Increased expression of neuropeptide Y and its mRNA in STZ- diabetic rats

目的：研究糖尿病大鼠下丘脑和胰腺神经肽Y的mRNA及蛋白表达情况,以探讨NPY和糖尿病的关系。方法：建立链脲佐菌素（STZ）诱导的糖尿病大鼠模型,设立糖尿病、糖尿病胰岛素治疗及对照组,饲养24周后处死动物。用原位杂交和免疫组化检测下丘脑和胰腺NPY的mRNA及蛋白表达情况。结果：1.糖尿病大鼠下丘脑NPY的mRNA及蛋白表达均增加,NPY的mRNA表达主要在弓状核,说明弓状核是NPY产生的主要部位。2.给予胰岛素治疗后,STZ糖尿病大鼠下丘脑的NPY的mRNA及蛋白表达均较糖尿病组明显下降,说明胰岛素缺乏是STZ糖尿病大鼠下丘脑NPY增多的重要原因之一。3.下丘脑NPY增高的糖尿病大鼠具有多饮、多食;胰岛素治疗后其NPY下降,糖尿病大鼠的多饮、多食明显缓解,证实NPY参与STZ糖尿病大鼠的某些病理生理过程。4.首次揭示在STZ糖尿病大鼠胰岛中NPY的mRNA及蛋白表达增加。胰岛素NPY阳性细胞的分布也发生改变,由主要分布在周边变为整个胰岛散在分布,给予胰岛素治疗后,胰岛中的NPY和mRNA及蛋白表达未见明显改变。结论：糖尿病下丘脑NPY的增多,主要参与糖尿病的多饮、多食等病理生理过程。虽然糖尿病胰岛的NPY增多原因及其作用还不完全清楚,但为今后进一步的研究提供了重要线索。     

慢性肾功能衰竭大鼠下丘脑组织和血浆食欲素A及神经肽Y水平的变化及其意义

目的　探讨大鼠慢性肾功能衰竭 (CRF)动物模型的下丘脑组织和血浆食欲素A及神经肽Y(NPY)水平的变化及其意义。方法　将 41只 2 0 0～ 2 50 g雄性Wister大鼠分为 :正常组、假手术组和CRF组。术后 4、 8、 1 2周分批断头处死大鼠 ,取血浆和下丘脑组织标本。用放射免疫法测定血浆和下丘脑组织食欲素A和NPY。用生化自动分析仪测定血清肌酐。结果　CRF大鼠术后4、 8和 1 2周血肌酐水平均高于假手术组。其术后 1 2周的血浆食欲素A水平高于假手术组 (2 64pg/ml± 62pg/mlvs 1 83pg/ml± 56pg/ml,P =0 0 39)。CRF大鼠术后 1 2周的下丘脑食欲素A水平明显低于假手术组 (1 0 5fmol/mg± 2 7fmol/mg湿重vs 1 7 4fmol/mg± 3 9fmol/mg湿重 ,P =0 0 2 3)。CRF大鼠术后 8周 (7 1 pmol/ml± 1 7pmol/mlvs 5 0 pmol/ml± 0 5pmol/ml,P =0 0 1 )和1 2周 (7 9pmol/ml± 1 1pmol/mlvs 4 8pmol/ml± 1 1 pmol/ml,P =0 0 0 0 8)的血浆神经肽Y水平高于假手术组 ,其术后 1 2周的下丘脑神经肽Y水平明显低于假手术组 (70fmol/mg± 2 3fmol/mgvs1 1 3fmol/mg± 31fmol/mg湿重 ,P =0 0 33)。 结论　 (1 )CRF大鼠血浆食欲素A和NPY水平有逐渐增高趋势 ,肾功能减退可能导致食欲素A和NPY排泄障碍。 (2 )CRF时下丘脑组织食欲素     

