甘精胰岛素联合格列美脲强化治疗初发2型糖尿病疗效观察

目的探讨甘精胰岛素联合格列美脲强化治疗初发2型糖尿病临床疗效。方法对照组在常规治疗基础上加用甘精胰岛素治疗;研究组在对照组治疗基础上加用来格列美脲。两组患者治疗过程中均根据血糖变化情况及时调整给药剂量,记录其治疗前后空腹血糖变化情况及治疗过程中低血糖发生率,给予统计学分析并得出结论。结果两组初发2型糖尿病患者经不同方案给药治疗后,空腹血糖检测值均较治疗前显著降低,但研究组患者下降幅度更为明显(<0.05)。结论应用甘精胰岛素联合格列美脲治疗初诊2型糖尿病患者可显著降低其血糖含量,治疗有效性及安全性均较为满意,保障患者生活质量。     

甘精胰岛素与格列美脲联合治疗口服降糖药控制不佳 2型糖尿病的疗效

目的 观察甘精胰岛素与格列美脲联合治疗口服降糖药控制不佳2型糖尿病的疗效。方法 选择2018年6月~2019年3月在我院诊治的90例口服降糖药控制不佳2型糖尿病患者作为研究对象,随机分为对照组和观察组,各45例,对照组采用格列美脲治疗,观察组在对照组基础上联合甘精胰岛素治疗,对比两组临床治疗疗效、空腹血糖（FPG）、餐后2h血糖（2hPG）、糖化血红蛋白（HbA1c）水平以及低血糖发生情况。结果 治疗后,观察组治疗总有效率（93.33%）与对照组治疗总有效率（91.11%）比较,差异无统计学意义（P＞0.05）。治疗后两组FPG、2hPG、HbA1c水平均较治疗前降低,差异有统计学意义（P＜0.05）;观察组FPG、2hPG与对照组比较,差异无统计学意义（P＞0.05）;观察组HbA1c与对照组比较,差异有统计学意义（P＜0.05）;观察组低血糖发生率（17.78%）低于对照组（35.56%）,差异有统计学意义（P＜0.05）。结论 口服降糖药控制不佳2型糖尿病患者采用甘精胰岛素联合格列美脲治疗疗效理想,且可降低治疗期间低血糖发生率,安全性高,值得临床应用。     

甘精胰岛素联合二甲双胍治疗2型糖尿病的疗效

目的 观察甘精胰岛素联合二甲双胍治疗2型糖尿病的临床疗效。方法 选取2015年1月~2018年12月于我院内分泌科诊治的应用甘精胰岛素联合二甲双胍治疗的2型糖尿病患者48例设为观察组,另选同期单独应用甘精胰岛素治疗2型糖尿病患者48例设为对照组,比较两组临床治疗总有效率、空腹血糖（FBG）、餐后2 h血糖（PBG）、糖化血红蛋白（HbAlc）、平均血糖达标时间以及临床不良反应情况。结果 观察组治疗总有效率为93.75%,高于对照组的81.25%（P＜0.05）;治疗后两组FBG、PBG、HbAlc均低于治疗前,且观察组低于对照组（P＜0.05）;观察组血糖达标时间为（5.71±1.15）d,短于对照组的（9.90±2.16）d（P＜0.05）;观察组不良反应发生率为6.25%,低于对照组的16.67%（P＜0.05）。结论 甘精胰岛素联合二甲双胍治疗2型糖尿病,可促进血糖水平控制,提高治疗效果,且用药安全性高,具有重要的临床应用价值。     

