秦绵祛风胶囊对鹌鹑高尿酸血症模型的治疗作用

目的观察秦绵祛风胶囊对鹌鹑高尿酸血症的影响。方法通过喂饲用酵母配制的造模饲料造成鹌鹑高尿酸血症模型,设秦绵祛风胶囊高、中、低3个剂量组并以苯溴马隆为阳性对照,在造模的同时连续灌胃药35d,检测血中黄嘌呤氧化酶、尿酸、血尿素氮和三酰甘油及粪便中尿酸含量。结果模型动物血清中黄嘌呤氧化酶、尿酸和三酰甘油水平及粪便中尿酸含量较正常对照组明显升高。秦绵祛风胶囊各剂量组均可显著降低鹌鹑血清中的尿酸和三酰甘油水平,同时升高粪便中尿酸含量,对血清中黄嘌呤氧化酶活性影响不大。结论秦绵祛风胶囊具有降脂降尿酸的功能,其机制可能是通过提高动物排泄尿酸的能力,从而降低血中尿酸的含量。     

链脲佐菌素加高糖高脂饮食复制大鼠2型糖尿病模型

目的链脲佐菌素加高糖高脂饮食诱导大鼠2型糖尿病模型的建立。方法Wistar大鼠分别高糖高脂饲料喂养4、6、8周后．采血检测空腹血糖及血清胰岛素,按30m/kg体重剂量一次性腹腔内注射链脲佐菌素,7d后再次采血检测糖尿病鼠空腹血糖及血清胰岛素。结果与对照组比较,高糖高脂喂养大鼠血清胰岛素明显上升（P〈0．05）,但血糖无变化,糖尿病鼠血糖及血清胰岛素均皿著高于对照组（P〈0．05）。结论高脂高糖饲料喂养6周后,小剂量（30mg／kg）注射链脲佐菌素（STZ）诱导2型糖尿病大鼠模型,所建札的2型糖脲病模型与文献报道的方法相比成模率较高,死亡率较少。     

不同嘌呤含量食源性低聚肽对高尿酸血症的作用研究

目的 测定不同食物来源食源性低聚肽的嘌呤含量，研究不同嘌呤含量食源性低聚肽对高尿酸血症大鼠模型血尿酸水平、肾功能和肾脏结构的影响。方法 通过高效液相色谱测定10种不同取材的食源性低聚肽进行嘌呤含量，大豆肽为高嘌呤，绿豆肽和豌豆肽为中嘌呤，海洋鱼骨肽、海洋鱼蛋白肽、玉米肽、小麦肽、大米肽、白蛋白肽和核桃肽为低嘌呤。选取大豆肽、绿豆肽和海洋鱼蛋白肽为高、中、低嘌呤食源性低聚肽作为大鼠灌胃干预物质。10%果糖构建高尿酸血症大鼠模型；实验分为对照组、模型组、别嘌呤醇组和高、中、低嘌呤含量食源性低聚肽灌胃组，分别在建模7 d、14 d、21 d和28 d取血检测各组大鼠血尿酸、血肌酐和血尿素氮，在28 d实验结束后取肾组织通过HE染色观察肾脏的组织学改变。结果 高嘌呤含量的大豆肽在实验4个时间点具有降低血尿酸的作用(P<0.05)，建模7 d、14 d、21 d、28 d，模型组血尿酸值分别为(98.7±4.3)μmol/L、(95.6±2.3)μmol/L、(95.2±2.3)μmol/L、(60.15±14.5)μmol/L；高嘌呤大豆肽组血尿酸值分别为(72.4±19.2)μmol/...     

黄连素对实验性2型糖尿病大鼠黄嘌呤氧化酶的影响

目的观察黄连素对实验性2型糖尿病大鼠血清、肾脏中黄嘌呤氧化酶(XOD)活性的影响及肾脏组织学改变。方法采用小剂量链脲佐菌素加高糖高脂饲料喂养的方法建立Wistar大鼠2型糖尿病模型,成模后给予黄连素0.1g.kg-1.d-1灌胃治疗8周,检测大鼠空腹血糖(FPG)的变化,血清和肾脏中黄嘌呤氧化酶(XOD)活性的变化,观察肾脏组织学改变。结果与糖尿病组相比,黄连素治疗组血清和肾组织黄嘌呤氧化酶(XOD)活性明显降低(P<0.01)。黄连素组大鼠肾脏组织仅见内皮细胞数目稍有增加,较糖尿病组大鼠有所改善。结论黄连素可降低大鼠体内黄嘌呤氧化酶活性、延缓DM肾脏的发生和发展。     