新诊断2型糖尿病患者β细胞功能分析

目的了解新诊断2型糖尿病患者胰岛β细胞功能改变。方法检测352例新诊断2型糖尿病患者空腹血糖、胰岛素及胰岛素原,行静脉葡萄糖耐量试验,评价胰岛素曲线下面积(AUC)、胰岛素急性分泌时相(AIR)及稳态模型β细胞功能指数(Homa β)及胰岛素抵抗指数(HomaIR)。结果糖尿病患者 AUC 较正常者明显减低(834.2 pmol/L vs 7934.7 pmol/L,中位数,P<0.001);AIR 缺失(-33.7 pmol/L vs 6962.0 pmol/L,P<0.001)。分层分析显示当患者空腹血糖>7.0 mmol/L 时其 AIR 即明显减弱(317.3 pmol/L),大于9.0 mmol/L 时消失。糖尿病患者 Homa β约为正常者的30%(3.7±0.9 vs 5.9±0.9,P<0.001),空腹胰岛素原(PI)及其与胰岛素比值(PI/I)显著升高(22.6 pmol/L±14.7 pmol/L vs 11.5 pmol/L±7.1 pmol/L,P<0.001;30.1%±20.5%vs12.1%±9.6%,P<0.001)。结论新诊断2型糖尿病患者胰岛β细胞功能受损主要表现在 AIR 缺失和 AUC 显著下降,Homa β明显降低,以及胰岛素分泌质量下降。     

游离脂肪酸诱导的胰岛素抵抗对血浆ghrelin水平的影响

目的　探讨正糖 高胰岛素钳夹及游离脂肪酸 (FFA)对大鼠血浆ghrelin浓度的影响。方法　建立清醒状态下大鼠正常血糖 高胰岛素钳夹技术 ,在钳夹前后分别测定大鼠血浆ghrelin浓度 ,脂质灌注组大鼠 12只 ,生理盐水组 12只为对照 ,并用 3 3 H葡萄糖作为示踪剂测定了胰岛素介导的外周和肝糖的代谢。结果　在胰岛素钳夹中 ,脂质灌注组大鼠血浆FFA明显增加 (从 74 2 μmol/L±5 1μmol/L到 2 346 μmol/L± 2 38μmol/L ,P <0 0 1)。脂质灌注组葡萄糖输注率 (GIR)明显低于对照组( 2 0 0 2 4 0min ,平均 12 6mg·kg-1·min-1± 1 5mg·kg-1·min-1vs 34 0mg·kg-1·min-1± 1.6mg·kg-1·min-1,P <0 0 1)。到钳夹结束时 ,下降至相应对照值的 35 % ( 2 4 0min ,12 0mg·kg-1·min-1± 1 9mg·kg-1·min-1vs 34 7mg·kg-1·min-1± 1 7mg·kg-1·min-1,P <0 0 1)。对照组肝糖产率 (HGP)明显被抑制 ( 88% ) ,从 19 0mg·kg-1·min-1± 4 5mg·kg-1·min-1降至 2 3mg·kg-1·min-1± 0 9mg·kg-1·min-1(P <0 0 1)。脂质输注组胰岛素对HGP的抑制作用明显障碍 ( 2 0 0 2 4 0min ,从 18 7mg·kg-1·min-1± 3 0mg·kg-1·min-1到 2 3 2mg·kg-1·min-1± 3 1mg·kg-1·min-1,P <0 0 5 )。钳夹术结束时 ,对照     

Functional magnetic resonance imaging and immunohisto-

Background The hypothalamus plays a central role in the regulation of metabolism by sensing metabolic demands and releasing regulatory neurotransmitters. This study investigated the response of the hypothalamus to glucose ingestion in rats by blood oxygen level-dependent functional magnetic resonance imaging (BOLD-fMRI) and immunohistochemical techniques to determine the role of the hypothalamus in glycoregulation during disturbances in carbohydrate metabolism. Methods The signal intensity of the hypothalamus was monitored by fMRI for 60 minutes after oral glucose intake in 48 healthy rats (age 14 months), which included 24 normal weight rats (weighing (365±76.5) g) and 24 overweight rats (weighing (714±83.5) g). Then, 12 rats (6 normal, 6 overweight) underwent a repeat fMRI scan after consuming an equivalent amount of water without glucose on a separate day. The procedure for fMRI with water intake was the same as for glucose ingestion. fMRI data was processed using time cluster analysis and intensity averaging method. After fMRI, the expression of neuropeptide Y (NPY) and 5-hydroxytryptamine (5-HT) in the hypothalamus of all rats was determined by immunohistochemistry. Positive cells for NPY or 5-HT were counted. Results There was a transient, but significant, decrease in fMRI signal intensity in all rats (mean (3.12±0.78)%) in the hypothalamus within 19.5–25.5 minutes of oral glucose ingestion. In overweight rats, the decrease in signal intensity in response to the glucose ingestion was more markedly attenuated than that observed in normal weight rats ((2.2±1.5)% vs (4.2±0.7)% inhibition, t=2.12, P&lt;0.05). There was no significant response in the hypothalamus after oral water ingestion. The percentage of NPY positive cells in obese rats were slightly lower than those in control group (21% vs 23%, t=0.71, P&gt;0.05); but there was no significant difference between the two groups; the percentage of 5-HT positive cells in obese rats were significantly lower than those in the control group (22% vs 31%, t=3.25, P&lt;0.01).Conclusions There is a transient, but significant, decrease in BOLD signal intensity in the hypothalamus following glucose ingestion, which is similar to that observed in humans. The response of the hypothalamus to glucose ingestion was different in overweight and normal weight rats. The percentage of NPY positive cells in obese rats were lower than those in the control group, although this difference was not statistically significant. The percentage of 5-HT positive cells in obese rats was significantly lower than those in the control group.     

