马齿苋治疗糖尿病的探讨

马齿苋用于治疗糖尿病载于传统中医文献。通过实验研究,观察到马齿苋对糖尿病小鼠有降血糖及修复胰岛细胞形态结构的作用,其中丰富的n-3脂肪酸含量可能起着重要的作用。     

菠萝蜜低聚肽对db/db糖尿病小鼠血糖的影响

 关于菠萝蜜的研究显示其具有一定的降血糖作用,但尚未有关于菠萝蜜低聚肽（Jack-fruit oligopeptides,JOPs）降血糖的研究。通过菠萝蜜低聚肽干预,研究其对db/db糖尿病模型小鼠血糖的影响作用。将db/db糖尿病小鼠模型,随机分为3个菠萝蜜低聚肽组（0.2 g/kg·bw、0.4 g/kg·bw、0.8 g/kg·bw）以及糖尿病模型对照组、二甲双胍对照组、乳清蛋白对照组;并选用db/m小鼠作为非糖尿病小鼠空白对照。经过为期6周的干预,检测小鼠空腹血糖、糖耐量实验血糖曲线下面积及组织中糖原含量。结果表明,菠萝蜜低聚肽可显著降低db/db糖尿病小鼠空腹血糖水平,显著降低糖耐量实验血糖曲线下面积（P<0.05）,其效果以0.4 g/kg·bw剂量组最为显著。菠萝蜜低聚肽干预可有效降低糖尿病小鼠的血糖水平,改善糖耐量,具有辅助降血糖作用。     

糖消平胶囊对四氧嘧啶致糖尿病小鼠糖代谢的影响

目的:观察糖消平胶囊对四氧嘧啶致糖尿病小鼠糖代谢的影响,为糖消平胶囊防治2型糖尿病及其并发症提供科学依据.方法:采用四氧嘧啶建立糖尿病小鼠模型,观察糖消平胶囊对小鼠空腹血糖、糖耐量、糖异生及肝糖原等糖代谢指标的影响.结果:糖消平胶囊能明显降低模型小鼠的空腹血糖,改善糖耐量的异常,在降低血糖的同时,能有效抑制糖异生的升高,促进肝糖原的储备和利用,增加机体肝糖原的含量.结论:糖消平胶囊具有明显的抗糖尿病作用,其作用与改善糖代谢有关.     

免疫初乳对正常和实验性糖尿病小鼠血糖的影响

目的研究免疫初乳对正常小鼠和四氧嘧啶致糖尿病小鼠血糖的影响.方法用正常小鼠和糖尿病模型小鼠研究免疫初乳调节血糖的作用.连续30d给予正常小鼠和四氧嘧啶糖尿病模型小鼠免疫初乳,30d后眼眶取血,取其血清测定小鼠空腹血清血糖.结论免疫初乳能显著降低四氧嘧啶致高血糖小鼠的血糖水平并提高其糖耐量,且高剂量免疫初乳组的效果好于低剂量组的效果.但免疫初乳对正常小鼠的血清血糖及糖耐量没有影响.     

虎眼万年青提取物降血糖作用的实验研究

观察虎眼万年青提取物对糖尿病模型小鼠血糖质量浓度以及糖尿病相关特征的水平的影响.采用四氧嘧啶腹腔注射法制造糖尿病小鼠模型,随机分为五组,醇提物高、中、低剂量组,二甲双胍阳性药物组,模型小鼠溶剂对照组,正常小鼠空白对照组,观察各组小鼠血糖质量浓度以及其他相关指标的变化水平.结果表明,模型各组的血糖质量浓度升高,经灌胃给以醇提物14 d后,血糖质量浓度明显下降,其他糖尿病症状也相应减轻.而空白组小鼠血糖值无明显变化.可见虎眼万年青乙醇提取物对于四氧嘧啶所致的糖尿病小鼠有治疗作用.     

