胰岛素对糖尿病兔牙槽骨缺损修复的影响

目的：探讨胰岛素对糖尿病兔牙槽骨缺损修复治疗的效果,为糖尿病所致的牙周炎提供临床治疗的依据,方法：40只大耳白兔随机分为4组：A组制备健康兔的牙槽骨缺损;B组为胰岛素组,制备健康兔牙槽骨缺损后,用胰岛素治疗;C组为糖尿病组,制备糖尿病兔牙槽骨缺损;D组为糖尿病胰岛素治疗组,制备糖尿病兔牙槽骨缺损后,用胰岛素治疗。每组10只,缺损制备后4、8周各处死5只,对各组成骨情况进行组织学观察及测定。结果：组织学观察A、B、D组修复区可见大量新骨形成,以B组为显著;C组仅见少许成骨,多为纤维组织。新生骨面积比和成骨细胞数在4、8周时均为D组大于c组,B组大于A组,组间差异有统计学意义（P〈0．05）。证明应用胰岛素促进糖尿病兔缺损牙槽骨形成新骨的效果明显。结论：胰岛素能够促进糖尿病兔牙槽骨缺损的戍骨,为,临床上治疗糖尿病并发牙周炎提供一种新的手段。     

舒血宁注射液联合前列地尔注射液治疗糖尿病周围血管病变的临床疗效观察

目的:观察联合应用舒血宁注射液与前列地尔注射液治疗糖尿病周围血管病变的临床疗效和安全性.方法:以药物降低血糖为基础,舒血宁注射液与前列地尔注射液联合应用于78例糖尿病周围血管病变患者,14天为一个疗程,患者在治疗前后行双下肢动脉彩色多普勒超声检测.结果:治疗后,患者的股动脉、胭动脉及足背动脉管径较治疗前显著增加,血流速度较治疗前明显加快(P＜0.05).间歇性跛行症状好转,肢体皮温上升,足背动脉开始有搏动.治疗中无不良反应,亦无出血倾向.结论:舒血宁注射液与前列地尔注射液联合治疗糖屎病周围血管病变是一种安全有效的治疗方法.     

The association between serum selenium and gestational diabetes mellitus: A systematic review and meta-analysis

BackgroundResults of the studies about association between serum selenium concentration and gestational hyperglycemia are inconsistent. Some studies have demonstrated that women with gestational diabetes mellitus (GDM) have lower Se concentrations while contrary results are reported in other studies.AimThe aim of this study is to compare the serum Se concentration in women with GDM and normoglycemic pregnant women via a systematic review and meta-analysis.MethodsA computerized literature search on four databases (PubMed, Cochrane register of control trials, Scopus and Google scholar) was performed from inception through August 2013. Necessary data were extracted and random effects model was used to conduct the meta-analysis.ResultsSix observational studies (containing 147 women with GDM and 360 normoglycemic pregnant women) were found, which had compared serum Se concentration in women suffering from GDM with normal pregnant ones. Our meta-analysis revealed that serum Se concentration was lower in women with GDM compared to normoglycemic pregnant women (Hedges = −1.34; 95% CI: −2.33 to −0.36; P < 0.01). Stratified meta-analysis demonstrated that concentration of Se in the sera of women with GDM was lower than normal pregnant women both in second and third trimesters, but the result was not significant in second trimester (second trimester: Hedges = −0.68; 95% CI: −1.60−0.25; P = 0.15, third trimester: Hedges = −2.81; 95% CI: −5.21 to −0.42; P < 0.05). It was also demonstrated that serum Se status was lower in pregnant women with impaired glucose tolerance (IGT) compared to normoglycemic pregnant women (Hedges = −0.85; 95% CI: −1.18 to −0.52).ConclusionThe available evidences suggest that serum Se concentration is significantly lower in pregnant women with gestational hyperglycemia compared to normal pregnant women.     

