20两种实验性糖尿病模型小鼠的比较

目的：通过对链脲佐菌素（STZ）模型鼠和db／db模型鼠的糖尿病模型鼠的特点以及对三类降糖药反应性的比较,客观评价两种糖尿病模型鼠在药物研究中的应用价值。方法：离乳、雄性BALB／c小鼠高脂饲料喂养4周后,空腹12hSTZ（45mg／kg）腹腔注射,连续3次,一周后检测糖耐量受损、空腹血糖大于8．0mmol／L的为STZ模型鼠。将STZ模型鼠和8周龄空腹血糖大于8．0mmol／L的db／db模型鼠各随机分组,每组8只分别给予罗格列酮（12mg／kg）、格列苯脲（45mg／kg）、胰岛素（1U／kg）和生理盐水（0．1mL／10g）,每天1次,连续给药4周后检测两模型鼠及其对照组糖脂代谢相关的生化指标及激素水平。结果：STZ模型鼠和db／db模型鼠分别与正常BALB／c鼠、C57BL鼠对比,STZ模型鼠和db／db模型鼠均口服葡萄糖耐量试验（OG—TT）异常,空腹血糖、血TG和TC显著升高。但STZ模型鼠的胰岛素与C肽水平低于正常;而db／db鼠血C肽、胰岛素浓度显著升高;3种降糖药给药4周后STZ模型鼠的空腹血糖均明显降低,OGTT显著改善;罗格列酮对db／db模型鼠也可显著降低空腹血糖并改善糖耐量,但相同剂量的格列苯脲和胰岛素对db／db模型鼠的空腹血糖和糖耐量无影响。给予3倍剂量的胰岛素,db／db模型鼠才表现出空腹血糖的显著降低。结论：STZ模型鼠胰岛功能受损并有一定程度的胰岛素抵抗,对3种降糖药均敏感。db／db模型鼠表现出高度的胰岛素耐受,对内源性和外源性的胰岛素都不敏感,对罗格列酮的敏感性与STZ模型鼠相当。     

基因缺陷型2型糖尿病模型动物db/db小鼠早期生物学特性研究

目的研究基因缺陷型2型糖尿病模型动物db/db小鼠的早期生物学特性,为db/db小鼠应用于降糖药物的研究奠定基础。方法采用db/db小鼠为模型组动物,db/m小鼠为对照组动物,测定两组小鼠的体质量、食量、饮水量、空腹血糖、正常饮食血糖、糖耐量、胰岛素耐量;于第14周眼底静脉丛取血,分离血清,测定糖化血清蛋白（GSP）、三酰甘油（TG）、总胆固醇（TC）;取肝、胰腺、腹部脂肪等主要脏器组织进行组织病理学检查。结果与对照组比较,db/db小鼠体质量、食量、饮水量显著增加;空腹血糖及正常饮食血糖显著升高,整个实验期血糖水平稳定;糖耐量异常、胰岛素耐量异常,对外源胰岛素敏感性显著降低;血清GSP、TG、TC含量显著升高,腹部脂肪质量显著增加,肝组织不同程度的空泡变性,脂肪组织中脂肪细胞体积增大,胰腺中胰岛细胞胞浆减少、血管扩张。结论 db/db小鼠早期脂质代谢紊乱,血糖、血脂显著升高,糖耐量及胰岛素耐量异常,血糖水平稳定,是研究2型糖尿病较为理想的模型。     

