Ficolin-3、TRF及hs-CRP联合检测在2型糖尿病早期诊断中的价值

目的 检测2型糖尿病(T2DM)患者,T2DM的期人群及健康人群血清中纤维凝胶蛋白-3 (Ficol-in-3)、转铁蛋白(TRF)、超敏C反应蛋白(hs-CRP)水平,来探讨血清中Ficolin-3、TRF及hs-CRP水平与T2DM的关系.方法 选择大连医科大学附属第一医院T2DM患者33例,T2DM前期组41(包括29例糖耐量减低者和12例空腹血糖受损者)及健康对照组30例,比较各组间Ficolin-3、TRF及hs-CRP的水平,分析3者与T2DM间的关系.结果 (1)血清Ficolin-3水平:在T2DM前期组(26.1±10.5) μg/mL及T2DM组(28.1±8.5)μg/mL均高于正常对照组(20.8±11.7 μg/mL,P＜0.05),T2DM前期组与T2DM组无显著性差异(P＞0.05);(2)血清TRF水平:T2DM前期组(261.3±51.1) mg/dL明显高于正常对照组(236.5±31.9 mg/dL,P＜0.05),T2DM组(242.0±57.7) mg/dL与正常对照组、T2DM组与T2DM前期组均无显著性差异(P＞0.05);(3)血清hs-CRP水平:T2DM组(3.12±3.47) mg/L明显高于正常对照组(1.19± 1.41) mg/L和T2DM前期组(1.70±1.97mg/L,P＜ 0.05),T2DM前期组与正常对照组无显著性差异(P＞0.05).结论 血清Ficolin-3、TRF和hs-CRP的水平可以有助于2型糖尿病的早期诊断,对T2DM的早期预防及病情发展有一定的预测价值.     

鱼鳞胶原蛋白对小鼠皮肤伤口愈合的影响

目的：探索鱼鳞胶原蛋白对糖尿病小鼠皮肤伤口愈合的影响。方法通过水提法提取鱼鳞胶原蛋白,利用链脲佐菌素建立小鼠糖尿病模型,实时定量荧光PCR （ real time PCR ）检测糖尿病小鼠伤口处血管生长因子（ vascular endothelial growth factor,VEGF）、表皮细胞生长因子（Epidermal Growth Factor,EGF）mRNA表达,并检测伤口处超氧化物歧化酶（Superox-ide Dismutase,SOD）、过氧化氢酶（ catalase,CAT）含量。结果鱼鳞胶原蛋白0.5 mg组及1 mg组可促进糖尿病小鼠伤口愈合。治疗第15天,鱼鳞胶原蛋白1 mg组愈合率可达94.14％;鱼鳞胶原蛋白1 mg组可明显促进伤口处VEGF、EGF mRNA表达,并且可增加伤口处SOD、CAT含量。结论水提法提取的鱼鳞胶原蛋白具有良好的相容性,可促进糖尿病小鼠伤口愈合,具有潜在的临床应用价值。     

雌激素α受体PvuⅡ和XbaⅠ基因多态性与产后抑郁障碍的相关性

目的探讨雌激素α受体(ERα)基因多态性与产后抑郁障碍发生的关联性,为产后抑郁障碍发生的病因机制提供遗传学证据,进而为疾病基因诊断与治疗提供理论基础。方法选取产后抑郁障碍产妇(产后抑郁组)与健康产妇(正常对照组)各45例,运用限制性片段长度多态性聚合酶链式反应分析法、基因记数法统计两组ERα基因的基因型和等位基因频率,分析ERαPvuⅡ和XbaⅠ多态性与产后抑郁的关联性。结果产后抑郁组与正常对照组ERαPvuⅡ基因型及等位基因(P与p)频率分布差异有统计学意义(P<0.05),产后抑郁组与正常对照组ERαXbaⅠ基因型及等位基因(X与x)频率分布差异无统计学意义(P>0.05),ERαPvuⅡ与XbaⅠ联合基因型分布差异无统计学意义(P>0.05)。结论 ERαPvuⅡ基因多态性与产后抑郁障碍发病有相关性,XbaⅠ基因型突变对于产后抑郁障碍发病无相关性,联合基因分析,产后抑郁产妇与健康产妇整体基因型分布相似。     

Metformin increases insulin sensitivity and basal glucose clearance in Type 2 (non-insulin dependent) diabetes mellitus