Ameliorative effect of vanadyl(IV)–ascorbate complex on high-fat high-sucrose diet-induced hyperglycemia,insulin resistance,and oxidative stress in mice

There is mounting evidence demonstrating causative links between hyperglycemia, oxidative stress, and insulin resistance, the core pathophysiological features of type 2 diabetes mellitus. Using a combinational approach, we synthesized a vanadium–antioxidant (i.e., l-ascorbic acid) complex and examined its effect on insulin resistance and oxidative stress. This study was designed to examine whether vanadyl(IV)-ascorbate complex (VOAsc) would reduce oxidative stress, hyperglycemia, and insulin resistance in high-fat high-sucrose diet (HFSD)-induced type 2 diabetes in mice. Male C57BL/6J mice were fed a HFSD for 12 weeks to induce insulin resistance, rendering them diabetic. Diabetic mice were treated with rosiglitazone, sodium l-ascorbate, or VOAsc. At the end of treatment, fasting blood glucose, fasting serum insulin, homeostasis model assessment-insulin resistance index, and serum adipocytokine levels were measured. Serum levels of nitric oxide (NO) parameters were also determined. The liver was isolated and used for determination of malondialdehyde, reduced glutathione, and catalase levels, and superoxide dismutase and glutathione peroxidase activities. VOAsc groups exhibited significant reductions in serum adipocytokine and NO levels, and oxidative stress parameters compared to the corresponding values in the untreated diabetic mice. The results indicated that VOAsc is non-toxic. In conclusion, we identified VOAsc as a potentially effective adjunct therapy for the management of type 2 diabetes.     

Increased resistin may suppress reactive oxygen species production and inflammasome activation in type 2 diabetic patients with pulmonary tuberculosis infection

Although it has been known for decades that patients with type 2 diabetes mellitus (DM) are more susceptible to severe tuberculosis (TB) infection, the underlying immunological mechanisms remain unclear. Resistin, a protein produced by immune cells in humans, causes insulin resistance and has been implicated in inhibiting reactive oxygen species (ROS) production in leukocytes. Recent studies suggested that IL-1β production in patients with Mycobacteria tuberculosis infection correlates with inflammasome activation which may be regulated by ROS production in the immune cells. By investigating the level of resistin in different patient groups, we found that serum resistin levels were significantly higher in severe TB and DM-only groups when compared with mild TB cases and healthy controls. Moreover, elevation of serum resistin correlated with impairment of ROS production of neutrophils in patients with both DM and TB. In human macrophages, exogenous resistin inhibits the production of ROS which are important in the mycobacterium-induced inflammasome activation. Moreover, macrophages with defective ROS production had poor IL-1β production and ineffective control of mycobacteria growth. Our results suggest that increased resistin in severe TB and DM patients may suppress the mycobacterium-induced inflammasome activation through inhibiting ROS production by leukocytes.     

Determination of potential role of antioxidative status and circulating biochemical markers in the pathogenesis of ethambutol induced toxic optic neuropathy among diabetic and non-diabetic patients

The present study was designed to explore the antioxidative status and circulating biochemical markers having a potential role in the pathogenesis of ethambutol (EMB) induced toxic optic neuropathy (TON) among diabetic and non-diabetic patients.Fifty patients under complete therapy of EMB for tuberculosis were included in the present study. Inclusion criteria for patients were to receive EMB everyday during treatment, a dose of 25 mg/kg for initial 2 months and 15 mg/kg during the rest of therapy period. We conducted color vision and visual acuity test for all patients.Fifteen out of fifty EMB induced TON patients, were found to be diabetic. Color vision and visual acuity test results were evaluated for diabetic and non-diabetic as well as twenty age matched controls. The results demonstrated a significant pattern of circulating biochemical markers between the studied groups. Data regarding hematological (RBC, p value = 0.02; Hemoglobin, p value = 0.02), hepatic (total bilirubin, p value = 0.01), renal (urea, p value = 0.03; creatinine, p value = 0.007), lipid (total cholesterol, p value = 0.01; total triglycerides, p value = 0.03) and antioxidative (superoxide dismutase, p value = 0.005; glutathione, p value = 0.02; catalase, p value = 0.02) profile showed a highly significant difference among the studied groups specially patients with diabetes. Malondialdehyde (MDA) level had gone significantly up in diabetic TON patients (p value = 0.02), in comparison to other antioxidants and vitamins (Vit). Vit-A, E, B₁, B₁₂ and Zinc seem to be playing a major role in the pathogenesis of TON, specially Vit-E and B₁ surpassed all the antioxidants as having highly significant inverse relationships with MDA (MDA vs Vit-E, r = −0.676^** and MDA vs Vit-B₁, r = −0.724^** respectively).We conclude that during the ethambutol therapy the decreased levels of Vit-E and Vit-B₁ possibly play a role in the development of TON and may be used as therapeutic agents to lessen the deleterious effects of ethambutol.     