Interaction of Dietary Composition and PYY Gene Expression in Diet-induced Obesity in Rats

Dietary obesity ,induced by exposure to highfat food,is the rodent model that most closely re-sembles human obesity . Comparing rats that areresistant or prone to diet-induced obesity serves thedual purpose of illustrating the molecular adapta-tions that prevent obesity and identifying genesthat become dysregulated by high fat diets .Neuropeptide Y ( NPY) and peptide YY(PYY) are closely related polypeptides which arecomposed of 36 amino acides and share considera-ble homology . While NPYa…     

Ghrelin对糖尿病大鼠摄食的影响

目的探讨Ghrelin在糖尿病大鼠摄食过量调控中的作用。方法21只大鼠随机分为：①正常对照组（N＋NS组）7只,腹腔注射枸橼酸缓冲液1mL,皮下注射生理盐水（NS）0．1mL;②实验组14只,采用链脲佐菌素（sTz）腹腔注射制作糖尿病大鼠模型,48h后随机分为糖尿病组（STZ＋NS组）7只,皮下注射NS0．1mL,糖尿病＋胰岛素组（sTz＋INS组）7只,皮下注射人胰岛素0．1mL（7U）。各组均每天注射2次,共注射14d。每天检测各组大鼠血糖水平、摄食量及体质量的改变;实验结束检测血清瘦素、生长激素水平,以及下丘脑神经肽Y（NPY）mRNA和胃GhrelinmRNA表达。结果注射STZ后5d,STZ＋NS组血糖水平持续高于27．8mmol／L;STZ＋INS组血糖水平逐渐下降,最终在8d后与N＋NS组无显著差异（P〉0．05）;STZ＋NS组摄食量较N＋NS组显著增多,体质量显著减少（F一9．56～29．25,q一6．46～9．56,P〈O．05）;STZ＋INS组与STZ＋NS组比较,大鼠摄食量显著减少,体质量显著增加（q=3．70～9．15,P％0．05）。与N＋NS组相比,STZ＋NS组血浆胰岛素、瘦素及生长激素水平显著降低,而STZ＋INS组血浆瘦素及生长激素水平显著升高（F=26．31～214．28,q=3．21～11．28,P〈0．05）。STZ＋NS组血浆Ghrelin水平显著高于N＋Ns组（F=52．31,q=12．41,P〈0．05）,STZ＋INS组血浆Ghrelin水平趋于正常（P〉0．05）。STZ＋NS组下丘脑NPYmRNA表达较N＋NS组显著增高（F=97．96,q—17．78,P〈O．05）。结论糖尿病大鼠血浆Ghrelin、瘦素水平以及下丘脑NPY表达的改变,可能与糖尿病摄食过盛形成有关。     