非洛地平对动脉粥样硬化大鼠血清SOD及MDA的影响

目的:通过腹腔注射维生素D3与高脂饲料诱导相结合建立大鼠动脉粥样硬化模型,用非洛地平进行干预,探讨非洛地平对动脉粥样硬化大鼠血清超氧化物歧化酶(SOD)及丙二醛(MDA)的影响.方法:30只雄性SD大鼠随机分为3组,每组10只,分别为正常组(正常饮食)、模型组(高脂饮食+腹腔注射维生素D3)和非洛地平组[高脂饮食+腹腔注射维生素D3+非洛地平(5 mg/kg*d)].喂养6周后用黄嘌呤氧化法检测血清SOD,硫代巴比妥酸比色法检测血清MDA.比较各组以上指标的差异.结果:模型组较正常组血清SOD明显降低,血清MDA明显升高(P＜0.01);非洛地平组较模型组血清SOD升高,血清MDA降低(P＜0.01).结论:非洛地平能够明显抑制动脉粥样硬比病变过程中的脂质过氧化损伤.     

洛伐他汀对高糖诱导大鼠近端肾小管上皮细胞钠钾ATP酶活性的影响

目的洛伐他汀对高糖诱导的原代大鼠近端上皮小管上皮细胞（PTEC）钠钾ATP酶（Na＋,K＋-ATPase）活性的影响。方法采用显微微分离法体外培养大鼠PTEC,进行免疫细胞免疫化学方法鉴定细胞类型。将细胞分为正常对照组[达氏改良伊格尔（DMEM）培养液]、高糖组（25mmol／L）、高糖加小剂量洛伐他汀（高糖＋0．1μmol／LLOV）,高糖加中剂量LOV（1．0μmol／L）组,高糖加大剂量LOV（10．0μmol／L）组,检测洛伐他汀对肾小管上皮细胞氧化应激水平,液闪法测定PTEC的Na＋,K＋-ATPase活性。结果高糖组Na＋,K＋-ATPase活性显著高于正常对照组,小剂量组、中剂量组明显减低,大剂量组显著性减低。结论高糖诱导的PTECNa＋,K＋-ATPase活性明显升高,洛伐他汀对高糖诱导的原代PTEC的Na＋,K＋-ATPase活性的升高有明显抑制作用。     

糖目清袋泡剂在糖尿病大鼠抗氧化损伤中的作用

目的:观察糖目清袋泡剂对糖尿病大鼠氧化损伤的影响.方法:用四氧嘧啶诱发糖尿病大鼠模型,分别以高、低剂量糖目清袋泡剂及糖脉康颗粒治疗,并设立正常对照组及模型对照组,治疗3个月后,检测各组大鼠血糖及血清SOD值.结果:糖目清高、低剂量组及糖脉康组治疗后,大鼠血糖值明显低于模型对照组(P＜0.01);糖目清高、低剂量组大鼠血清SOD活性升高,与模型对照组间有非常显著差异(P＜0.01).结论:糖目清袋泡剂能降低血糖,提高糖尿病大鼠SOD活性,减轻氧化损伤.     

大鼠骨骼肌糖酵解限速酶在不同训练负荷过程中的变化

背景:糖酵解系统在运动时能量的消耗和利用中起重要作用,不同的训练科目的主要供能系统不同,会引起战士机体不同的适应性变化.目的:探讨不同训练负荷条件对大鼠骨骼肌相关糖酵解限速酶磷酸果糖激酶、己糖激酶和丙酮酸激酶活性的影响.方法:参照BEDFORD TG标准,建立无氧、有氧和有氧无氧交替运动大鼠跑台训练模型,并设置正常对照组.各组动物训练结束后即刻处死,应用酶偶联法检测SD大鼠骨骼肌磷酸果糖激酶、己糖激酶和丙酮酸激酶的活性.结果与结论:经过不同时间的跑台训练,无氧组大鼠骨骼肌磷酸果糖激酶活性均明显升高(P<0.05),交替运动组在训练至6周时磷酸果糖激酶活性增加(P<0.05),而有氧组磷酸果糖激酶活性在训练2周和4周后均下降(P<0.05).各组己糖激酶活性在训练4周和6周后均升高(P<0.05),其中无氧组最高(P<0.05),交替运动组己糖激酶活性高于有氧运动组(P<0.05).而无氧运动2和4周组丙酮酸激酶活性较对照组有所下降(P<0.05). 结果提示,大鼠骨骼肌糖酵解限速酶的活性不仅受运动方式的影响,而且在相同运动方式下还与训练时间的长短有关.长时间的训练,尤其是包含高速无氧训练的运动项目更能提高骨骼肌糖酵解限速酶的活性.     

