans under euglycemic conditions.     

车前子对抗高脂血症大鼠脂质过氧化作用

背景:近年研究发现,车前草种子外壳是很好的可溶性膳食纤维源,可用来添加到食品中,调整胆固醇含量。目的:观察车前子对高脂血症大鼠血脂及其体内脂质过氧化作用的干预结果。设计:完全随机分组设计,对照动物实验。单位:河北省新药药理毒理实验室。材料:①选用健康一级SD大鼠24只,鼠龄60～70d,体质量(210±22)g,雌雄不拘。②基础饲料由河北省实验动物中心配制,各成分质量分数:面粉0.25,麸皮0.1,玉米面0.22,豆饼0.22,鱼粉0.08,骨粉0.02,草粉0.05,食盐0.01,酵母粉0.02,葵花子0.03。高脂饲料由河北省实验动物中心配制,各成分质量分数:基础饲料0.9,胆固醇0.015,猪油0.08,猪胆盐0.003。③测定血脂试剂盒由保定长城临床试剂公司出品;测超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶活力和丙二醛水平试剂盒由南京建成生物工程研究所提供。方法:实验于2004-06/12在河北省新药药理毒理研究实验室完成。①随机将24只大鼠分为3组:正常对照组,模型组,车前子组,每组8只。正常对照组:进食基础饲料。模型组:进食高脂饲料。车前子组:进食高脂饲料 车前子15g/kg,普通饮水。实验动物分笼饲养,每只摄食25g/d,自由饮水,实验周期为12周。②实验结束时,麻醉大鼠,采用相应试剂盒测定血清三酰甘油、总胆固醇、高密度脂蛋白胆固醇水平;采用相应试剂盒测血清超氧化物歧化酶、过氧化氢酶活力和丙二醛水平,心肌组织超氧化物歧化酶活力及丙二醛含量,肝组织过氧化氢酶和谷胱甘肽过氧化物酶活力。③两组间计量资料差异比较采用t检验。主要观察指标:造模12周后,各组大鼠血脂水平及机体抗氧化能力比较。结果:大鼠24只均进入结果分析。①造模12周后,模型组大鼠血清和心肌组织超氧化物歧化酶活力明显低于正常对照组和车前子组(P<0.05),血清丙二醛水平和心肌丙二醛含量均明显高于正常对照组和车前子组(P<0.05)。②造模12周后,模型组大鼠血清和心肌组织过氧化氢酶和肝组织谷胱甘肽过氧化物酶活力均明显低于正常对照组和车前子组(P<0.05)。③造模12周后,模型组大鼠血清总胆固醇和三酰甘油水平明显高于正常对照组和车前子组(P<0.05),血清高密度脂蛋白胆固醇水平和高密度脂蛋白胆固醇/总胆固醇明显低于正常对照组和车前子组(P<0.05)。结论:提示15g/kg剂量车前子可明显降低高脂血症大鼠血脂,增加机体抗氧化能力。     

Changes in hepatic metabolism through simulated weightlessness: decrease of glycogen and increase of lipids following prolonged immobilization in the rat

The effect of simulated weightlessness on hepatic metabolisms of carbohydrates and lipids was investigated in rats that were chronically immobilized by means of a suspension harness. During the 10-day period of the suspension, the animals showed a substantial decrease in the hepatic glycogen content, whereas the content of hepatic total lipids was markedly elevated. Similar results were obtained when the “suspended” animals were provided with a regular amount of nutrients by a force-feeding procedure. In the suspended animals, hepatic parenchymal cells were filled with large fat droplets, and hepatic triglyceride contents were elevated. The prolonged immobilization led to a slight, but significant, increase in glucose-6-phosphatase activity in the liver, suggesting that an increased glycogen breakdown might have occurred in the suspended animals. However, it was unlikely that the increased amount of glucose produced by the glycogen breakdown was utilized as a substrate for the lipogenesis in the liver, because hepatic lipogenic enzyme activities were unaffected by the suspension. The results suggest that the hepatic lipids accumulate in animals exposed to a prolonged immobilization state, presumably due to a decreased lipolysis and/or a suppressed lipoprotein mobilization from the liver into the blood stream.     

Decreased insulin sensitivity and muscle enzyme activity in elderly subjects

Skeletal muscle glycogen deposition, and the activation of muscle glycogen synthase and pyruvate dehydrogenase during a hyerinsulinaemic euglycaemic clamp have been measured in six young and six elderly males matched for body mass index, physical activity and diet. Clamp glucose requirement (insulin, 0.1 U kg-1 h-1) was significantly lower in the older subjects (8.0 +/- 0.4 mg kg-1 min-1) than in younger subjects (10.5 +/- 0.6 mg kg-1 min-1, P less than 0.02). Although the older subjects had a 6.5% decrease in lean body mass, clamp glucose requirement expressed per unit of lean body mass was also significantly decreased in the older subjects (10.2 +/- 0.5 vs. 12.4 +/- 0.6 mg kg-1 min-1, P less than 0.05). The increase in muscle glycogen with the clamp was decreased by 33% in the older subjects (elderly: 13.1 +/- 1.3 mg g-1 protein, young: 19.6 +/- 2.2 mg g-1 protein; P less than 0.05), and was strongly correlated with clamp glucose requirement (r = 0.72, P less than 0.01). Glucose-6-phosphate independent glycogen synthase activity increased significantly between fasting and the end of the clamps in both groups (P less than 0.001), but was lower at the end of the clamp in the older subjects (P less than 0.05). Glycogen synthase activity at the end of the clamp correlated with both clamp glucose requirement (r = 0.83, P less than 0.01) and muscle glycogen deposition (r = 0.73, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)