阿托伐他汀对冠心病患者血浆神经肽Y及胰岛素抵抗的影响

目的：观察阿托伐他汀对冠心病患血浆神经肽及Y及胰岛素抵抗的影响。方法：测定39例冠心病患（冠心病组）调脂治疗（阿托伐他汀，10mg/d，疗程4周）前后及27例健康人（正常对照组）血脂、血浆神经肽Y、空腹血糖、血清胰岛素，计算胰岛素敏感指数。分析神经肽Y与空腹血清胰岛素和胰岛系敏感指数的相关性。结果：（1）冠心病组血清总胆固醇、甘油三酯、低密度脂蛋白胆固醇、血浆神经肽Y、空腹血糖、血清胰岛素明显高于对照组，胰岛素敏感指数显降低；（2）冠心病组神经肽Y与空腹血清胰岛素和胰岛素敏感指数的密切相关性；（3）冠心病组调脂治疗后血浆神经肽Y水平显降低，胰岛素敏感指数明显提高，血清总胆固醇、甘油三酯、低密度脂蛋白胆固醇明显下降。结论：阿托伐他汀可显降低冠心病患血浆神经肽Y水平，并能改善胰岛素抵抗状态，且调脂疗效肯定。     

Messenger RNA expressions of vasopressin system and aquaporin-2 in adriamycin-induced nephrotic rats and effects of astragalus membranaceus

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不同糖耐量个体胰岛β细胞功能观察及评价

目的评价正常糖耐量（NGT）、糖调节受损（IGR）、新诊断2型糖尿病（T2DM）个体胰岛β细胞功能及其相关指标的适用性。方法178例入选者行口服和静脉葡萄糖耐量试验。检测胰岛素生成指数（ΔI30/ΔG30）、胰岛素急性分泌时相（AIR）、β细胞功能指数（HOMA β）、空腹胰岛素原（FPI）及胰岛素原／胰岛素（PI／I）比值反映胰岛素分泌功能。结果IGR组的ΔI30／ΔG30、AIR较NGT组分别下降了38％、39％,HOMA β轻度下降（19％）;T2DM组的胰岛β细胞功能降低更明显,其中AIR下降84％,ΔI30／ΔG30下降70％、HOMA β下降62％。T2DM组FPI和PI／I比值也比NGT组明显升高（24．4pmol／L±18．0pmol／L or 10．9pmol／L±6．7pmol／L;14．7％±10．5％or10．0％±6．5％,P〈0．05）。ΔI30／ΔG30和AIR相关性好（r=0．75,P〈0．001）。结论IGR患者主要表现胰岛素分泌时相缺陷和HOMA β降低,至糖尿病阶段则伴有胰岛素分泌质量下降。ΔI30／ΔG30和AIR均可准确反映IGR患者胰岛β细胞功能,而在新诊断2型糖尿病患者中AIR更适用,若应用ΔI30／ΔG30须校正胰岛素抵抗。     

针刺对糖尿病模型大鼠血浆神经肽 Ｙ的影响

目的：观测针刺对链脲左菌素（sterptozotcin,STZ）诱导的糖尿病模型大鼠血浆神经肽 Ｙ（neurpeptideＹ,ＮＰＹ）的影响。方法：ＳＴＺ诱导的糖尿病模型大鼠随机分为模型组、治疗组、防治组,其余正常大鼠作为对照组,每组10只。防治组于造模前１周开始针刺预防,取穴双侧“后三里”、胰俞穴,每日 １次,共治疗 １４次。治疗组大鼠取穴同防治组大鼠,于造模后第 １天给予针刺治疗,每日针刺 １次,共 ７次。疗程结束后用血糖仪检测大鼠空腹血糖,用放射免疫分析法检测大鼠胰岛素和 ＮＰＹ。结果：与模型组比较,针刺治疗和防治明显降低糖尿病大鼠的血糖水平（Ｐ＜0.05）,升高胰岛素水平（Ｐ＜0.05）,降低 ＮＰＹ水平（Ｐ＜0.05）;且防治组效果优于治疗组（Ｐ＜0.05）。结论：针刺降低糖尿病大鼠血糖的同时使胰岛素、ＮＰＹ水平降低,可能是针刺防治糖尿病血管并发症的机制之一;针刺防治结合效果优于单纯的针刺治疗。     