Abstract The effects of metformin on glycaemia, insulin and c-peptide levels, hepatic glucose production and insulin sensitivity (using the euglycaemic, hyperinsulinaemic clamp) were evaluated at fortnightly intervals in 9 Type 2 diabetic patients using a stepwise dosing protocol: Stage 1 - no metformin for four weeks; stage 2 - metformin 500mg mane; stage 3 - metformin 500mg thrice daily; stage 4 – metformin 1000mg thrice daily. Results are expressed as Mean ± SEM. Fasting blood glucose decreased from basal values (9.7 ±1.0 mmol/L) by 13% at stage 2, 34% at stage 3 and 41% at stage 4 (p<0.02 vs basal for all stages; p<0.02 stage 2 vs stage 3). Post-prandial glycaemia was significantly improved only with metformin 3000mg/day (p<0.05). Fasting, meal-stimulated and total insulin and c-peptide levels showed no change. Hepatic glucose output did not change significantly with metformin. Insulin sensitivity, measured as total glucose utilisation during hyperinsulinaemia, increased from stage 1 (10.3 ± 2.1 μmoL/kg/min) by 23% at stage 3 (p < 0.05) and by 29% at stage 4 (p < 0.02). Basal metabolic clearance of glucose increased compared to stage 1 (1.69 ±0.16 mL/kg/min) by 30% at stage 2, 53% at stage 3 and 44% at stage 4 (all p <0.02). This study demonstrates that improved efficiency of glucose utilisation, both basally and under conditions of euglycaemic hyperinsulinaemia, is the basis of metformin's antihyperglycaemic action.     

Linkage analysis of the human insulin receptor gene in Type 2 (non-insulin-dependent) diabetic families and a family with maturity onset diabetes of the young

Summary The possibility of linkage between the human insulin receptor gene locus and diabetes was examined in three Type 2 (non-insulin-dependent) diabetic families and one family with maturity onset diabetes of the young. Insulin receptor gene haplotypes were established using BglII, Rsal and Sstl restriction enzyme digests of genomic DNA from all available family members. The digested DNA was subjected to agarose gel electrophoresis, Southern blotted, and hybridised to ³²P-labelled human insulin receptor gene cDNA. In the pedigree with maturity onset diabetes of the young, formal linkage analysis allowed exclusion of close linkage between the insulin receptor locus and diabetes (logarithm of the odds for linkage versus non-linkage was –5.35 at recombination fraction of 0.01). This confirms the absence of linkage between insulin receptor and diabetes which has been reported in two similar pedigrees. In the three Type 2 diabetic families there were a minimum of 4 recombinants between the insulin receptor locus and diabetes, which makes a direct role for insulin receptor defects unlikely. The importance of using realistic estimates of penetrance when performing linkage analysis in a disease with a late age of onset is emphasised. In contrast to the one previous linkage analysis study of the insulin receptor gene, no specific association of diabetes with the rare Sstl Sl(-) allele was observed in either the maturity onset diabetes of the young or the Type 2 diabetic families.     

Dawn phenomenon in Type 1 (insulin-dependent) diabetic adolescents: influence of nocturnal growth hormone secretion

Summary In order to reassess the role of growth hormone in the dawn phenomenon, we studied eight C-peptide negative diabetic adolescents, who are likely to exhibit important nocturnal growth hormone surges. The insulin infusion rate necessary to maintain euglycaemia was predetermined in each patient from 22.00 hours to 01.00 hours, and then kept constant until 08.00 hours resulting in stable free insulin levels. Blood glucose rose from 4.3±0.7 mmol/l at 01.00 hours to 7.1±1.1 mmol/l at 08.00 hours (p<0.01) secondary to an increased hepatic glucose production. All the subjects presented an important growth hormone secretion, ranging from 20 to 66 ng/ml (peak values) and from 3619 to 8621 ng·min· ml^–1 (areas under the curve). The insulin infusion rate selected for each patient was positively correlated with the nocturnal growth hormone secretion (area under the curve) (r=0.87, p<0.01). On the other hand, there was no relationship between the nocturnal growth hormone secretion and the magnitude of the early morning blood glucose rise (r=–0.48, p>0.2). We conclude that, in Type 1 (insulin-dependent) diabetic adolescents, the dawn phenomenon exists but is moderate despite important growth hormone surges; the nocturnal growth hormone secretion influences the nocturnal insulin requirements but not the dawn phenomenon itself, if insulinisation is adequate.     