千金黄连方对db/db小鼠血糖的影响

目的 探讨千金黄连方对2型糖尿病模型动物db/db小鼠血糖的影响。方法 C57BL/6J小鼠10只（雌雄各半）作为对照组,将db/db小鼠60只（雌雄各半）按血糖值随机分为6组：模型组、二甲双胍（0.25 g·kg^-1）组、金芪降糖片（4.2 g·kg^-1）组和千金黄连方高、中、低剂量（生药13.00、6.50、3.25 g·kg^-1）组。每天ig给药1次,给药体积20 mL·kg^-1,对照组及模型组ig给予等量去离子水。血糖仪测定千金黄连方给药1次对糖耐量、空腹血糖的影响及多次给药对空腹血糖、糖耐量、混合饮食餐后血糖、淀粉耐量（碳水化合物饮食餐后血糖）的影响;连续给药12周后,试剂盒法检测血清中糖化血清蛋白（GSP）、糖化血红蛋白（GHb）、胰岛素水平;小鼠放血处死后,剪开腹部,取腹部脂肪称质量,计算脂肪系数;HE染色后对肝组织进行病理学检查。结果 给药1次,与模型组比较,给药后1~2 h千金黄连方高剂量能显著降低小鼠空腹血糖值和糖耐量血糖值（P<0.05、0.01）。与模型组比较,多次给予千金黄连方能显著降低小鼠空腹血糖值、显著降低葡萄糖耐量血糖值、显著降低混合饮食餐后血糖值和淀粉耐量血糖值（P<0.05、0.01、0.01）。与模型组比较,千金黄连方高、中、低剂量组小鼠GHb、GSP及胰岛素水平均显著下降（P<0.05、0.01、0.001）;高、中剂量组小鼠腹部脂肪系数显著下降（P<0.05、0.01）;高、低剂量对肝脏空泡变性程度有减轻作用。结论 千金黄连方能显著降低db/db小鼠空腹血糖,改善糖耐量异常及增强胰岛素敏感性,显著减少腹部脂肪系数,对肝细胞的损伤也有一定的改善作用;其降血糖作用与二甲双胍相当,强于金芪降糖片,其改善胰岛素抵抗、增加胰岛素敏感性的作用强于二甲双胍和金芪降糖片。     

Pharmacologic profile and insulin secretagogue effect of linogliride (McN-3935), a new,orally effective hypoglycemic agent

Linogliride (McN-3935) [N-(1-methyl-2-pyrrolidinylidene)-N'-phenyl-4-morpholinecarboximidamide] was selected for clinical evaluation as a potential orally effective hypoglycemic agent for treatment of noninsulin-dependent diabetes mellitus. Linogliride is structurally unrelated to sulfonylureas and biguanides. It produced a dose-dependent hypoglycemic effect in nondiabetic rats, mice, and dogs. The minimum effective oral doses that lowered fasting blood glucose levels and improved glucose tolerance were 1–5 mg/kg. Comparison of the dose-response curves from fasting rat studies showed linogliride to be approximately two times more potent than the related compound pirogliride and approximately eight times more potent than tolbutamide. Tolerance to its hypoglycemic effect did not develop in rat and dog 3-day repeat dose studies. Linogliride did not alter plasma lactic acid levels in normal and streptozotocin-induced diabetic rats, and it improved glucose tolerance whether the glucose was administered orally or parenterally. In nondiabetic rats and dogs, decreases in fasting blood glucose levels following linogliride administration were associated with elevated (two- to fourfold) plasma insulin concentrations. Linogliride was inactive in depancreatized diabetic dogs. In genetically diabetic (db/db) mice and streptozotocin-induced diabetic rats, linogliride (25–100 mg/kg p.o.) produced variable, nondose-dependent reductions of blood glucose levels, unlike the sulfonylureas, which were consistently ineffective in these diabetic rodent models. In conclusion, although the observed activity in diabetic rodent models is suggestive of a potential nonpancreatic mechanism, the experimental evidence to date indicates that the acute effectiveness of linogliride as a hypoglycemic agent is due primarily to stimulation of insulin release.     

FR258900, a novel glycogen phosphorylase inhibitor isolated from Fungus No. 138354. II. Anti-hyperglycemic effects in diabetic animal models

A novel glycogen phosphorylase inhibitor FR258900 was isolated from the cultured broth of a fungal strain No. 138354. We examined the hypoglycemic effects of FR258900 in diabetic animal models. FR258900 treatment significantly reduced the plasma glucose concentrations during oral glucose tolerance tests in diabetic mice models, including db/db mice and STZ-induced diabetic mice. Furthermore, FR258900 treatment resulted in rapid decrease in the plasma glucose levels in db/db mice. These improvements in glucose disposal were accompanied by increased liver glycogen contents, suggesting that the glucose lowering effects of FR258900 were attributed to suppressed hepatic glycogen breakdown and increased hepatic glycogen synthesis. Taken together, our results suggest that glycogen phosphorylase is a potentially useful target in new therapies against diabetes.     