超重及糖耐量异常个体胰岛素慢速脉冲分泌模式研究

目的应用胰岛素慢速脉冲分泌模式检测、分析技术探讨正常糖耐量(NGT)、超重及糖耐量异常(IGT)个体胰岛素慢速脉冲分泌模式的特点。方法10例NGT个体、6例超重个体及3例IGT个体分别在混合餐情况下,每15min取血一次,连续进行24h,测定各时点的血糖、胰岛素、C肽值,结合时间序列的有关分析方法进行分析。结果(1)在混合餐情况下,胰岛素慢速脉冲每餐后出现2~4个,夜间出现3~4个左右,全天可出现12~15个,首个脉冲发生时间往往出现在餐后30~60min,最大脉冲往往出现在餐后45~90min,此分布特点在正常对照组、超重组、IGT组间差异无统计学意义;(2)在等比例进餐情况下,3组的24h胰岛素分泌率(ISR)平均脉冲幅度分别为357pmol/min±11pmol/min、820pmol/min±37pmol/min、666pmol/min±53pmol/min;(3)对照组的ISR脉冲平均周期为75min,超重组为75~90min,IGT组周期节律性不明显;(4)3组的互相关函数分别为0·72±0·11、0·80±0·11、0·51±0·11。结论利用时间序列的分析方法可以发现胰岛素慢速脉冲分泌模式的特点。     

Improvement of the function of islet beta and alpha cells by intervention against glucotoxicity: experiment with rats

OBJECTIVE: To investigate the effects of intervention against glucotoxicity on improvement of the function and pathological changes of islet beta and alpha cells. METHODS: Thirty-six male Sprague Dawley rats were randomly divided into four equal groups: normal control (NC) group, fed with standard chow, high-fat (HF) group, fed with extra high-fat chow; diabetes mellitus (DM) control group, fed with high-fat chow for 8 weeks followed by 30 mg/kg streptozotocin injection to establish DM models; and insulin (INS) group, treated with subcutaneous injection of long-acting insulin (glargine, 0.5 U x kg(-1) x d(-1)) for 4 weeks after the establishment of DM models. 48 h, 2 weeks, and 4 weeks after the STZ injection to the 2 DM groups oral glucose tolerance test (OGTT) was performed to all rats. Peripheral blood samples were collected from the caudal vein. Serum insulin level was assayed by radioimmunoassay. Total serum cholesterol (TC) and triglyceride (TG) were measured by enzyme-colorimetric method. By the end of experiment the rats were killed with their pancreases taken out. Immunohistochemistry was used to observe the morphological changes of the islet beta and alpha cells. Beta cell and alpha cell masses were calculated by the proportions of positive area in the islet. Proinsulin mRNA level was detected by RT-PCR. Insulin protein content in islets was detected by Western blotting. RESULTS: Four weeks after the insulin intervention against glucotoxicity, the fasting blood glucose and blood glucose 2 h after sugar-taking of the INS group were both significantly lower than those of the DM group (both P < 0.01). The relative beta cell mass of the INS group was 0.38 +/- 0.08, significantly bigger, 2.45 times, that of the DM group (0.11 +/- 0.05, P < 0.01). The relative alpha cells mass in islets of the INS group was 0.16 +/- 0.04, significantly lower, by 43%, than that of the DM group (0.28 +/- 0.15, P < 0.01). The insulin contents in beta cells of the INS group was 0.58 +/- 0.03, significantly higher, by 70.6%, than that of the DM group (0.34 +/- 0.14, P < 0.01). The proinsulin mRNA level of the INS group was 1.52 +/- 0.14, significantly higher, by 20.6%, than that of the DM group. CONCLUSION: The morphology of islet beta, alpha cells in diabetic rats was improved by four weeks of Intervention against glucotoxicity improves the pathology of islet beta and alpha cells in diabetic and insulin synthesis.     

Early metabolic defects for developing diabetes mellitus among offspring of patients with type 2 diabetes are independent of gender