艾塞那肽联合甘精胰岛素对肥胖2型糖尿病效果观察

目的：对艾塞那肽联合甘精胰岛素在2型糖尿病患者中的治疗效果进行观察。方法选取我院2012年4月~2014年4月68例2型肥胖糖尿病患者,将所有患者分成两组,每组34例,1组作为对照组进行胰岛素治疗,2组作为实验组进行艾塞那肽联合甘精胰岛素治疗。治疗后对两组患者的空腹血糖、餐后2h血糖、血脂等情况进行比较。结果实验组平均空腹血糖为(5.83±0.71)mmol/L,餐后2h血糖为(7.32±1.05)mmol/L,糖化血红蛋白水平为(6.15±0.72)%;对照组患者空腹血糖水平为(11.26±1.34)mmol/L,餐后2h血糖为(14.31±2.06)mmol/L,糖化血红蛋白水平(9.93±1.51)%,P<0.05。两组患者胆固醇、甘油三酯、低密度脂蛋白水平存在明显差异,但高密度脂蛋白水平差异不大。结论：艾塞那肽联合甘精胰岛素在2型糖尿病患者中的治疗效果较为显著,能够有效的对患者血糖进行控制,降低患者发病率。     

甘精胰岛素联合诺和锐强化治疗初诊2型糖尿病的疗效观察

目的 探讨胰岛素强化治疗初诊2型糖尿病的最佳方案.方法 将38例初诊的2型糖尿病随机分组为A组甘精胰岛素组(19例),B组中性鱼精蛋白锌胰岛素组NPH(19例),分别三餐前联用门冬胰岛素,观察两组病人治疗前后各项临床指标变化.结果 两组治疗方案均能较好的控制血糖,甘精胰岛素组血糖达标时间、低血糖发生率、胰岛素总量低于NPH组(P<0.01).结论 甘精胰岛素联合门冬胰岛素是初诊2型糖尿病强化治疗的首选方案.     

甘精胰岛素用在2型糖尿病合并上消化道出血的生物学探讨

目的通过分析甘精胰岛素治疗2型糖尿病合并上消化道出血急性期血糖控制的优势,评价其生物学特点。方法选取46例上消化道出血合并糖尿病的患者,随机分为两组:A组23例,治疗方法采用静脉点滴葡萄糖时加用中和量短效胰岛素,并于早晨8时皮下注射甘精胰岛素,根据空腹血糖调整用量;B组23例,静脉点滴葡萄糖时加用中和量短效胰岛素,根据随机血糖结果调整短效胰岛素用量。两组随机血糖控制目标值均在10.0mmol/L以下,且内科止血治疗措施基本相同。通过观察患者黑便、胃管内抽取物、低血糖症状、日均血糖的平均指标、胰岛素用量和便潜血转阴时间等指标,评价甘精胰岛素在治疗中的优势,并进行生物学特性分析。结果 A组日均血糖(9.6±1.1)mmol/L,甘精胰岛素总量为(16±1.2)U,中和量短效胰岛素用量为(20±3.5)U,未出现低血糖现象;B组日均血糖值控制在(11.6±0.7)mmol/L,短效胰岛素用量平均(50±4.2)U,有3人出现低血糖现象,两组间有显著统计学差异,P0.05;两组便潜血转阴时间相同。结论提示在消化道出血急性期间,用甘精胰岛素控制血糖,病人低血糖反应少,胰岛素用量小,此源于其良好的生物学特性。     

利拉鲁肽联合甘精胰岛素治疗2型糖尿病患者临床疗效

目的:分析2型糖尿病(T2DM)患者采取利拉鲁肽联合甘精胰岛素治疗的临床疗效。方法:选取本院于2016-02-2018-12期间收治的88例T2DM患者,随机分为两组,利拉鲁肽联合甘精胰岛素组作为研究组(n=46),单纯采用甘精胰岛素治疗组作为对照组(n=42),比较两组治疗后空腹血糖(FPG)、餐后2h血糖(2hPG)和糖化血红蛋白(HbAlc)水平变化,甘精胰岛素日用量、血糖达标时间及低血糖发生率。结果:与同组治疗前比较,两组患者治疗后FPG、2hPG、HbAlc水平均降低(P0.01);研究组治疗后FPG、2hPG、HbAlc、甘精胰岛素日使用剂量均低于对照组,血糖达标时间短于对照组,且低血糖发生率低于对照组,差异均有统计学意义(P0.01)。结论:利拉鲁肽联合甘精胰岛素联合治疗T2DM临床疗效显著,能改善血糖水平,减少胰岛素用量,缩短血糖达标时间以及降低不良反应发生率,值得临床推广应用。     

