门体分流对肝脏及胰岛细胞功能的影响

本实验动态观察犬行门腔和肠腔端侧分流术后对肝脏和胰岛细胞功能的影响。分析两组分流术后肝脏形态学改变和门脉血中胰岛素浓度与肝血流量变化之间的关系后,作者认为肝血流量减少是肝功能恶化的主要因素,两组分流术后周围血和门脉血中胰岛素和胰高糖素水平均降低,且同时有胰岛A,B细胞数量减少和胰腺空泡变性等。上述变化门腔分流组较肠腔分流血为明显。由此提示,门体分流术,尤其是全门体分流术可损害胰腺内分泌功能。     

STUDIES OF EFFECTS OF PORTASYSTEMIC SHUNT ON THE FUNCTION OF HEPATIC AND PANCREATIC ISLET CELLS

The present study was aimed at dynamic observation of the ef fects of end to side portacaval shunt (PCS) and end to side mesocaval shunt (MCS) in dogs on the functions of the liver and pancreatic islet cells. According to correlation between the changes of plasma insulin level in the portal vein and hepatic flow and liver morphology after PCS and MCS, we conclude that the depletion of hepatic flow is the major factor in the deterioration of liver functions. The levels of insulin and glucagon in both the peripheral vein and the portal vein were decreased after PCS and MCS. There was also depletion of pancreatic islet A and B cells and vacuolar degeneration of the pancreas. These changes were more signifcant in PCS than in MCS, suggesting that portasystemic shunt, especially total portasystemie shunt, might damage pancreatic endocrine functions.     

DYNAMIC OBSERVATION ON THE CHANGES OF PLASMA SOMATOSTATIN AND GLUCAGON DURING THE DEVELOPMENT OF CIRRHOSIS AND AFTER PORTACAVAL SHUNTING IN THE CIRRHOTIC RATS

In the present study we observed dynamically and systemically the changes of plasma somatostatin and glucagon in the peripheral and portal vein, and the changes of pancreatic immunopathology in the course of development of cirrhosis induced by CCl_4 and after portacaval shunt (PCS) in the cirrhotic rats as well as investigated their causes and correlationship. The results showed that hyperglucagonemia was caused by spontaneous portosystemic shunting and surgically induced portacaval anastomosis. Moreover, there was much higher level of glucagon in the portal vein with corresponding increase of A cells in PCS rats than those in the controls, indicating that another cause for elevation of glucagon was hypersecretion of pancreatic A cells. Our data demonstrated that both deterioration of liver function and portosystemic shunting might not be responsible for the elevated level of somatostatin in the cirrhotic rats with PCS. However, there was a closed positive correlation between plasma glucagon and somatostatin. Thus it was concluded that hyperglucagonemia stimulated the release of somatostatin. In view of the fact the elevated level of glucagon was much higher than that of somatostatin, there was probably a relative lack of somatostatin in cirrhosis with portal hypertension.     

分流术及断流术对门静脉高压症病人血胰岛激素水平的影响

本文报告不同术式对门静脉高压症病人血胰岛激素水平影响的临床实验研究结果。21例肝硬变门静脉高压症病人外周血和门脉血IRI、IRG水平均显著升高。DSCS和PAD能不同程度改善病人胰岛素血症,但未能改善病人胰高糖素血症;MCS术后胰岛素血症和胰高糖素血症则较术前加重。     

人工虫草多糖降血糖作用及其机制研究

目的：研究人工虫草多糖的降血糖作用及其机制。方法：用正常小鼠和四氧嘧啶糖尿病小鼠模型，以血糖、糖化血清蛋白、糖耐量等为指标研究人工虫草多糖的降糖作用；用高浓度葡萄糖和胰岛素诱导脂肪细胞胰岛素抵抗模型，观察人工虫草多糖对葡萄糖摄取的影响。结果：人工虫草多糖对正常小鼠血糖水平无明显影响，但能显著降低四氧嘧啶糖尿病小鼠的血糖水平和糖基化血清蛋白含量，明显改善糖尿病小鼠的糖耐量，提高胰岛素抵抗脂肪细胞的葡萄糖摄取水平。结论：人工虫草多糖对糖尿病小鼠有较好的降糖作用，促进胰岛素抵抗脂肪组织的葡萄糖摄取可能是其降糖作用机制之一。     