The aim of the study was to investigate if the female offspring of patients with Type 2 diabetes have more metabolic defects for developing diabetes mellitus than their male counterparts. Thirty-four offspring (10 males, 24 females) of patients with Type 2 diabetes mellitus aged 28.9 +/- 1.5 years (mean +/- SEM) underwent a standard oral glucose tolerance tests (OGTT; 75 g glucose in 300 ml water). Anthropometric indices, plasma lipids and blood pressure were measured while insulin resistance (IR) and sensitivity (%S) were assessed using the Homeostasis Model Assessment (HOMA) method. All the offspring had normal glucose tolerance but high HOMA-derived IR values (27.2 +/- 4.2 vs. 22.5 +/- 2.7 pmol/mmol/l, p > 0.05) and low %S (48.1 +/- 5.1 vs. 50.6 +/- 3.9%, p > 0.05), all of which did not differ on gender comparisons. Multiple linear regression analyses suggest that gender had no influence on the outcome of the result (p = 0.37). Again, body mass index (BMI), fasting serum insulin, plasma glucose, triglyceride, total cholesterol, HDL-cholesterol and LDL-cholesterol were all similar in both genders (p > 0.05). The results suggest that though the offspring manifested metabolic defects for developing diabetes in later life, this susceptibility is independent of gender in the population studied. Further studies with a larger sample size are warranted to confirm these findings in this population.     

胰岛素及胰岛素受体在大鼠变应性气道炎症中的作用

目的探讨1型糖尿病与支气管哮喘之间拮抗关系的可能机制以及胰岛素及其受体在气道变应性炎症中的作用。方法将64只雄性SD大鼠随机分为8组,每组8只A组哮喘组;D组糖尿病组;I组胰岛素组;AD组哮喘+糖尿病组;AI组哮喘+胰岛素组;DI组糖尿病+胰岛素组;ADI组哮喘+糖尿病+胰岛素组;C组对照组。通过腹腔注射链脲菌素溶液的方法复制大鼠1型糖尿病模型;皮下注射卵白蛋白,14d后超声雾化吸入卵白蛋白复制大鼠气道变应性炎症反应模型。检测外周血细胞分类、血糖及血清胰岛素水平;收集支气管肺泡灌洗液行细胞计数、分类;HE染色观察肺脏病理变化;用免疫组化方法观察肺脏胰岛素受体的分布;用半定量RT-PCR测定肺组织胰岛素受体mRNA表达。结果糖尿病组血糖显著高于非糖尿病组,A、AI、ADI组大鼠激发后出现以嗜酸性粒细胞及中性粒细胞细胞增高为主的气道炎症反应。AD组气道炎症反应介于有哮喘组与非哮喘组之间。ADI、AI组、A组胰岛素水平(分别为27mIU/L±8mIU/L;83mIU/L±12mIU/L;71mIU/L±12mIU/L),均高于其相应对照(DI、I、C组,分别为15mIU/L±4mIU/L;64mIU/L±9mIU/L;49mIU/L±14mIU/L)。免疫组化显示胰岛素受体广泛分布于肺组织内,A、AI、ADI组肺泡腔内、血管及支气管周围浸润染色阳性细胞明显增多。糖尿病组胰岛素受体mRNA表达显著高于非糖尿病组(0.2588±0.0809vs0.0896±0.0308,P=0.00)。结论低剂量胰岛素可明显增强大鼠气道变应性炎症反应。炎症状态下机体胰岛素分泌增多。气道变应性炎症反应时肺组织内浸润的炎症细胞表面及支气管壁分泌细胞胰岛素受体增多。     

Foetomaternal complications in pregnancies with diabetes mellitus: association with the amount of insulin requirement, mean terminal blood glucose and HbA1C levels

Pregnancy hyperglycaemia can lead to foetomaternal complications. Normoglycaemia with exercise, diet and/or insulin can alter outcomes. The insulin requirement itself may alter outcomes independently. Two hundred and forty patients of pregnancy with diabetes mellitus were selected of which 176 belonged to gestational diabetes mellitus and 64 pregestational diabetes mellitus groups. Insulin requirement of pregestational diabetes mellitus group was 1.8 times higher than the gestational diabetes mellitus group. There were no insulin related increased complications in either group. The foetal complications were higher in pregestational diabetes mellitus group (62.5%) than in the gestational diabetes mellitus group (27.3 and 40% in < 15 units or > or = 15 units insulin requirement respectively). The terminal glycaemic parameters (fasting plasma glucose, 2 hours postprandial plasma glucose, HbA1C%) were not different in case of gestational diabetes mellitus between those with and without foetal complications, except for fasting plasma glucose where 'with complications' fasting plasma glucose was lower than without (79.4 +/- 13.14 versus 75.28 +/- 3.68 mg/dl). For pregestational diabetes mellitus patients those without complications had a significantly lower level of all the parameters (fasting plasma glucose 69.75 +/- 0.5 versus 122 +/- 14.14 mg/dl, postprandial plasma glucose 95 +/- 7.4 versus 131.5 +/- 12.02 mg/dl; HbA1C 6.8 +/- 0.28 versus 7.3 +/- 3.6%) compared with those having complications. Maternal complications could not be segregated as all the subgroups had a very incidence of caesarean section (60%-100%). However, when lower segment caesarean section was excluded and maternal complications segregated, for gestational diabetes mellitus patients, only fasting plasma glucose was significantly lower in cases without complications while in pregestational diabetes mellitus patients the fasting plasma glucose as well as HbA1C were significantly lower in cases without complications.     