Insulin autoantibody polymorphisms with greater discrimination for diabetes in humans

Summary Insulin autoantibodies, like islet cell antibodies, are found not only in the sera of newly diagnosed Type 1 (insulin-dependent) diabetic patients and their relatives, but also in patients with other autoimmunities who do not develop diabetes. Insulin autoantibodies are oligo/monoclonal and frequently binding-site restricted. As determinant selection is genetically determined, we questioned whether certain polymorphisms of insulin autoantibodies, identified by their binding site on the insulin molecule, could better discriminate for Type 1 diabetes, which is also HLA determined. First, we raised monoclonal antibodies to human insulin by classic fusion methods in order to determine the range of antibody polymorphism, and identified five distinct types by their binding profiles to a panel of insulin variants, using an enzyme-linked immunosorbent assay. Two of these polymorphisms, type A and type B, were subsequently found in insulin autoantibody positive human sera using the same panel of insulin variants, and successfully distinguished diabetes-related from diabetes-unrelated individuals. Thus, the type B polymorphism was responsible for binding in 60% of 41 insulin autoantibody positive individuals with polyautoimmune disease but no personal or family history of diabetes (diabetes unrelated), but in only 2% of a group which comprised 17 newly-diagnosed insulin autoantibody positive Type 1 diabetic patients, 19 insulin autoantibody positive discordant twins of Type 1 diabetes and six insulin autoantibody positive healthy siblings of Type 1 diabetic patients (diabetes related) (p<0.01). Isolation of the type A polymorphism alone reduced the proportion of false negatives in the insulin autoantibody test for diabetes relatedness from 49% to 20% without diminishing its specificity. Thus, insulin autoantibody polymorphisms are more discriminating than the nominal antibody, due possibly to linkage between immune response genes determining response to the type A epitope on the one hand, and susceptibility to Type 1 diabetes on the other.     

胰岛素短期强化治疗对初诊2型糖尿病患者胰岛β细胞功能的影响

目的　观察胰岛素短期强化治疗对初诊 2型糖尿病患者胰岛β细胞功能的改善作用及降糖效果。方法对 2 4例初诊 2型糖尿病患者应用胰岛素泵进行 2周的胰岛素强化治疗 ,治疗第 15天时对比治疗前后静脉葡萄糖耐量试验所诱发的胰岛素第 1时相的分泌、胰岛素曲线下面积及由 Homa模型计算胰岛素分泌指数 (Homa B)、胰岛素抵抗指数 (Homa A) ,同时观察空腹血糖、餐后 2小时血糖变化 ;3个月时对比糖化血红蛋白变化。结果　患者空腹血糖及餐后 2小时血糖分别在治疗 (3.7± 1.8)天、 (5 .5± 1.7)天达到控制标准 ,胰岛 β细胞功能显著改善 ,静脉葡萄糖耐量试验各时点的胰岛素分泌及 Homa B值较治疗前明显升高 (P<0 .0 5 ) ,Hom a A指数下降(P<0 .0 5 )。随访 3个月 ,13例患者单纯控制饮食即可维持血糖控制标准 ,糖化血红蛋白由治疗前的 (9.8± 1.2 ) %降至 (6 .3± 0 .7) %。结论　胰岛素短期强化治疗可明显改善及恢复初诊 2型糖尿病患者胰岛素第 1时相分泌 ,不同程度的缓解病情     

A case control study on HDL associated PON1 enzyme level in Northern Indian type 2 diabetes mellitus patients

Aim

To evaluate the serum paraoxonase 1 activity and determine its association with duration in type 2 Diabetes mellitus patients.

Quality of diabetes care predicts the development of cardiovascular events: results of the QuED study

Background and aimIn the context of the QuED Study we assessed whether a quality of care summary score was able to predict the development of cardiovascular (CV) events in patients with type 2 diabetes.Methods and resultsThe score was calculated using process and intermediate outcome indicators (HbA_1c, blood pressure, low-density lipoprotein cholesterol, microalbuminuria) and ranged from 0 to 40. Overall, 3235 patients were enrolled, of whom 492 developed a CV event after a median follow-up of 5 years. The incidence rate (per 1000 person-years) of CV events was 62.4 in patients with a score ≤10, 54.8 in those with a score between 15 and 20, and 39.8 in those with a score >20. In adjusted multilevel regression models, the risk to develop a CV event was 89% greater in patients with a score of ≤10 (rate ratio [RR] = 1.89; 95% confidence interval [CI] 1.43–2.50) and 43% higher in those with a score between 10 and 20 (RR = 1.43; 95% CI 1.14–1.79), as compared to those with a score >20. A difference between centers of 5 points in the mean quality score was associated with a difference of 16% in CV event risk (RR = 0.84; 95% CI 0.72–0.98).ConclusionOur study documented for the first time a close relationship between a score of quality of diabetes care and long-term outcomes.