新诊断2型糖尿病患者一相胰岛素分泌和胰岛素敏感性评估

目的评估新诊断2型糖尿病患者一相胰岛素分泌与胰岛素敏感性。方法对332例新诊断2型糖尿病患者按照精氨酸刺激试验的结果分为胰岛功能正常组和异常组来评估其胰岛素分泌和胰岛素敏感性的状况。结果（1）胰岛功能正常组的体重、体重指数（BMI）、腰围、臀围、股围、空腹血清真胰岛素和甘油三酯均显著高于胰岛功能异常组（均P〈0．01）；（2）校正性别、年龄、BMI和腰臀比后，胰岛功能正常组的真胰岛素增值（△TI）和胰岛素抵抗指数（HOMA—IR）均显著高于胰岛功能异常组（均P〈0．01）；（3）胰岛素分泌功能正常伴胰岛素抵抗的个体，胰岛素分泌功能正常不伴胰岛素抵抗的个体，胰岛素分泌功能缺陷伴胰岛素抵抗的个体和胰岛素分泌功能缺陷不伴胰岛素抵抗的个体分别占总人数的35．11％、5．02％、29．78％和30．09％。结论2型糖尿病个体可分为单纯胰岛功能异常、单纯胰岛素抵抗及胰岛功能异常伴胰岛素抵抗3类，其诊断和治疗需依据此病理生理状态的评估。     

体重指数与胰岛素抵抗及血脂异常的关系（附260例报告）

根据体重指数将260例2型糖尿病患分为3组,观察与胰岛素作用指数及血脂异常之间的关系。结果发现：体重指数正常组,胰岛素作用指数及血脂在正常范围。而超重和肥胖组,胰岛素作用指数下降,甘油三酯和胆固醇增高,高密度脂蛋白下降。体重指数越高,后改变越明显。说明肥胖与胰岛素抵抗及脂代谢紊乱密切相关。     

体重指数与胰岛素抵抗及血脂异常的关系 (附260例报告)

根据体重指数将260例2型糖尿病患者分为3组,观察与胰岛素作用指数及血脂异常之间的关系.结果发现体重指数正常组,胰岛素作用指数及血脂在正常范围.而超重和肥胖组,胰岛素作用指数下降,甘油三酯和胆固醇增高,高密度脂蛋白下降.体重指数越高,后者改变越明显.说明肥胖与胰岛索抵抗及脂代谢紊乱密切相关.     

2型糖尿病微量白蛋白尿与胰岛素抵抗及血脂的关系

目的探讨2型糖尿病患者尿白蛋白排泄与胰岛素抵抗和血脂的关系以及胰岛素抵抗在糖尿病肾病(DN)中发生的作用.方法将80例2型糖尿病患者按尿白蛋白排泄率(UAER)分为正常蛋白尿组和微量白蛋白尿组,对血糖、胰岛素、胰岛素敏感指数(1SI)、血脂、血尿酸、纤维蛋白原、糖化血红蛋白、肌酐等代谢指标进行比较分析,并对UAER与相关因素进行多元回归分析.结果两组间ISI、甘油三酯、尿酸、高密度脂蛋白水平存在显著性差异(P＜0.05或P＜0.01);Persean相关显示UAER与ISI、甘油三酯、低密度脂蛋白、尿酸、糖化血红蛋白、年龄相关;在以UAER为自变量的线性多元回归分析中显示在P＜0.05水平有ISI、甘油三酯、低密度脂蛋白和肌酐进入回归模型.结论在2型糖尿病患者合并白蛋白尿时存在胰岛素敏感性减低和脂代谢紊乱,胰岛素抵抗和脂代谢紊乱对MAU的产生有重要作用.     

2型糖尿病合并非酒精性脂肪肝患者的胰岛素、血脂及脂联素的变化

对2型糖尿病合并非酒精性脂肪肝患者的脂联素、空腹血糖、胰岛素及甘油三酯、胆固醇进行监测,并与不合并非酒精性脂肪肝2型糖尿病组及正常对照组进行比较.结果糖尿病组脂联素、胰岛素敏感指数较正常对照组降低(P均<0.05);合并脂肪肝组与不合并脂肪肝组比较,脂联素水平、胰岛素敏感指数明显降低,甘油三酯、胆固醇水平明显增高;差异均有统计学意义(P均<0.05).认为2型糖尿病合并非酒精性脂肪肝与脂联素、胰岛素抵抗、脂代谢紊乱有关.     