格列美脲联合甘精胰岛素治疗2型糖尿病12周后对血糖水平和体重指数的影响

目的:观察格列美脲联合甘精胰岛素治疗2型糖尿病(T2DM)对血糖水平和体重指数(BMI)的影响。方法:选取本院2018-01-2018-06 T2DM患者50例,随机平分为对照组和试验组,对照组给予单纯注射甘精胰岛素治疗(0.2U/kg·d),试验组给予口服格列美脲(2-4mg/次,1次/天)联合注射甘精胰岛素治疗,12周后,分析比较两组患者空腹血糖(FPG)、餐后2h血糖(2hPG)、糖化血红蛋白(HbA1c)以及BMI等指标的水平变化。结果:治疗后两组FPG、2hPG、HbA1c和BMI水平均较同组治疗前降低(P0.01),且试验组血糖水平及其血糖达标率均优于对照组(P0.01)。结论:格列美脲联合甘精胰岛素治疗T2DM能有效降低血糖及BMI指标,提高血糖达标率。     

瑞格列奈联合甘精胰岛素治疗糖尿病60例临床观察

目的 探讨瑞格列奈联合甘精胰岛素治疗糖尿病的临床疗效.方法 选取本院2009年1月～10月收治的糖尿病患者120例,随机分为两组,每组各60例.治疗组采用甘精胰岛素联合瑞格列奈治疗,对照组采用胰岛素泵持续皮下注射治疗,对比观察两组病例的临床疗效.结果 两组强化治疗前一般情况差异无统计学意义,治疗后两组患者胰岛B细胞功能均得到明显改善.结论 瑞格列奈联合甘精胰岛素治疗口服降糖药控制不良的糖尿病患者可改善血糖控制水平,提高治疗达标率,同时低血糖风险较低,值得临床推广使用.     

胰岛素治疗46例2型糖尿病临床分析

目的 观察胰岛素治疗对2型糖尿病患者血糖控制的效果。方法：对46例2型糖尿病患者短期皮下注射胰岛素强化治疗后继续胰岛素联合口服降糖药物治疗，边用药、边监测血糖，观察用药7-14天，并跟踪半年。结果 血糖达到理想控制状态，胰岛素治疗后患者的空腹血糖、餐后2小时血糖、HbA，C明显低于治疗前，P〈0．01。其中7例只需饮食、运动治疗便可获得良好的血糖控制。结论 2型糖尿病患者在糖尿痛教育、饮食控制、运动疗法、监测血糖的基础上，通过适当的胰岛素治疗，其病情均可得到良好的控制，并保护健存的胰岛B细胞功能，且副作用轻微。     

Comparative efficacy of exenatide versus insulin glargine on glycemic control in type 2 diabetes mellitus patients inadequately treated with metformin monotherapy

PurposeComparative efficacy of exenatide versus insulin glargine primarily on glucemic control, and secondarily on body mass index (BMI), lipid profile and blood pressure, in type 2 diabetes mellitus (T2DM) patients suboptimally treated with metformin monotherapy.Material/MethodsForty-seven inadequately treated T2DM patients on metformin assigned to exenatide (n=18) or insulin glargine (n=29) for 26 weeks. Glycosylated hemoglobin (HbA1c), serum lipids, BMI, systolic and diastolic blood pressure, and adverse events, including episodes of hypoglycemia and gastrointestinal symptoms, were recorded.ResultsEither treatment had a similar favorable mean reduction in HbA1c. However, more patients in exenatide group achieved HbA1c ≤ 7% at the 26th week compared with insulin glargine group (p=0.036). Insulin glargine group had significantly more episodes of hypoglycemia compared with exenatide group (p=0.039). Gastrointestinal adverse events were non-significantly higher in the exenatide group. A significantly greater BMI reduction was observed in exenatide group, whereas BMI was not altered in insulin glargine group. Total and LDL cholesterol (p=0.012), and triglycerides (p=0.016) significantly decreased, whereas HDL cholesterol increased (p=0.021) in the exenatide group, whereas only total cholesterol decreased in insulin glargine group. Changes in systolic and diastolic blood pressure were insignificant in both groups.ConclusionsExenatide provided similar reduction in HbA1c, but fewer episodes of hypoglycemia, compared with insulin glargine. Exenatide had also a favorable effect on weight loss, although more gastrointestinal adverse events. Exenatide may provide a justified alternative in second line treatment of T2DM, but more trials are required to elucidate its long-term safety and cost-effectiveness.     