高糖高脂膳食和链脲佐菌素诱导2型糖尿病模型的建立

目的：研究高糖高脂膳食和链脲佐菌素诱导2型糖尿病大鼠模型的建立。方法：高糖高脂饲料喂养Wistar雄性大鼠4周，然后用亚致病剂量链脲佐菌素腹腔注射。结果：高糖高脂饮食4周后，大鼠出现高胰岛素血症和胰岛素抵抗，链脲佐菌素注射后大鼠出现高血糖症。结论：本研究通过饮食方法结合小剂量链脲佐菌素注射成功制备了2型糖尿病模型，并可作为研究T2DM及其并发症的理想动物模型。     

链脲佐菌素结合高糖高脂饮食诱导2型糖尿病大鼠模型

目的:研究如何运用链脲佐菌素(streptozotocin,STZ)结合高糖高脂饮食诱导2型糖尿病大鼠模型.方法:40只健康雄性SD大鼠随机分为高脂组、糖尿病对照组、正常组.高脂组用STZ 60 mg/kg一次性左下腹腔注射,并结合4周的高糖高脂饮食.糖尿病对照组用相同剂量STZ一次性左下腹腔注射,普通饲料喂养4周.正常组用相同剂量的柠檬酸缓冲液一次性左下腹腔注射,普通饲料喂养4周.于注射药物后72 h及1、4、8、12周等不同时间点测量空腹体重、血糖、尿糖等指标,进行统计分析.结果:高脂组与糖尿病对照组、正常组相比空腹血糖、体重明显增加,差异有显著性(P<0.05).高脂组与糖尿病对照组相比血糖增高并能保持长时间的稳定、尿糖强阳性.结论:STZ一次性左下腹腔注射结合高糖高脂饮食4周可成功诱导2型糖尿病大鼠模型.     

罗格列酮联合中效胰岛素治疗初发2型糖尿病的临床观察

目的 探讨罗格列酮和中效胰岛素对初发2型糖尿病的降糖效果.方法 18例初发的2型DM病人应用罗格列酮8mg/d,加用中效胰岛素治疗12周后全部停药,分别在12周和26周测空腹血糖（FBG）、餐后2h血糖（2hPG）、糖化血红蛋白（HBA1c）.结果 治疗3个月后糖化血红蛋白平均下降1.85%,空腹血糖平均下降4.02 mmol/L,餐后血糖平均下降5.79mmol/L;治疗6个月后糖化血红蛋白平均下降1.82%,空腹血糖平均下降3.36 mmol/L,餐后血糖平均下降5.2 mmol/L.结论 罗格列酮联合中效胰岛素治疗初发2型糖尿病疗效可靠,有很好的后续作用.     

Improved glycemic control and lipid profile and normalized fibrinolytic activity on a low-glycemic index diet in type 2 diabetic patients.

OBJECTIVE: To evaluate the effects of varying the glycemic index (GI) of carbohydrate-rich foods on metabolic control in type 2 diabetic patients. RESEARCH DESIGN AND METHODS: In a randomized crossover study, 20 patients, 5 women and 15 men, were given preweighed diets with different GIs during two consecutive 24-day periods. Both diets were composed in accordance with dietary recommendations for people with diabetes. The macronutrient composition and type and amount of dietary fiber were identical. Differences in GI were achieved mainly by altering the structure of the starchy foods. RESULTS: Peripheral insulin sensitivity increased significantly and fasting plasma glucose decreased during both treatment periods. There was a significant difference in the changes of serum fructosamine concentrations between the diets (P < 0.05). The incremental area under the curve for both blood glucose and plasma insulin was approximately 30% lower after the low- than after the high-GI diet. LDL cholesterol was significantly lowered on both diets, with a significantly more pronounced reduction on the low-GI diet. Plasminogen activator inhibitor-1 activity was normalized on the low-GI diet, (-54%, P < 0.001), but remained unchanged on the high-GI diet. CONCLUSIONS: A diet characterized by low-GI starchy foods lowers the glucose and insulin responses throughout the day and improves the lipid profile and capacity for fibrinolysis, suggesting a therapeutic potential in diabetes.     