Effects of hepatotrophic factors on the liver after portacaval shunt in rats with portal hypertension

Background Portacaval shunt （PCS） prevent hepatotrophic factors from flowing into the liver, but they enter directly the systemic circulation and worsen liver injury. This study was designed to investigate the effects of hepatotrophic factors through the portal vein on the liver in rats with portal hypertension after portacaval shunt. Methods Intrahepatic portal hypertension （IHPH） was induced by intragastric administration of carbon tetrachloride, and end-to-side PCS was performed. Eight normal rats served as controls, and eight rats with IHPH served as IHPH model （IHPH group）. Another 32 rats with IHPH-PCS were randomly subdivided into 4 groups： normal saline （NS） given to 8 rats, hepatocyte growth factor （HGF） 8, insulin （INS） 8, hepatocyte growth factor and insulin （HGF＋INS） 8. Hepatotrophic factors were infused into the portal vein through an intravenous catheter. Portal venous pressure （PVP） was measured. The levels of serum alanine aminotransferase （ALT） and aspartate aminotransferase （AST） were tested biochemically and those of hyaluronic acid （HA） and laminin （LN） were measured by radioimmunoassay. Hepatic fibrosis was assessed histologically and the expression of collagens type I and In were detected immunohistochemically. Ultrastructural change of hepatocytes and the number of mitochondria were observed under an electron microscope. The data were compared between groups and subgroups by Student-Newman-Keuls procedure with SPSS 10.0. Results PVP was significantly higher in the IHPH rats than in the control rats （P〈0.05）. The levels of serum ALT, AST, HA, and LN, hepatic fibrosis score, the amount of collagen deposition, collagens type I and III increased more significantly in the IHPH group than in the control rats （P〈0.05）. The number of mitochondria decreased more significantly in the IHPH rats than in the control rats （P〈0.05）. The levels of serum ALT, AST, HA and LN as well as hepatic fibrosis score, the amount of collagen deposition, and the amount of collagens type I and M in the HGF and HGF＋INS rats were significantly lower than those in the NS rats （P〈0.05）. The damage to hepatocyte ultrastructure was markedly alleviated and the number of mitochondria was increased more significantly in the HGF and HGF＋INS rats than in the NS rats under an electron microscope. Conclusions Perfusion of exogenous hepatotrophic factors through the portal vein can alleviate liver injury, minimize the damage to the ultrastructure of hepatocyte, protect liver function, and lessen hepatic fibrosis in rats with portal hypertension after PCS.     

Effects of nitric oxide inhibitor on prostacyclin biosynthesis in portal hypertensive rats

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Mechanism of overproduction of plasma prostacyclin in portal hypertensive rats