西红柿凝集素修饰脂质体对小鼠口服吸收胰岛素的促进作用西红柿凝集素修饰脂质体对小鼠口服吸收胰岛素的促进作用

目的研究西红柿凝集素修饰的胰岛素脂质体在小鼠胃肠道吸收作用。方法采用碳二亚胺交联法制备西红柿凝集素(TL)修饰的磷脂酰乙醇胺(PE),将TL-PE掺入胰岛素脂质体中制成凝集素修饰脂质体并证实TL凝集活性不受影响。分别对正常小鼠及糖尿病模型小鼠灌胃给予350 u·kg^-1胰岛素的修饰脂质体溶液,用葡萄糖酶试剂盒测定小鼠血糖,并与同剂量普通胰岛素脂质体比较。结果正常小鼠中,西红柿凝集素修饰脂质体在4 h血糖降至初始水平的(85±5)%,8 h降至(54±11)%,12 h为(57±6)%。胰岛素普通脂质体几乎没有降糖作用,与生理盐水对照组相当。糖尿病模型小鼠中,西红柿凝集素修饰脂质体在4 h血糖降至初始水平的(38±13)%,8 h降至(50±15)%,12 h为(50±16)%。结论西红柿凝集素修饰的脂质体可能通过与细胞表面特异性受体的结合作用促进大分子药物的胃肠吸收。     

Anti-diabetic and hypolipidemic effects of aqueous-extract from the flower of Inula japonica in alloxan-induced diabetic mice

The anti-diabetic and hypolipidemic effects of aqueous-extract from the flower of Inula japonica (IJ) and its two fractions (IJR and IJP) were investigated in alloxan-induced diabetic mice. An oral glucose tolerance test (OGTT) of IJ was also performed in normal and diabetic mice. The results showed that IJ (1000 mg/kg), IJR (500 mg/kg) and IJP (250 mg/kg) significantly reduced blood glucose levels in diabetic mice by oral administration (p<0.01). IJ and IJP markedly decreased serum triglyceride concentrations (p<0.05) in diabetic mice. Their hypoglycemic activities were better than gliclazide (40 mg/kg) and compared with metformin (250 mg/kg). IJ raised plasma insulin levels in alloxan-induced diabetic mice. IJ, IJR and IJP significantly decreased the consumption of water and food in diabetic mice. OGTT showed that IJ slightly lowered blood glucose levels in normal mice, but significantly decreased blood glucose in diabetic mice between 60-150 min after a glucose load (p<0.05). The data indicated that IJ has both anti-diabetic and hypolipidemic effects.     

Effects of new hypoglycemic agent 2-piperazinyl-4-methyl-amino-5-methylthieno [2,3-d]pyrimidine dihydrochloride hydrate

The antidiabetic effects of 2-piperazinyl-4-methylamino-5-methylthieno [2,3-d]pyrimidine dihydrochloride hydrate (Compound-(I] were investigated in various animals and in various conditions. Compound-(I) is a new hypoglycemic agent structurally unrelated to sulfonylurea and biguanide. It produced dose dependent hypoglycemic effects (10-100 mg/kg) in rats and mice under fed, fasted and glucose tolerated states. However, it was ineffective in fasted guinea pigs even when given at 100 mg/kg. In normal fed rats and mice, hypoglycemic effects of Compound-(I) were estimated to be 3-19 times and 12-70 times more potent than tolbutamide and phenformin, respectively. Compound-(I) also produced hypoglycemic action in streptozocin diabetic rats and genetically diabetic KK mice. Especially, its hypoglycemic effect was observed at the dose as low as 3 mg/kg p.o. in KK mice. However, elevation of blood lactate was accompanied by lowering of blood glucose after oral administration of Compound-(I) in normal rats and mice and in streptozocin diabetic rats, while these effects were not observed in guinea pigs. In addition, plasma insulin significantly increased after administration of Compound-(I) in both normal and KK mice, while this increase in plasma insulin was not so prominent in fed rats. This elevation in plasma insulin might be produced by alpha 2-adrenergic antagonism at pancreatic B cell as Compound-(I) suppressed epinephrine induced hyperglycemia by elevating plasma insulin. In conclusion, Compound-(I) seems mainly to produce hypoglycemic action through extrapancreatic mechanism which increases blood lactate associated with anaerobic glycolysis or inhibition of gluconeogenesis. In addition, elevation of plasma insulin also might be responsible for hypoglycemic effects.     