Plasma adiponectin and insulin resistance in Korean type 2 diabetes mellitus

Insulin resistance, which implies impairment of insulin signaling in the target tissues, is a common cause of type 2 diabetes. Adipose tissue plays an important role in insulin resistance through the dysregulated production and secretion of adipose-derived proteins, including tumor necrosis factor-alpha, plasminogen activator inhibitor-1, leptin, resistin, angiotensinogen, and adiponectin. Adiponectin was estimated to be a protective adipocytokine against atherosclerosis, and also to have an anti-inflammatory effect. In this study, the relationship between fasting plasma adiponectin concentration and adiposity, body composition, insulin sensitivity (ITT, HOMAIR, QUICK), lipid profile, fasting insulin concentration were examined in Korean type 2 diabetes. The difference in the adiponectin concentrations was also examined in diabetic and non-diabetic subjects, with adjustment for gender, age and body mass index. 102 type 2 diabetics and 50 controls were examined. After a 12-h overnight fast, all subjects underwent a 75 gram oral glucose tolerance test. Baseline blood samples were drawn for the determinations of fasting plasma glucose, insulin, adiponectin, total cholesterol, triglyceride, LDL-cholesterol, and HDL-cholesterol. The body composition was estimated using a bioelectric impedance analyzer (Inbody 2.0). The insulin sensitivity was estimated using the insulin tolerance test (ITT), HOMAIR and QUICK methods. In the diabetic group, the fasting adiponectin concentrations were significantly lower in men than in women. They were negatively correlated with BMI (r=-0.453), hip circumference (r=-0.341), fasting glucose concentrations (r=-0.277) and HOMAIR (r= -0.233). In addition, they were positively correlated with systolic blood pressure (r=0.321) and HDL-cholesterol (r= 0.291). The systolic blood pressure and HDL-cholesterol were found to be independent variables, from a multiple logistic regression analysis, which influenced the adiponectin concentration. Compared with the non-diabetic group, the adiponectin concentrations were significantly lower in the diabetic group, with the exception of obese males. In conclusion, the plasma adiponectin concentrations were closely related to the insulin resistance parameters in Korean type 2 diabetic patients.     

Fetal type lymphocytes in insulin dependent diabetes mellitus.

CD5+ B and gamma/delta T lymphocytes constituting a major population in the fetus and newborn infant, represent two small subsets of the B and T lymphocyte compartment in healthy adults. There is evidence for their potential involvement and relative expansion in autoimmune disorders. In insulin-dependent diabetes mellitus (IDDM) CD5+ B lymphocyte counts have been found to be increased or normal. The aim of our study was to determine the percentage of both "fetal type" lymphocyte subsets in peripheral blood of 22 recently diagnosed children with IDDM, in that of 13 high risk subjects (islet cell antibody (ICA) positive non-diabetic Ist degree relatives of diabetic children) and in 43 healthy controls. The percentage of gamma/delta TCR+ cells and of CD5+ B lymphocytes was found to be significantly (p < 0.0001 and p = 0.03, respectively) higher in the diabetic and prediabetic groups as compared to controls. Young children with IDDM associated antibodies carry a higher risk of developing clinical IDDM than older individuals. In our hands, the percentage of both CD5+ B and gamma/delta T lymphocytes was higher in the younger population. However, age-dependent decrease for both lymphocyte subpopulations in IDDM-prediabetic patients was less than in healthy controls. Since the above subpopulations are supposed to play a role in immune response to conserved structures, these observations would suggest a higher capacity of older individuals to 'natural autoimmunity" and would explain at least in part the increased risk of antibody positive young children to develop IDDM.     