OBJECTIVE: To evaluate the role of increased portal pressure and portosystemic shunting in elevated level of prostacyclin (PGI2) in portal hypertension. METHODS: Thirty-six male Sprague-Dawley rats were divided into four groups: prehepatic portal hypertension (PHPH, 8 rats), intrahepatic portal hypertension (IHPH, 9), end-to-side portacaval shunt (PCS, 8), and sham-operated controls (SO, 11). Two weeks after surgery, free portal pressure (FPP) was measured; systemic and splanchnic hemodynamics was studied by radioactive microsphere technique and blood sample from the femoral artery was obtained to measure the level of plasma 6-keto-PGF1 alpha with radioimmunoassay. RESULTS: The FPP (mmHg) in IHPH, PHPH, PCS and SO rats was 13.10 +/- 1.02, 12.10 +/- 1.52, 3.0 +/- 0.82 and 6.86 +/- 0.69, respectively. The value of FPP was significantly increased in IHPH, PHPH rats and significantly decreased in PCS rats when compared to SO rats. Cardiac index (CI) and portal venous inflow (PVI) were in the order of PCS > PHPH > IHPH > SO rats. Portosystemic shunting (PSS) in PCS, PHPH, IHPH was 99.7 +/- 0.29%, 76.02 +/- 20.62% and 30.34 +/- 10.18%, respectively. The concentrations of plasma 6-keto-PGF1 alpha (ng/ml) in PHPH, IHPH, PCS and SO rats were 6.93 +/- 2.43, 5.09 +/- 2.27, 2.36 +/- 1.01 and 1.56 +/- 0.61, respectively. The concentrations of plasma PGI2 in PHPH, IHPH and PCS rats were significantly higher than those in SO rats. Furthermore, the concentrations of plasma PGI2 in PHPH and IHPH rats were also significantly higher than those in PCS rats. Moreover, a closed positive correlation existed between plasma PGI2 and FPP (r = 0.67, P < 0.001). CONCLUSIONS: The results of the present study suggest that the elevated PGI2 in portal hypertension is mainly due to the overproduction of PGI2 in vascular epithelium cells induced by increased portal pressure, whereas portosystemic shunting and liver dysfunction play a secondary role. In addition, the results of this study do not support that PGI2 mediated the hyperhemodynamics in portal hypertension.     

Changes in plasma glucagon concentration in patients with diabetes mellitus and its clinical significance]

To investigate the role of glucagon in the pathogenesis of diabetes, we observed change of plasma glucagon concentrations during glucose loading in normal subjects and patients with impaired glucose tolerance (IGT) and non-insulin dependent diabetes mellitus (NIDDM) using specific radioimmunoassay. The results showed that the fasting plasma glucagon levels in patients with IGT and NIDDM were similar to those of the normal subjects. The nadir of plasma glucagon level in the normal control occurred at 1-h after glucose loading and the changes of glucagon, glucose and insulin levels synchronized; but peaks of plasma glucose and insulin levels in the IGT and NIDDM patients were delayed at 2-h after glucose loading with the lowest glucagon level at 3-h. It was suggested that there were relative hyperglucagonemia and decrease of sensitivity of islet A cell to glucose in IGT and NIDDM patients. The present study also showed that hyperglucagonemia is related to the reduction of insulin secretion and might play an important role in the development of postprandial hyperglycemia in NIDDM.     

云南省景颇族居民糖尿病患病现状及其对生命质量的影响

目的 分析云南省景颇族居民糖尿病的患病现状及对其生命质量的影响.方法 采用随机抽样方法在云南省德宏州芒市抽取1 367名≥35岁景颇族居民进行问卷调查和血糖检测,采用SF-36进行生命质量的测定.结果 云南省芒市景颇族居民糖尿病的患病率为4.1%,其中男性为4.2%,女性为4.0%;景颇族糖尿病患者生理机能、生理职能、躯体疼痛、总体健康、生命力、社会功能、情感职能、精神健康、躯体综合得分和心理综合得分分别为(84.64±16.81)、(53.13±45.24)、(71.70±24.28)、(49.46±21.38)、(65.09±11.02)、(90.08±14.00)、(79.17±39.98)、(70.29±13.73)、(57.12±9.39)和(55.07±6.58)分.糖尿病患者的生理机能、生理职能、躯体疼痛、躯体综合得分均低于非糖尿病者(P<0.05).景颇族居民生命质量影响因素的多元线性回归分析结果显示,年龄越大的景颇族居民其生命质量的躯体综合得分和心理综合得分越低(P<0.01);男性的生命质量躯体综合得分和心理综合得分均低于女性(P<0.01);受教育水平越高的景颇族居民生命质量的躯体综合得分和心理综合得分越高(P<0.01);已婚景颇族居民生命质量的躯体综合得分高于未婚及离异者(P<0.01);患有糖尿病的景颇族居民生命质量的躯体综合得分低于未患糖尿病者(P<0.01).结论 加强景颇族老年人、低文化程度人群的健康教育,加强对糖尿病患者的管理,可有效提高景颇族居民的生命质量.     