Preservative effect of electrolyzed reduced water on pancreatic beta-cell mass in diabetic db/db mice

Oxidative stress is produced under diabetic conditions and involved in progression of pancreatic beta-cell dysfunction. Both an increase in reactive oxygen free radical species (ROS) and a decrease in the antioxidant defense mechanism lead to the increase in oxidative stress in diabetes. Electrolyzed reduced water (ERW) with ROS scavenging ability may have a potential effect on diabetic animals, a model for high oxidative stress. Therefore, the present study examined the possible anti-diabetic effect of ERW in genetically diabetic mouse strain C57BL/6J-db/db (db/db). ERW with ROS scavenging ability reduced the blood glucose concentration, increased blood insulin level, improved glucose tolerance and preserved beta-cell mass in db/db mice. The present data suggest that ERW may protects beta-cell damage and would be useful for antidiabetic agent.     

口服胰岛素微粒剂降血糖有效性及大鼠胃肠道有效吸收部位的研究

分别以葡萄糖氧化酶法、放射免疫分析法对服用微粒剂后的四氧嘧啶致糖尿病小鼠与狗的血糖、血清胰岛素进行测定 ,验证确有外源性胰岛素进入动物体内 ,在给药后 1h动物血清胰岛素增至最高 ,约 2h动物血糖降至最低 ,且作用强度、时间与血清胰岛素变化相对应。给药剂量在 4 0～35 0u/kg范围 ,存在量效关系 :Y(% ) =13 2 1- 1 70 7X(u/kg) ,r =0 9788。给小鼠腹腔注射葡萄糖 (2 g/kg)可见 ,微粒剂 (17u/kg)能对抗并减缓因注射外源还原性单糖引起的动物血糖升高 ,0 5h可抵抗百分率达 86 % (P <0 0 0 5 )。经四氧嘧啶糖尿病大鼠胃肠道不同部位给药发现 :给药部位不同 ,微粒剂降血糖程度有显著差别 ,其中经回肠部位给药效果最好 ,降血糖百分率达 5 6 %(P <0 0 1)。     

Sulfonyliminoimidazolidines, a new class of oral hypoglycemic agents. 3. Hypoglycemic activity and mode of action of 1-[p-[2-(crotonylamino)-ethyl]-phenylsulfonyl]-3-cyclohexyl-2-imino- imidazolidine (CGP 11 112)

1-[p-[2-(Crotonylamino)-ethyl]-phenylsulfonyl]-3-cyclohexyl-2-imino- imidazolidine (CGP 11 112) is a representative of a new class of oral hypoglycemic agents. It lowers blood glucose in normal animals and in streptozocin (streptozotocin)-diabetic rats. In normal mice, rats and dogs the hypoglycemic effect is more potent (range 3-30 times) and has a shorter duration than that of tolbutamide. CGP 11 112 increases plasma insulin after oral administration in normal animals and stimulates release of insulin in perifused rat islets in vitro (sulfonylurea-like effect). In streptozocin-diabetic rats CGP 11 112 decreases blood glucose with a potency comparable to that of phenformin. In contrast to phenformin, CGP 11 112 does not increase blood lactate in diabetic rats or inhibit intestinal absorption of glucose. An effect of CGP 11 112 on gluconeogenesis and glycogenolysis could not be demonstrated. It is suggested that the hypoglycemic activity in streptozocin-diabetic rats may be due to stimulation of glucose efflux from the circulation. In vitro, CGP 11 112 inhibits glucose oxidation and lipolysis in isolated rat fat cells.     