Fulminant type 1 diabetes mellitus observed in insulin receptor substrate 2 deficient mice

The objective of this study was to characterise the fulminant type 1 diabetes mellitus (DM) accompanying abrupt hyperglycaemia and ketonuria observed in insulin receptor substrate 2 (IRS2)-deficient mice. IRS2-deficient mice backcrossed onto the original C57BL/6J:Jc1 background (B6J-IRS2(-/-) mice) for more than 10 generations were used. Eight male IRS2-deficient mice with ketonuria and abrupt increase in plasma glucose concentrations over 25 mmol/l were used as the fulminant type 1 diabetic mice (diabetic mice) and 8 male IRS2-deficient mice (8 weeks old) without glycosuria were used as the control mice. Plasma metabolite, immunoreactive insulin (IRI) and C-peptide concentrations, hepatic energy metabolism related enzyme activities and histopathological change in pancreatic islets were investigated. The diabetic mice showed significantly higher plasma glucose and cholesterol concentrations and lower plasma IRI and C-peptide concentrations than the control mice. In livers of the diabetic mice, glycolytic and malate-aspartate shuttle enzyme activities decreased significantly and gluconeogenic, lipogenic and ketone body synthesis enzyme activities increased significantly compared to those in the control mice. The pancreatic islets of the diabetic mice decreased significantly in size and number of beta cells. The diabetic IRS2-deficient mice did not show the islet-related antibodies observed in the diabetic NOD mice in their sera. The characteristics of the diabetic IRS2-deficient mice resembled those of the human nonautoimmune fulminant type 1 DM. IRS2-deficient mice may be a useful animal model for studying the degradation mechanism of pancreatic beta cells in the process of development of fulminant type 1 DM.     

Association of FADS2 rs174575 gene polymorphism and insulin resistance in type 2 diabetes mellitus

BackgroundMany risk factors contribute to the pathogenesis of diabetes. Gene and lifestyle factors are considered to be the major contributors. A dietary pattern is attributed to be one of the lifestyle risk factors favoring diabetes. The present study aims to find an association between fatty acid desaturase (FADS) gene polymorphism and glycemic profile in type 2 diabetes mellitus (T2DM).MethodologyA total of 429 subjects were included in the study on the basis of inclusion and exclusion criteria, of which 213 and 216 subjects were diabetic and control, respectively. Body mass index was calculated. Fasting plasma glucose, glycated hemoglobin (HbA1c) and insulin were measured using commercially available kits. rs174575 of FADS2 was selected based on previous publications and identified using the dbSNP database. To compare the biochemical parameters with the genotype, the following three models were used: additive model (CC vs CG vs GG), dominant model (CC + CG vs GG), and recessive model (CC vs CG + GG).Results and DiscussionFBS, HbA1c, insulin, HOMA-IR, and HOMA-B exhibited a high and statistically significant difference between subjects and controls. The three models exhibited a statistically significant difference between FBS, HOMA-IR, and HOMA- B (p<0.05).ConclusionThe distribution of rs174575 genotype differed significantly between the subjects and controls in the present study. The study revealed that genetic variation in FADS2 is an additional facet to consider while studying the risk factors of T2DM.     

Reference value and cut-off value for diagnosis of insulin resistance in type 2 diabetes mellitus

The homeostasis model assessment-insulin resistance(HOMA-IR) index has been proposed to assess insulin resistance, which plays an important role in the pathogenesis of type 2 diabetes mellitus. However, it has not generally introduced into the outpatient care in Japan, because of lack in definite reference values. In this paper we studied the precision in the assay of immuno-reactive insulin and then the HOMA-IR index was determined in 90 healthy individuals and 281 type 2 diabetic patients. The reference value was calculated to be 1.77 +/- 0.44(mean +/- SD) in healthy individuals without obesity. Receiver operating characteristic curve analysis gave the cut-off values discriminating between healthy and diabetic subjects to be 2.53, 3.50 and 3.00 in non-obese, obese and total individuals, respectively. These values should be available for the diagnosis of insulin resistance in type 2 diabetes mellitus.