Insulin concentration in polytraumatized patients during infusion of glucose, fructose and sorbitol]

Serum insulin concentration was measured during infusion of glucose, fructose or sorbitol for several days in polytraumatized patients. The patients are divided in two groups, one group with normal glucose tolerance and a second group, where an extreme disturbance of the glucose utilization was found. In patients with normal glucose tolerance the glucose substitutes had the same metabolic effects as in metabolically healthy volunteers. In patients with disturbed glucose tolerance the glucose substitutes (fructose as well as sorbitol) effected an increase in blood glucose concentration and in serum insulin concentration. It is concluded that the increase in blood glucose concentration causes the increase in serum insulin concentration. Obviously, in a certain group of polytraumatized patients a "metabolic insulin resistence" exists. Therefore, glucose utilization is decreased despite an increase in serum insulin. In most cases the metabolic disturbance in these patients is mastered, if glucose substitutes are used instead of glucose as energy source. However, in many cases glucose can be administered only if insulin is given additionally.     

Quantitative Determination of Proteinuria by Closs’ Polythionate Method

A methodological investigation of the glucose oxidase method for determination of glucose is described. The importance of eliminating substances reducing H₂O₂ generated from glucose and other substances causing unspecific oxidation of the chromogen is emphasized. On the basis of this study a method has been constructed which gives accurate glucose values in whole blood, plasma, and red blood cells.     

山奈酚对2型糖尿病大鼠糖脂代谢及胰岛素抵抗的影响

目的探讨PPARγ激动剂山奈酚对糖尿病大鼠血糖、胰岛素抵抗及血脂生化水平的影响。方法高糖高脂饲料喂养加腹腔注射链脲佐菌素建立2型糖尿病大鼠模型,实验组灌胃给予山奈酚50、100、200 mg/(kg.d),灌胃给药10周后,葡萄糖氧化酶法进行空腹血糖测定,放射免疫法进行血浆胰岛素水平测定,酶法测定血浆总胆固醇、甘油三酯、尿素氮和肌酐含量。结果与模型组相比,山奈酚治疗组空腹血糖值及胰岛素抵抗均有所下降,血脂生化水平也有所降低,与模型组比较存在显著性差异。结论山奈酚可有效降低空腹血糖和胰岛素抵抗,改善糖脂代谢紊乱。     

Ketogenic Diets and Thermal Pain: Dissociation of Hypoalgesia,Elevated Ketones,and Lowered Glucose in Rats

Ketogenic diets (KDs) are high-fat, low-carbohydrate formulations effective in treating medically refractory epilepsy, and recently we demonstrated lowered sensitivity to thermal pain in rats fed a KD for 3 to 4 weeks. Regarding anticonvulsant and hypoalgesic mechanisms, theories are divided as to direct effects of increased ketones and/or decreased glucose, metabolic hallmarks of these diets. To address this point, we characterized the time course of KD-induced thermal hypoalgesia, ketosis, and lowered glucose in young male rats fed ad libitum on normal chow or KDs. A strict 6.6:1 (fat:[carbohydrates + protein], by weight) KD increased blood ketones and reduced blood glucose by 2 days of feeding, but thermal hypoalgesia did not appear until 10 days. Thus, ketosis and decreased glucose are not sufficient for hypoalgesia. After feeding a 6.6:1 KD for 19 days, decreased thermal pain sensitivity and changes in blood chemistry reversed 1 day after return to normal chow. Effects were consistent between 2 different diet formulations: a more moderate and clinically relevant KD formula (3.0:1) produced hypoalgesia and similar changes in blood chemistry as the 6.6:1 diet, thus increasing translational potential. Furthermore, feeding the 3.0:1 diet throughout an extended protocol (10–11 weeks) revealed that significant hypoalgesia and increased ketones persisted whereas low glucose did not, demonstrating that KD-induced hypoalgesia does not depend on reduced glucose. In separate experiments we determined that effects on thermal pain responses were not secondary to motor or cognitive changes. Together, these findings dissociate diet-related changes in nociception from direct actions of elevated ketones or decreased glucose, and suggest mechanisms with a slower onset in this paradigm. Overall, our data indicate that metabolic approaches can relieve pain.PerspectiveChronic pain is a common and debilitating condition. We show that a KD, a high-fat, very low carbohydrate diet well known for treating epilepsy, lowers sensitivity to thermal pain in rats. This reduced pain is not temporally correlated with hallmark diet-induced changes in blood glucose and ketones.     