Pharmacokinetic and pharmacodynamic properties of the glucokinase activator MK-0941 in rodent models of type 2 diabetes and healthy dogs

Glucokinase activators (GKAs) are small-molecule agents that enhance glucose sensing by pancreatic β cells and glucose metabolism by hepatocytes. There is strong interest in these agents as potential therapies for type 2 diabetes. Here, we report key pharmacokinetic and pharmacodynamic findings from preclinical studies of the GKA 3-[[6-(ethylsulfonyl)-3-pyridinyl]oxy]-5-[(1S)-2-hydroxy-1-methylethoxy]-N-(1-methyl-1H-pyrazol-3-yl)benzamide (MK-0941). Incubated in vitro with recombinant human glucokinase, 1 μM MK-0941 lowered the S(0.5) of this enzyme for glucose from 6.9 to 1.4 mM and increased the maximum velocity of glucose phosphorylation by 1.5-fold. In 2.5 and 10 mM glucose, the EC(50) values for activation of GK by MK-0941 were 0.240 and 0.065 μM, respectively. Treatment of isolated rat islets of Langerhans and hepatocytes with 10 μM MK-0941 increased insulin secretion by 17-fold and glucose uptake up to 18-fold, respectively. MK-0941 exhibited strong glucose-lowering activity in C57BL/6J mice maintained on a high-fat diet (HFD), db/db mice, HFD plus low-dose streptozotocin-treated mice, and nondiabetic dogs. In both mice and dogs, oral doses of MK-0941 were rapidly absorbed and rapidly cleared from the blood; plasma levels reached maximum within 1 h and fell thereafter with a half-life of ~2 h. During oral glucose tolerance testing in dogs, MK-0941 reduced total area-under-the-curve postchallenge (0-2 h) plasma glucose levels by up to 48% compared with vehicle-treated controls. When administered twice daily to mice for 16 days, and once daily to the dog for 4 days, MK-0941 remained efficacious on successive days. These findings support further investigation of MK-0941 as a potential therapeutic agent for treatment of type 2 diabetes.     

孕期咖啡因暴露致子代大鼠高脂饮食下胰腺形态和糖代谢功能改变

目的：研究孕期咖啡因暴露（PCE）子代高脂饮食（HFD）下胰腺形态和糖代谢功能变化。方法：孕鼠妊娠第11天给予咖啡因120 mg·kg^-1·d^-1至自然生产。出生后4周给予HFD至成年。于出生后第20周行口服糖耐量（OGTT）实验。24周处死后，观察胰腺形态，检测肝胰岛素受体（IR）、胰岛素受体底物2（IRS2）和葡萄糖转运体2（Glut2）的mRNA表达。结果：与对照组相比，PCE组子代出生1周体质量降低但体质量增长率均升高（P<0.05，P<0.01），第4~24周雄性体质量降低而雌性升高（P<0.05，P<0.01）。第20周PCE组雌性子代基础血糖水平升高而胰岛素水平降低，定量胰岛素敏感性检测指数（QUICKI）升高（P<0.01）。同时，绝对糖耐量减低而相对糖耐量增强。与对照组相比，第24周PCE组胰岛形态被破坏，出现大量脂肪空泡变性。雌性子代肝IR、IRS2和Glut2的mRNA表达升高（P<0.05，P<0.01）。结论：PCE成年子代HFD下呈现"高血糖、低血胰岛素"为主的糖尿病样反应且以雌性较为明显，其机制可能与胰岛形态和功能损伤所致的胰岛素分泌不足有关。     