中国新诊断2型糖尿病患者胰岛素分泌和胰岛素抵抗特点调查

胰岛素抵抗与胰岛素分泌缺陷是2型糖尿病的主要病理生理学缺陷。绝大多数的欧美2型糖尿病患者均肥胖，而肥胖所致的胰岛素抵抗被认为是导致该人群发生2型糖尿病的最主要因素。但是亚洲2型糖尿病患者中，肥胖者还不到半数。胰岛素抵抗抑或胰岛素分泌功能缺陷是亚洲糖尿病患者早期发病的主要因素尚不明了。本文调查了解中国新诊断的2型糖尿病人群胰岛素抵抗和胰岛素分泌功能的状况并观察格列齐特（达美康缓释片）强化治疗对其的影响。     

胰岛素抵抗与糖尿病脂代谢紊乱关系探讨

糖尿病(DM)不仅是糖代谢异常，而且是糖脂病。脂代谢紊乱对糖尿病及并发症发生有重要的作用。许多研究证明，肥胖和胰岛素抵抗与糖尿病有着十分重要的关系，这些病人早在糖代谢出现异常之前，就存在脂类代谢紊乱，我们观察研究了本院门诊和住院的108例2型糖尿病病人胰岛素敏感指数(IAI)与血脂及脂蛋白(a)水平的关系，现总结报告如下。     

60岁及以上非糖尿病人群代谢紊乱集簇与血清铁蛋白水平的关系

目的探讨60岁及以上人群代谢紊乱集簇与血清铁蛋白水平的关系。方法2008年6至7月人选上海市闵行区汀川社区60岁以上非糖尿病老年人3416名,测定血压、血脂、血糖、空腹胰岛素、尿白蛋白／肌酐比值、血清铁蛋白,采用稳态模型评价胰岛素抵抗指数和胰岛β细胞功能,计算胰岛素敏感指数及处置指数。根据上述结果将糖耐量正常者分为4组：胰岛素敏感＋胰岛素分泌减退组（SF2组,n=514）;胰岛素敏感＋胰岛素分泌正常组（SF,组,n=1049）;胰岛素抵抗＋胰岛素分泌减退组（SF,组,n=17）;胰岛素抵抗＋胰岛素分泌正常组（SF4组,n=516）。另根据代谢综合征诊断标准将全部研究对象分为代谢紊乱0组分组（MS0组,n=1564）、代谢紊乱1组分组（MS1组,n=1603）、代谢紊乱2组分组（MS2组,n=170）、代谢紊乱93组分组（MS3组,n=79）。各胰岛功能组及代谢紊乱组分别进行血清铁蛋白水平相关性分析。计数资料比较采用X^2检验,组间比较采用方差分析（Bonferroni法）。血清铁蛋白与各指标的相关性研究采用Spearman相关分析和多元逐步回归分析。结果随着代谢紊乱组分数目增加,血清铁蛋白、体质指数、体脂含量、收缩斥、舒张压、空腹血糖、总胆固醇、甘油三酯、尿白蛋白／肌酐比值、空腹胰岛素、胰岛素抵抗指数逐渐升高,胰岛素敏感指数及处置指数逐渐下降。高甘油三酯组、肥胖组患者血清铁蛋白水平分别高于正常甘油三酯组、正常体质量组。各代谢紊乱组（高甘油三酯、高胆同醇、高血压和肥胖组）中男性铁蛋白水平均高于女性。Spearman相关分析显示,空腹血糖、2h血糖、空腹胰岛素、体质指数、甘油三酯、总胆㈨醇、胰岛素抵抗指数、胰岛β细胞功能与血清铁蛋白呈显著正相关（P〈0．01）,胰岛素处置指数、胰岛素敏感指数与血清铁蛋白呈显著负相关（P〈0．01）。多元逐步回归分析显示,胰岛素抵抗指数、总胆固醇、体质指数、甘油三酯是影响老年代谢紊乱者血清铁蛋白水平的独立危险因素。结论60岁及以上人群血清铁蛋白升高与代谢紊乱集簇显著相关,血脂异常、肥胖和胰岛素抵抗是该年龄段人群血清铁蛋白升高的主要危险因素。     

Ⅱ型糖尿病家系中一级亲属的脂质代谢紊乱与胰岛素抵抗

为研究II型糖尿病家系中一级亲属的脂质变化和胰岛素抵抗，对25个II型糖尿病家系中非糖尿病一级亲属，糖耐量减低者，糖尿病患者进行了空腹血糖，空腹胰岛素，总胆固醇，甘油三酯和高密度脂蛋白测定，根据公式计算低密度脂蛋白及胰岛素敏感指数，并与家系中非糖尿病非糖耐量减低同胞的配偶进行了比照，结果发现，一级亲属，糖耐量减低者，糖尿病患者甘油三酯较正常对照组高，高密度脂蛋白，胰岛素敏感指数较正常对照组低，此结果提示，II型糖尿病患者的一级亲属在未患糖耐量减低和糖尿病之前存在脂代谢紊乱和胰岛素抵抗。     