糖脂毒性对肥胖大鼠β细胞功能和凋亡的影响研究

目的 探讨葡萄糖和游离脂肪酸（FFA）联合作用对胰岛β细胞功能与凋亡的影响及病理生理机制。方法 Wistar大鼠采用高脂饲料喂养制造胰岛素抵抗模型,取造模成功的肥胖胰岛素抵抗模型大鼠分为4个亚组,生理盐水组（OB-NS组, n=7）、高葡萄糖组（OB-GS组, n=9）、高游离脂肪酸组（OB-FFA组, n=8）和高糖高脂肪酸组（OB-FG组, n=9）。另取5只Wistar大鼠采用普通饲料喂养作为正常对照组。采用比色法检测FFA和β-羟丁酸（β-HBA）水平,采用静脉葡萄糖耐量试验（IVGTT）评价胰岛β细胞胰岛素分泌功能, 免疫组织化学方法检测β细胞胰岛素储备的能力, 并应用原位末端标记法(TUNEL)检测凋亡的β细胞。结果 肥胖大鼠葡萄糖输注率（GIR）低于正常对照〔（10.82±1.8 mg/kg·min) vs. (25.21±1.7 mg/kg·min), P<0.05〕,提示胰岛素抵抗模型成功建立。OB-FG组大鼠糖负荷后胰岛素分泌达峰时间延后且各时点胰岛素水平明显低于NC组和OB-NS组,差异有统计学意义（ P<0.05）。糖负荷后5、10、15和20 min时,OB-FG组血胰岛素水平也明显较OB-FFA组、OB-GS组降低,胰岛素和血糖比值及胰岛素释放指数也均低于NC组和OB-NS组,差异有统计学意义。免疫组织化学染色示,OB-FG组胰岛素储备在各高脂肥胖亚组中最低,远低于NC组和OB-NS组（ P<0.01）,OB-GS组和OB-FFA组胰岛素储备与OB-NS组比较也有不同程度降低（ P<0.05)。OB-FG组β细胞凋亡率高于NC组和OB-NS组（ P<0.01)。结论 糖脂联合毒性在引起肥胖大鼠酮体生成显著增加的同时也导致胰岛 细胞分泌功能障碍。     

加味半夏泻心汤对2型糖尿病大鼠血糖、血脂及胰岛细胞功能的影响

目的观察加味半夏泻心汤对2型糖尿病大鼠的血糖、胰岛素、血脂、血清、肿瘤坏死因子(TNF-)及胰岛细胞功能的影响。方法高糖高脂饲料喂养10周,腹腔注射链脲佐菌素(STZ)制备2型糖尿病大鼠模型,随机分为模型对照组、加味半夏泻心汤组、二甲双胍组,并设正常对照组。给药5周后取血,测定空腹血糖(FBG)、空腹胰岛素(FINS)、计算胰岛素抵抗指数(HOMA-IR)、胰岛素敏感指数(ISI)、胰岛细胞功能指数(HOMA-);检测胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白(HDL-C)、低密度脂蛋白(LDL-C)、游离脂肪酸(FFA)、TNF-的变化。结果加味半夏泻心汤能明显降低2型糖尿病大鼠FBG(P0.05),TC(P0.05)、TG(P0.05)、LDL-C(P0.05)、FFA(P0.05)、TNF-(P0.05),升高HDL-C、HOMA-(P0.05),降低HOMA-IR,升高ISI。结论加味半夏泻心汤在降糖、调脂、改善胰岛素抵抗,保护胰岛细胞功能方面作用显著,初步揭示该方治疗2型糖尿病具有一定的科学性和临床指导意义,其具体作用机制值得进一步研究。     