Reversal of glucose intolerance by by pioglitazone in high fat diet-fed rats

The present study was undertaken to determine the effect of pioglitazone (3, 10 and 30 mg/kg p.o.), an insulin sensitizer, on glucose intolerance in high fat diet- (HFD) fed rats (a nongenetic model of insulin resistance). In addition, the effect of pioglitazone (3, 10 and 30 mg/kg p.o.) on diet-induced changes in body weight, plasma glucose, insulin, triglyceride and total cholesterol levels were also determined. The feeding of HFD for 4 weeks produced a significant increase in body weight, total fat pad weight, basal/fasting plasma glucose, insulin, basal triglyceride (TG) and total cholesterol (TC) levels in male rats. Furthermore, the rats fed HFD exhibited fasting hyperglycemia and hyperinsulinemia as well as enhanced glycemic response to exogenously administered glucose (2 g/kg p.o.) during an oral glucose tolerance test (OGTT) at the end of 4 weeks of dietary manipulation, indicating that the rats had developed insulin resistance and glucose intolerance. Treatment with pioglitazone (10 and 30 mg/kg p.o.) once daily for 2 weeks significantly diminished the elevated basal plasma insulin and TG levels in HFD-fed rats. In addition, a statistically significant reduction in TC level was observed only with the high dose of pioglitazone (30 mg/kg p.o.). However, pioglitazone had no significant effect on body weight, total fat pad weight and basal plasma glucose level. Pioglitazone (10 and 30 mg/kg p.o.) significantly reduced fasting hyperglycemia and reversed oral glucose intolerance to normal in HFD-fed rats compared with control normal rats. The above findings suggest that pioglitazone has potent insulin-sensitizing and lipid-lowering properties in a HFD-fed rat model. In conclusion, the present study demonstrates that the adult male rats on a HFD for 4 weeks exhibited the characteristic features of obesity, insulin resistance and glucose intolerance, namely increased body weight, increased total fat pad weight, mild basal/fasting hyperglycemia, hyperinsulinemia, hypertriglyceridemia, hypercholesterolemia and impaired oral glucose tolerance, that closely resemble the human prediabetic obese insulin-resistant and glucose-intolerant state. Further treatment with pioglitazone once daily for 2 weeks significantly ameliorated changes in basal plasma insulin, TG and TC, and reversed oral glucose intolerance to normal in HFD-fed rats, suggesting its potential in the treatment of insulin resistance and glucose intolerance associated with abnormal lipid metabolism.     

Hypoglycemic effect of aqueous extract of Ammi visnaga in normal and streptozotocin-induced diabetic rats

The effect of the aqueous extract of Ammi visnaga (Apiaceae) on blood glucose levels was investigated in fasting normal and streptozotocin-induced diabetic rats after single and repeated oral administration. The aqueous extract of Ammi visnaga (AV) at a dose of 20 mg/kg significantly reduced blood glucose in normal rats six hours after a single oral administration (P < 0.005) and nine days after repeated oral administration (P < 0.05). This hypoglycemic effect is more pronounced in streptozotocin (STZ) diabetic rats (P < 0.001). Acute toxicity (LD50) and general behavioural effects of an aqueous extract of AV fruits was studied in mice. The LD50 of intraperitoneal (i.p.) and oral administration was 3.6 and 10.1 g/kg, respectively. These findings suggest that the aqueous extract of AV possess significant hypoglycemic effect in both normal and STZ diabetic rats and support, therefore, its claimed clinical use by the Moroccan population.     

丹皮多糖-2b降血糖作用的实验研究

目的：研究丹皮多糖－2b（CMP－2b)降血糖作用及作用机制。方法：用小鼠和大鼠建立葡萄糖性高血糖及四氧嘧啶性糖尿病模型，氢化可的松琥珀酸纳（HCSS)诱导胰岛素抵抗，观察丹皮多糖－2b对正常和高血糖模型动物的影响，并测定糖尿病动物SOD、Insulin、GHb、ApoA1等水平。结果：CMP－2b可降低葡萄糖和四氧嘧啶诱发的鼠高血糖，并能升高糖尿病小鼠SOD和大鼠ApoA1水平，降低GHb水平，改善小鼠胰岛素抵抗。结论：CMP－2b可有效地控制实验性高血糖，其降糖机理可能与改善机体对胰岛素的敏感性，促进外周组织对葡萄糖的利用有关。     

Qi盐对正常及糖尿病模型大鼠血糖的影响

目的观察Qi盐对正常小鼠和糖尿病模型大鼠的降血糖作用.方法尾静脉注射四氧嘧啶制作大鼠糖尿病模型,连续灌胃给Qi盐14 d,葡萄糖氧化酶法测血糖.结果Qi盐1.6,0.8,0.4 g·kg-1对正常小鼠血糖及糖耐量均无明显影响,但0.8,0.4 g·kg-1可降低四氧嘧啶模型大鼠血糖,改善糖耐量.结论Qi盐对糖尿病模型大鼠有降血糖作用.     