2型糖尿病胰岛素抵抗与颈动脉内膜厚度相关性分析

目的研究2型糖尿病胰岛素抵抗与颈动脉内膜中层厚度的关系。方法对该院2型糖尿病病人均做颈动脉彩超测定颈动脉内膜中层厚度(IMT),根据IMT分为正常组(IMT<0.9 mm)58例、IMT增厚组(IMT≥0.9 mm)63例,受试者均隔夜空腹8 h以上取静脉血检测空腹血糖、空腹胰岛素、低密度脂蛋白、高密度脂蛋白、总胆固醇、甘油三酯、糖化血红蛋白水平,测量身高、体重,计算BMI。同时计算稳态模型胰岛素抵抗(HOMA-IR)指数,分析2型糖尿病患者颈动脉IMT与胰岛素抵抗、血糖、血脂等因素之间的关系。结果 2型糖尿病患者颈动脉IMT主要与年龄、FINS、HOMA-IR有关,IMT增厚组FINS和HOMA-IR明显高于IMT正常组,说明胰岛素抵抗程度、代偿性高胰岛素血症与IMT增厚呈正相关。结论胰岛素抵抗可能与颈动脉内膜增厚有关。     

Precipitin reactions between insulin,proinsulin, insulin chains and insulin antibody

Summary Insulin antibody was produced in guinea pigs and the precipitins tested by double diffusion in agarose gel. Pork, beef and monocomponent insulin produced precipitin lines. Proinsulin also produced a precipitin line with these antisera but no lines appeared with either the A-chain or the B-chain of insulin. There was good correlation between the precipitin titre and the radioimmunoassay titre.     

Clinical utility of insulin and insulin analogs

Diabetes is a pandemic disease characterized by autoimmune, genetic and metabolic abnormalities. While insulin deficiency manifested as hyperglycemia is a common sequel of both Type-1 and Type-2 diabetes (T1DM and T2DM), it does not result from a single genetic defect—rather insulin deficiency results from the functional loss of pancreatic β cells due to multifactorial mechanisms. Since pancreatic β cells of patients with T1DM are destroyed by autoimmune reaction, these patients require daily insulin injections. Insulin resistance followed by β cell dysfunction and β cell loss is the characteristics of T2DM. Therefore, most patients with T2DM will require insulin treatment due to eventual loss of insulin secretion. Despite the evidence of early insulin treatment lowering macrovascular (coronary artery disease, peripheral arterial disease and stroke) and microvascular (diabetic nephropathy, neuropathy and retinopathy) complications of T2DM, controversy exists among physicians on how to initiate and intensify insulin therapy. The slow acting nature of regular human insulin makes its use ineffective in counteracting postprandial hyperglycemia. Instead, recombinant insulin analogs have been generated with a variable degree of specificity and action. Due to the metabolic variability among individuals, optimum blood glucose management is a formidable task to accomplish despite the presence of novel insulin analogs. In this article, we present a recent update on insulin analog structure and function with an overview of the evidence on the various insulin regimens clinically used to treat diabetes.     

Treatment of insulin lipoatrophy with monocomponent insulin

Summary A female diabetic with severe insulininduced lipoatrophy was successfully treated with a monocomponent (MC) Lente preparation. This patient was studied for over 6 years and, during periods of treatment with various insulins of different purity, a variety of reactions was observed in the adipose tissue. Evidence is presented that lipoatrophy may be caused by insulin impurities. Lipoatrophy occurring after treatment with recrystallized, mixed species Lente insulin was substantially reduced after treatment with 10 times recrystallized porcine Lente, but recurred on 4 times recrystallized beef Lente, also in areas where beef Lente was not injected. Beef insulin impurities seem more prone to produce lipoatrophy than pork insulin impurities. It is suggested that MC-insulin is the treatment of choice for this condition.     

ATP sensitizes the insulin receptor to insulin

Insulin receptor with high insulin binding and tyrosine kinase activities has been prepared from human placenta. Based on a molecular mass of 306 kDa for the receptor (the value obtained from the sum of the amino acid residues), this preparation is capable of binding 1.48 mol of insulin per mol of receptor. The receptor is free from phosphatase and ATPase activity and is not stimulated by sodium vanadate. Autophosphorylation is linear with respect to receptor concentration, and the 32P incorporated is stable even in the presence of a 100-fold excess of unlabeled ATP. The Km for ATP is 208 microM. N-Ethylmaleimide inhibits autophosphorylation. Alkylation with 3H-labeled N-ethylmaleimide results in the incorporation of 1.13 +/- 0.37 mol of N-ethylmaleimide per mol of insulin binding activity exclusively into the beta subunit of the receptor. The nonhydrolyzable ATP analog adenosine 5'-[beta,gamma-imido]triphosphate stimulates autophosphorylation of the receptor, an effect that is evident at ATP concentrations below 1 mM. The stimulatory effect of adenosine 5'-[beta,gamma-imido]triphosphate is the result of increasing the binding of insulin to the alpha subunit, and this reflects itself in a shift to the left of the insulin dose-response curve for autophosphorylation. The same is true for ATP. As a consequence, it is now possible to reconcile the concentration of insulin necessary for stimulating the autophosphorylation reaction with physiological levels and with the levels of insulin required for its classical biological effects.