江蓠藻膳食纤维的降血糖及抗氧化作用

观察江蓠藻膳食纤维对糖尿病小鼠的血糖,以及血清中某些抗氧化指标的效应,探讨其降血糖的可能作用机理.结果表明,江蓠藻膳食纤维能显著降低四氧嘧啶糖尿病小鼠的血糖值,且以中剂量(0.4 g.kg-1)江蓠藻膳食纤维的降血糖作用最佳.此外,江蓠藻膳食纤维可降低四氧嘧啶糖尿病小鼠血清中的丙二醛(MDA)浓度,提高超氧化物歧化酶(SOD)活性,改善糖尿病小鼠的氧化应激水平.     

苯并吡喃衍生物降血糖作用的研究

目的：观察苯并吡喃衍生物对正常小鼠及四氧嘧啶所致糖尿病小鼠血糖的影响。方法：通过随机分组,灌胃给药、对比,确定苯并吡喃衍生物对小鼠血糖的影响。结果：苯并吡喃衍生物对正常小鼠血糖无影响,对四氧嘧啶所致糖尿病小鼠有降血糖作用,结论：4b药有显著降血糖作用,其它各药有轻度降血糖作用。     

金线莲甲醇提取物的降血糖作用

研究金线莲甲醇提取物的降血糖作用及其机制.将正常小鼠和链尿佐菌素(STZ)诱导成功的糖尿病小鼠随机分成5组, 14 d后,分别测定小鼠的肝糖原、血糖、血脂及血清抗氧化指标.结果表明,金线莲甲醇提取物能显著降低糖尿病小鼠的血糖,使小鼠血清中超氧化物歧化酶(SOD)活性升高,丙二醛(MDA)浓度显著下降;能显著降低糖尿病小鼠血清中甘油三酯(TG)、总胆固醇(TC)的浓度,并使小鼠的肝糖原质量比显著增加.金线莲甲醇提取物有降血糖作用,其降糖机制可能与其调节血脂水平、增加外周组织对葡萄糖的利用及提高糖尿病小鼠的抗氧化能力有关.     

青钱柳叶降血糖作用研究

目的 研究青钱柳叶双水相提取物对糖尿病小鼠的降血糖作用。方法 通过高脂饮食联合腹腔注射链佐霉素（STZ）建立小鼠糖尿病模型,设置青钱柳叶双水相提取物高、中、低剂量组灌胃,连续14 d后测定空腹血糖值,检测血清中胰岛素（INS）、总胆固醇（T-CHO）、甘油三酯（TG）、高密度脂蛋白（HDL-C）、低密度脂蛋白（LDL-C）、极低密度脂蛋白含量（VLDL-C）,采用HE染色法观察实验性糖尿病小鼠肝脏和胰腺的病理学变化。结果 青钱柳叶双水相提取物中剂量能明显改善2型糖尿病小鼠体重减轻这一症状（P<0.01）,低剂量组降低糖尿病小鼠空腹血糖（P<0.05）,高剂量组显示出降低血清胰岛素的作用（P<0.05）,青钱柳叶双水相提取物能降低糖尿病小鼠血清中总胆固醇、甘油三酯、低密度脂蛋白的含量,增加高密度脂蛋白含量。二甲双胍组和青钱柳叶双水相提取物高、中、低剂量组小鼠的肝脏和胰腺的病变较模型组有不同程度的减轻。结论 青钱柳叶双水相提取物具有降低小鼠空腹血糖、降脂、改善胰岛素抵抗、保护胰岛细胞的作用,其降血糖的作用机制需进一步研究。     

剑麻皂素降血糖作用的研究

采用四氧嘧啶致糖尿病小鼠模型、肾上腺素引起的高血糖大鼠模型以及正常小鼠研究剑麻皂素的降血糖作用,在口服给药后,测定各模型动物的血糖水平。结果显示,剑麻皂素能明显降低四氧嘧啶糖尿病小鼠的血糖水平,对肾上腺素高血糖大鼠也有降血糖作用,对正常小鼠血糖没有影响。剑麻皂素对糖尿病动物具有明显的降血糖作用。     