适量运动联合食疗对二胎妊娠糖尿病患者血糖控制的研究

目的探讨运动联合个性化食疗对妊娠糖尿病患者的血糖控制效果,从而为二胎妊娠糖尿病孕妇的治疗提供临床依据。方法将临床上就诊的150例二胎妊娠糖尿病患者作为研究对象,年龄28~45岁,孕周24~28周,以运动和个性化食疗作为治疗手段,根据临床研究设计,随机分成运动组、食疗组、运动联合食疗组,每组50例,观察各组的临床疗效。结果与治疗前相比,运动组、食疗组、运动联合食疗组在经过1个月的坚持治疗后,患者空腹血糖及服糖后1、2、3h血糖都明显降低,差异有统计学意义(P<0.05);运动组和食疗组治疗总满意度差异无统计学意义(P>0.05),运动联合食疗组与运动组、食疗组的治疗总满意度差异有统计学意义(P<0.05)。结论适量运动联合食疗对二胎妊娠糖尿病患者血糖控制效果明显,值得临床推荐。     

普罗布考联合厄贝沙坦治疗糖尿病肾病的疗效观察

【目的】观察普罗布考联合厄贝沙坦治疗糖尿病肾病（DN）的疗效。【方法】60例DN患者随机分成治疗组和对照组。两组患者均在严格执行糖尿病饮食、减少蛋白摄入、控制血糖、血压达标的基础上,治疗组给厄贝沙坦150mg／d口服,同时给普罗布考每次0．5g,每天两次口服;对照组单用厄贝沙坦150mg／d口服。两组均随访3个月。【结果】两纽治疗后血清肌酐（Scr）、血丙二醛（MDA）、C反应蛋白（cRP）、尿白蛋白排泄率（UAER）均有降低（P〈0．05）;治疗组治疗后CRP和MDA、uAER较对照组明显下降（P〈0．05）。【结论】普罗布考与厄贝沙坦联合应用比单用厄贝沙坦能更有效地减轻蛋白尿和保护肾脏。     

Defective fatty acid uptake modulates insulin responsiveness and metabolic responses to diet in CD36-null mice

Deficiency of the membrane protein FAT/CD36 causes a marked defect in fatty acid uptake by various tissues and is genetically linked to insulin resistance in rats and humans. Here, we examined insulin responsiveness of CD36-/- mice. When fed a diet high in complex carbohydrates and low (5%) in fat, these animals cleared glucose faster than the wild-type. In vivo, uptake of 2-fluorodeoxyglucose by muscle was increased severalfold, and in vitro, insulin responsiveness of glycogenesis by the soleus was enhanced. Null mice had lower glycogen levels in muscle and liver, lower muscle triglyceride levels, and increased liver triglyceride content--all findings consistent with increased insulin-sensitivity. However, when the chow diet was switched to one high in fructose, CD36-/- mice but not wild-type mice developed marked glucose intolerance, hyperinsulinemia, and decreased muscle glucose uptake. High-fat diets impaired glucose tolerance equally in both groups, although CD36 deficiency helped moderate insulin-responsive muscle glucose oxidation. In conclusion, CD36 deficiency enhances insulin responsiveness on a high-starch, low-fat diet. It predisposes to insulin resistance induced by high fructose and partially protects from that induced by high-fat diets. In humans, CD36 deficiency may be an important factor in the metabolic adaptation to diet and in susceptibility to some forms of diet-induced pathology.     

Selective COX2 inhibition improves whole body and muscular insulin resistance in fructose‐fed rats

Background The effects of cyclooxygenase‐1 (COX1) and cyclooxygenase‐2 (COX2) inhibition on insulin resistance in subjects with the metabolic syndrome remain elusive. Aims of this study were to examine the effects of COX1 and COX2 inhibitors on whole body and muscular insulin resistance in fructose‐fed rats, an animal model of the metabolic syndrome. Materials and methods The rats on regular or 60% fructose‐enriched diets for 6 weeks were further divided into rats combined with or without piroxicam (a selective COX1 inhibitor) or celecoxib (a selective COX2 inhibitor) treatment for an additional 2 weeks. Euglycaemic hyperinsulinaemic clamp (EHC) with a tracer dilution method was performed at the end of the study. Results The present result showed that fructose‐induced increases in systolic blood pressure and fasting plasma insulin levels were significantly suppressed in rats treated with celecoxib but not piroxicam. In the EHC period, celecoxib significantly reversed fructose‐induced decreases in whole body glucose uptake, mainly by glucose storage. Hepatic glucose production and whole body glycolysis were not significantly changed among groups. Celecoxib but not piroxicam significantly reversed fructose‐induced decreases in glycogen synthase activities in red and white quadriceps muscles and insulin‐stimulated membrane GLUT4 recruitment in soleus muscles. Celecoxib and piroxicam both significantly diminished fructose‐induced increases in plasma thromboxane B2 and 6‐keto prostaglandin (PG) F1α; but only celecoxib treatment significantly attenuated a fructose‐induced increase in 8‐isoprostane levels. Plasma PGE metabolites were not different among groups. Conclusions This study demonstrates that a therapeutic dose of celecoxib, but not piroxicam, could significantly attenuate fructose‐induced whole body and muscular insulin resistance in rats.