Effects of Portulaca Oleracea on Insulin Resistance in Rats with Type 2 Diabetes Mellitus

Insulinresistance(IR)isthecommon patho physiologicalbasisforagroupofmetabolicabnormali tiescalledinsulinresistancesyndrome,whichin cludestype 2diabetesmellitus(T2DM),obesity,lipidmetabolicdisturbance,primaryhypertensionandatherosclerosis.ItwasoncereportedthataChinesemedicinalherb,Portulacaoleracea,usedalonecouldeffectivelytreatdiabetesmellitusinhumans(1) asithastheactionofamelioratinghyperlipidemia,andpreventingandcuringatherosclerosis(2,3).Butexper imentalstudyofPortulacaoleraceaoninsulinr…     

糖脂平胶囊的降糖降脂作用

目的 研究糖脂平胶囊的降糖和降脂作用。方法 用四氧嘧啶造成高血糖大鼠，小鼠模型，用高脂饲料造成小鼠高脂模型分别观察本品的降糖和降脂作用；用正常大鼠，小鼠观察血清胰岛素水平和葡萄糖耐量变化。结果 本品对大，小鼠的高血糖有明显的降糖作用。对正常大鼠及小鼠血糖无影响；提高血清胰岛素水平及葡萄糖的耐受性。对高脂饲养引起的小鼠亚急性甘油三酯及总胆固醇升高，有降脂作用，增加高密度脂蛋白水平。结论 本品具有降糖和降脂作用。     

高脂饮食导致胰岛素抵抗物质基础的实验研究

目的探讨高脂饮食所致肥胖导致胰岛素抵抗的物质基础。方法将30只雄性Wistar大鼠分为正常对照组、高脂组,正常对照组喂饲普通块料,高脂组喂饱和脂肪酸提供59%热卡的高脂饲料。各组共喂饲3月后测定体重,空腹血糖,糖负荷30、60、120min血糖,空腹胰岛素,胰岛素耐量,血脂,血清游离脂肪酸谱。结果与正常对照组比较,高脂组大鼠从第4周开始体重明显升高,空腹血糖和糖负荷30、60、120min血糖,糖耐量试验中葡萄糖曲线下面积,皮下注射胰岛素后40、90、120min血糖,胰岛素耐量试验中葡萄糖曲线下面积,血清胰岛素,胰岛素抵抗指数,血清瘦素,血清胆固醇和甘油三酯含量均明显升高。高脂组大鼠血清游离脂肪酸谱中饱和脂肪酸明显升高、不饱和脂肪酸明显下降。结论肥胖导致胰岛素抵抗的物质基础与脂肪代谢异常,特别是和饱和脂肪酸的升高、不饱和脂肪酸的下降有关。     

NIDDM患者血清性激素变化与胰岛素抵抗的关系

为探讨非胰岛素依赖型糖尿病（ＮＩＤＤＭ） 患者血清性激素变化及其与胰岛素抵抗的关系, 应用放射免疫法检测了６０ 例５０ 岁以上ＮＩＤＤＭ 患者血清雌二醇 （Ｅ２）、睾酮（Ｔ） 等性激素水平。结果： 男性患者Ｅ２ 升高, Ｔ呈下降趋势, Ｅ２／Ｔ比值显著高于正常对照 （Ｐ＜ ０． ０５）; 女性患者Ｅ２ 较对照组显著降低（Ｐ＜ ０． ０１）, Ｔ略高于正常, Ｅ２ ／Ｔ比值平衡失调。Ｅ２、Ｅ２／Ｔ与空腹血糖 （ＦＢＧ）、空腹胰岛素（ＦＩｎｓ） 呈正相关, 与胰岛素敏感性（ＩＳ） 呈负相关。认为ＮＩＤＤＭ 患者存在严重的性激素失调及胰岛素抵抗, 在“胰岛素抵抗—糖代谢紊乱—性激素内环境失衡”之间, 可能有规律性的内在联系。     