Loss of pancreatic islet tolerance induced by beta-cell expression of interferon-gamma

Interferon-gamma (IFN-gamma) is produced during the response to infection and participates in immunostimulatory events. We have previously reported the induction of diabetes in transgenic mice (ins-IFN-gamma) in which the expression of the lymphokine IFN-gamma is directed by the insulin promoter. This diabetes is a result of the progressive destruction of pancreatic islets that occurs with the influx of inflammatory cells. Here we demonstrate that this islet cell loss is mediated by lymphocytes, that engrafted histocompatible islets are destroyed, and that lymphocytes from the transgenic mice are cytotoxic to normal islets in vitro. These results indicate that the pancreatic expression of IFN-gamma can result in a loss of tolerance to normal islets, consistent with its role as an inducer of costimulatory activity, which is essential for lymphocyte activation during an immune response.     

PDGF signalling controls age-dependent proliferation in pancreatic β-cells

Determining the signalling pathways that direct tissue expansion is a principal goal of regenerative biology. Vigorous pancreatic β-cell replication in juvenile mice and humans declines with age, and elucidating the basis for this decay may reveal strategies for inducing β-cell expansion, a long-sought goal for diabetes therapy. Here we show that platelet-derived growth factor receptor (Pdgfr) signalling controls age-dependent β-cell proliferation in mouse and human pancreatic islets. With age, declining β-cell Pdgfr levels were accompanied by reductions in β-cell enhancer of zeste homologue 2 (Ezh2) levels and β-cell replication. Conditional inactivation of the Pdgfra gene in β-cells accelerated these changes, preventing mouse neonatal β-cell expansion and adult β-cell regeneration. Targeted human PDGFR-α activation in mouse β-cells stimulated Erk1/2 phosphorylation, leading to Ezh2-dependent expansion of adult β-cells. Adult human islets lack PDGF signalling competence, but exposure of juvenile human islets to PDGF-AA stimulated β-cell proliferation. The discovery of a conserved pathway controlling age-dependent β-cell proliferation indicates new strategies for β-cell expansion.     

Non-tolerance and autoantibodies to a transgenic self antigen expressed in pancreatic beta cells

Transgenic mice expressing simian virus 40 T antigen under control of the insulin gene regulatory region vary in their response to this protein. Each lineage is characteristically either tolerant to T antigen, or not, in which case autoantibodies arise with high frequency, and lymphocytes infiltrate and disrupt the pancreatic islets. Both non-tolerance and the autoimmune response appear to result from delayed onset of T antigen expression during beta cell development.     

马尾松花粉硫酸酯化多糖对2型糖尿病小鼠血糖的影响

探讨马尾松花粉硫酸酯化多糖对2型糖尿病小鼠血糖的影响.通过高糖高脂饲料联合35 mg/kg剂量一次性腹腔注射STZ成模.成模后将小鼠分为5组（空白组、模型组、200 mg/kg·d PPM60组、200 mg/kg·d SPPM60组、200 mg/kg·d二甲双胍组）,口服治疗4周.第4周末检测体重、血糖、胰岛素水平、口服糖耐量测试、胰岛素敏感指数等,组织学分析各组小鼠胰岛形态的变化.结果显示模型组小鼠血糖水平升高,胰岛素敏感和糖耐量水平受到损坏.与空白组小鼠相比,模型组小鼠的胰岛形态受损明显.经PPM60治疗后高血糖症得到改善（P＜0.05）,但是胰岛素水平和胰岛素敏感性变化差异性不显著.经SPPM60和二甲双胍治疗后高血糖症（P＜0.01）、高胰岛素血症（P＜0.01）以及胰岛素敏感性（P＜0.01）得到改善,胰岛形态受损情况得到一定恢复.SPPM60组与PPM60组相比,各指标均出现明显的改善.     