黄芪多糖对糖尿病大鼠神经肽Y及其Y_2受体表达的影响

目的：探讨黄芪多糖（APS）对糖尿病大鼠肾脏神经肽Y（NPY）及其Y2受体（Y2R）表达的影响。方法：采用腹腔注射链脲佐菌素（STZ）制备糖尿病大鼠动物模型,随机分为对照组、糖尿病组和黄芪多糖干预组;采用放射免疫法检测血浆和肾皮质NPY水平,实时荧光定量PCR方法检测肾皮质NPYmRNA的表达,免疫组织化学方法检测肾皮质Y2R蛋白表达,同时检测大鼠的血糖、尿白蛋白排泄率（UAER）、肾重/体重。结果：①APS干预能显著削弱糖尿病大鼠血糖、UAER和肾重/体重的增加;②APS干预后显著降低糖尿病大鼠血浆和肾皮质NPY水平（P〈0.01）;③APS干预组大鼠肾皮质NPYmRNA和Y2R蛋白表达显著低于糖尿病组（P〈0.05）。结论：APS对糖尿病肾病的保护作用机制可能与下调肾脏NPY及其Y2R的表达有关。     

下丘脑胰岛素及其受体在高血压大鼠的变化及与血压的关系

目的 探讨下丘脑胰岛素及其受体在高血压大鼠的变化及与血压的关系.方法 比较自发性高血压大鼠(spontaneous hypertensive rats,SHR)与正常血压Wistar大鼠对照下丘脑的胰岛素含量、胰岛素受体最大结合容量(maximum binding capacity,Bmax)和平衡解离常数(equilibrium dissociation constant,KD),观察下丘脑前区微量注射胰岛素对平均动脉血压(mean arterial pressure,MAP)的影响.结果 下丘脑胰岛素含量SHR高于Wistar大鼠,而血浆胰岛素与Wistar大鼠无明显变化.SHR下丘脑胰岛素受体Bmax显著低于Wistar大鼠,KD值无显著变化.SHR下丘脑前区微量注入0.2 pmol胰岛素,在注射1 h后MAP显著下降,Wistar大鼠组MAP无变化.结论 下丘脑胰岛素在高血压发生发展过程可能起到保护作用,抑制血压的过度升高.     

二甲双胍对慢性暴露于高糖及高游离脂肪酸的HIT-T15细胞胰岛素受体酪氨酸蛋白激酶活性的影响

目的 观察二甲双胍(MF)对慢性高糖和高脂处理后的HIT-T15细胞(β细胞系)胰岛素受体(IRc)酪氨酸蛋白激酶(TPK)活性的影响,探讨MF对β细胞糖脂毒性,即β细胞胰岛素抵抗的改善作用机制.方法 实验分为对照组、对照 MF组、高糖组、高糖 MF组、高脂组、高脂 MF组.将HIT-T15细胞分别接种于含有5.5 mmol/L、16.7 mmol/L葡萄糖(G)及0.5 mmol/L软脂酸的培养液中,培养48 h后,加入2.5 μg/mL MF干预24 h.用放射性酶分析法测定β细胞IRc TPK活性.结果 高糖[(52.5±18.6) pmol/(min·μg), P＜0.01],且与对照组相比差异无统计学意义.MF对对照组HIT-T15细胞IRc TPK活性无明显影响.结论 高糖和高脂可抑制β细胞IRc TPK活性.MF能明显改善受高糖及高脂所抑制的HIT-T15细胞IRc TPK活性,且恢复到接近正常水平.提示MF对糖脂毒性所致β细胞胰岛素抵抗的改善作用可能与增加IRc TPK活性有关.