硫辛酰维格列汀对2型糖尿病（T2DM）大鼠降糖作用的研究

目的观察硫辛酰维格列汀对2型糖尿病大鼠血糖的影响。方法选用雄性Wistar大鼠,高脂高糖饲料喂养4周后小剂量注射链脲佐菌素建立2型糖尿病模型,随机将大鼠分为正常对照组、糖尿病模型组、胰岛素糖尿病组、硫辛酰维格列汀糖尿病组。分别测定给药后0、0．5、1、2、3、4、5、6、7、8、9、10、12、24h的血糖变化。结果注射链脲佐菌素72h后造模大鼠血糖均明显高于注射前（P％0．05）和正常对照组（P〈0．05）。与正常对照组和糖尿病模型组相比,胰岛素糖尿病组在注射胰岛素后0．5～4h,血糖变化差异有统计学意义（P〈0．05）;硫辛酰维格列汀糖尿病组在灌胃给药3～10h,血糖变化差异有统计学意义（P〈0．05）。结论硫辛酰维格列汀和胰岛素有不同程度的降血糖作用,相比胰岛素,硫辛酰维格列汀降糖作用更加持久。     

滋阴益气活血泄浊法对db／db小鼠糖代谢的影响

目的：探讨滋阴益气活血泄浊法对db／db小鼠整体水平糖代谢的影响。方法选取12~14周龄雄性db／db小鼠,按空腹血糖及体质量随机分成模型组、阿卡波糖组、石斛合剂序贯组（以下简称序贯组）;选db／m为正常对照组。连续灌胃给药共6个循环（42d）。治疗前测各药物对淀粉耐量影响。每2周期测空腹血糖（FBG）,实验结束前测口服葡萄糖耐量（OGTT）和测定糖化血清蛋白（GSP）、血清胰岛素（Ins）以及各药物干预后的肠上皮α-葡萄糖苷酶活性。结果石斛合剂1方和2方单次给药均能明显降低db／db小鼠淀粉耐量30,60,120min血糖;随治疗循环数增加,序贯组的FBG逐步下降;与模型组比较,序贯组FBG、GSP和Ins显著下降（P<0.05）,改善葡萄糖耐量;石斛合剂1方、2方降低肠上皮α-葡萄糖苷酶活性（P<0.05）。结论石斛合剂有明确的α-葡萄糖苷酶抑制作用,序贯治疗能降低db／db小鼠的血糖相关指标,降低高胰岛素血症,表明滋阴益气活血泄浊法的降糖机制可能与抑制α-葡萄糖苷酶活性有关。     

Hypoglycemic and antiperglycemic effects of Semecarpus anacardium linn in normal and alloxan-induced diabetic rats

The effect of ethanolic extract of dried nuts of Semecarpus anacardium on blood glucose level was investigated in both normal and alloxan induced diabetic rats. The blood glucose levels were measured at 0, 1, 2 and 3 hours after the treatment. The ethanolic extract of S. anacardium (100 mg/kg) reduced the blood glucose of normal rat from 84 +/- 1.4 to 67 +/- 1.7 mg/dl, 3 hours after oral administration of the extract (P < 0.05). It also significantly lowered blood glucose level in alloxan induced diabetic rat from 325 +/- 2.2 to 144 +/- 1.4 mg/dl, 3 hours after oral administration of the extract (P < 0.05). The antihyperglycemic activity of S. anacardium was compared with tolbutamide, an oral hypoglycemic agent.