Signalling through CD30 protects against autoimmune diabetes mediated by CD8 T cells

Autoantigens found on pancreatic islets can move to draining lymph nodes, where they are able to cause the activation and consequent deletion of autoreactive T cells by a mechanism termed cross-tolerance. This deletion depends on signalling through CD95 (also known as Fas), a member of the superfamily of tumour-necrosis-factor receptors. Here we describe a new mechanism that protects against autoimmunity: this mechanism involves another member of this superfamily, CD30, whose function was largely unknown. CD30-deficient islet-specific CD8-positive T cells are roughly 6,000-fold more autoaggressive than wild-type cells, with the transfer of as few as 160 CD30-deficient T cells leading to the complete destruction of pancreatic islets and the rapid onset of diabetes. We show that, in the absence of CD30 signalling, cells activated but not yet deleted by the CD95-dependent cross-tolerance mechanism gain the ability to proliferate extensively upon secondary encounter with antigen on parenchymal tissues, such as the pancreatic islets. Thus, CD30 signalling limits the proliferative potential of autoreactive CD8 effector T cells and protects the body against autoimmunity.     

小鼠胰腺IAPP与SS共存的免疫组化研究

采用免疫组织化学ＰＡＰ邻片单染，显示正常成年及生后发育不同时期小鼠胰腺胰岛淀粉样多肽免疫反应细胞（ＩＡＰＰ－ＩＲ细胞）和生长抑素免疫反应细胞（ＳＳ－ＩＲ细胞），并对上述细胞进行了形态学计量。目的是观察小鼠生后发育期间胰岛淀粉样多肽（ＩＡＰＰ）与生长抑素（ＳＳ）的共存关系，结果表明：在生后发育不同时期，小鼠胰腺组织都有部分ＩＡＰＰ－ＩＲ细胞和ＳＳ－ＩＲ细胞形态相似，定位一致，同一细胞既呈ＩＡＰＰ免疫     

小熊猫胰的组织解剖学研究

小熊猫的胰呈“L”形，分为右叶和左叶．右叶，又称胰头，左叶又可分为胰体和胰尾两部分．胰小叶明显．胰管1条，与胆总管共同开口于十二指肠乳头．腺泡属浆液性腺泡，腺腔内有细胞质淡染的泡心细胞；胰岛染色浅淡，为大小不等的细胞团．     

Conserved mechanisms of glucose sensing and regulation by Drosophila corpora cardiaca cells

Antagonistic activities of glucagon and insulin control metabolism in mammals, and disruption of this balance underlies diabetes pathogenesis. Insulin-producing cells (IPCs) in the brain of insects such as Drosophila also regulate serum glucose, but it remains unclear whether insulin is the sole hormonal regulator of glucose homeostasis and whether mechanisms of glucose-sensing and response in IPCs resemble those in pancreatic islets. Here we show, by targeted cell ablation, that Drosophila corpora cardiaca (CC) cells of the ring gland are also essential for larval glucose homeostasis. Unlike IPCs, CC cells express Drosophila cognates of sulphonylurea receptor (Sur) and potassium channel (Ir), proteins that comprise ATP-sensitive potassium channels regulating hormone secretion by islets and other mammalian glucose-sensing cells. They also produce adipokinetic hormone, a polypeptide with glucagon-like functions. Glucose regulation by CC cells is impaired by exposure to sulphonylureas, drugs that target the Sur subunit. Furthermore, ubiquitous expression of an akh transgene reverses the effect of CC ablation on serum glucose. Thus, Drosophila CC cells are crucial regulators of glucose homeostasis and they use glucose-sensing and response mechanisms similar to islet cells.     

Identification and processing of proglucagon in pancreatic islets.

Immunoprecipitation and tryptic peptide analysis of newly synthesized proteins from rat islets have identified an 18,000 molecular weight (MW) protein as proglucagon. Conversion of this precursor was kinetically similar to the conversion of proinsulin and resulted in the formation of both pancreatic glucagon and a 10,000-MW protein lacking this hormonal sequence.