低分子壳聚糖对实验性糖尿病大鼠血糖的调节作用

目的:观察低分子壳聚糖对链脲佐菌素(STZ)诱导的实验性糖尿病大鼠血糖的调节作用。方法:腹腔一次性注射STZ复制大鼠糖尿病模型,观察低分子壳聚糖的降血糖效应及其对大鼠体重和血胰岛素含量的影响。结果:STZ诱导的糖尿病大鼠血糖升高、体重降低(P<0.01),血胰岛素无明显变化(P>0.05)。低分子壳聚糖可显著降低糖尿病模型大鼠的血糖浓度,使血胰岛素含量升高(P<0.01),并能对抗体重的降低(P<0.01)。结论:低分子壳聚糖对实验性糖尿病有明显的治疗效果,其作用与降低血糖浓度,增加胰岛素分泌有关。     

短期胰岛素治疗对糖尿病大鼠内脏脂肪抵抗素mRNA表达的影响

目的观察短期胰岛素治疗后糖尿病(DM)大鼠内脏脂肪组织抵抗素(resistin)mRNA表达及血清抵抗素水平的变化。方法采用小剂量链脲佐菌素(STZ)注射联合高糖高脂饲料喂养制备糖尿病大鼠模型,予胰岛素控制部分糖尿病大鼠血糖,设立空白对照组、血糖未控制组、血糖控制组。分别检测3组大鼠血清抵抗素水平及内脏脂肪组织抵抗素mRNA的表达;观察3组大鼠血清抵抗素、游离脂肪酸(FFA)、三酰甘油(TG)、总胆固醇(TC)水平及内脏脂肪抵抗素mRNA表达的变化。结果与空白对照组比较,血糖未控制组大鼠血清抵抗素及内脏脂肪组织抵抗素mRNA的表达显著增高[(696.23±187.77)vs(538.31±142.14);(62.26±25.79)vs(10.15±12.13),P<0.05];与血糖控制组大鼠比较,血糖未控制组大鼠内脏脂肪组织抵抗素mRNA的表达亦显著增高[(62.26±25.79)vs(10.45±2.99),P<0.05]。血糖控制组大鼠FFA较血糖未控制组大鼠FFA水平显著降低[(0.53±0.16)vs(0.73±0.19),P<0.05],而TC水平显著增高[(1.92±0.16)vs(1.22±0.38),P<0.05]。结论短期的胰岛素治疗能降低糖尿病大鼠内脏脂肪组织抵抗素mRNA的表达,可能与血糖控制后胰岛素抵抗改善及胰岛素负调节抵抗素mRNA表达有关。     

不同手术方式对肝硬变大鼠线粒体呼吸功能的影响

对大鼠肝硬变门静脉高压症及不同术式对其肝脏功能的影响进行观测以评价各术式的治疗效果。动物分为肠腔侧侧分流术、远端脾分流术、门奇断流术、肝硬变及正常对照组。     

实验性糖耐量异常动物模型的建立

目的 :建立一种典型稳定的糖耐量异常 (IGT)动物模型。方法 :雄性Wistar大鼠生后 2 4h内一次性腹腔注射链脲佐菌素(STZ) 80mg/kg ,10周后检测经腹腔葡萄糖耐量试验及血清胰岛素水平 ,16周后复查。结果 :实验组与正常对照组比较空腹血糖 ,胰岛素水平无统计学意义 (P >0 0 5 ) ;糖负荷后血糖明显升高 ,IGT ,血清胰岛素水平低于正常对照组。结论 :新生大鼠一次性腹腔注射STZ可成功制备IGT动物模型