APOA2 ?256T>C polymorphism interacts with saturated fatty acids intake to affect anthropometric and hormonal variables in type 2 diabetic patients

Recent studies have established the interaction between APOA2 −256T>C polymorphism and dietary saturated fatty acids intake in relation to obesity on healthy individuals. In the current study, we investigate the effects of this interaction on anthropometric variables and serum levels of leptin and ghrelin in patients with type 2 diabetes. In this cross-sectional study, 737 patients with type 2 diabetes mellitus (290 males and 447 females) were recruited from diabetes clinics in Tehran. The usual dietary intake of all participants during the last year was obtained by validated semiquantitative food frequency questionnaire. APOA2 genotyping was performed by real-time PCR on genomic DNA. No significant relation was obtained by univariate analysis between anthropometric variables and APOA2 genotypes. However, after adjusting for age, gender, physical activity and total energy intake, we identified a significant interaction between APOA2-saturated fatty acids intake and body mass index (BMI). After adjusting for potential confounders, serum levels of ghrelin in CC genotype patients were significantly higher than T allele carriers (p = 0.03), whereas the case with leptin did not reveal a significant difference. The result of this study confirmed the interaction between APOA2 −256T>C polymorphism and SFAs intake with BMI in type 2 diabetic patients. In fact, homozygous patients for the C allele with high saturated fatty acids intake had higher BMI. The APOA2 −256T>C polymorphism was associated with elevated levels of serum ghrelin.     

糖尿病大鼠ghrelin和nesfatin-1表达动力学及其调控

目的:探讨STZ诱导糖尿病大鼠ghrelin和nesfatin-1动力学及分泌调节变化。方法:STZ诱导糖尿病大鼠模型;采用葡糖糖脱氢酶分析法测量血浆葡萄糖水平;免疫放射分析检测血浆ghrelin、nesfatin-1、胰岛素、胰岛素样生长因子1(IGF-1)、生长激素(GH)含量;采用real-time PCR检测ghrelin m RNA水平变化;免疫组化观察ghrelin和nesfatin-1免疫活性细胞数量。结果:糖尿病大鼠体重显著降低(t=23.16,P<0.01),血糖水平显著升高(t=22.55,P<0.01),血浆胰岛素和IGF-1水平显著降低(t=6.50,t=24.13,P<0.01),但GH水平显著升高(t=3.30,P<0.05)。糖尿病大鼠血浆总ghrelin(t=7.03,P<0.01)和活性ghrelin(t=3.33,P<0.05)水平均显著升高,血浆nesfatin-1水平则显著降低(t=6.24,P<0.01);糖尿病大鼠血浆总ghrelin与GH(r=0.81,P<0.01)和IGF-1水平(r=-0.58,P<0.01)呈显著相关性;与对照组大鼠相比,糖尿病大鼠胃总ghrelin(t=16.86,P<0.01)和活性ghrelin(t=3.30,P<0.05)水平均显著降低;而胃nesfatin-1(t=7.93,P<0.01)水平则显著升高。胃总ghrelin水平与血浆IGF-1水平呈明显相关性(r=0.65,P<0.01);与对照组大鼠相比,糖尿病大鼠胃ghrelin m RNA表达水平显著升高(t=16.8,P<0.01),胃底ghrelin免疫活性细胞数量显著减少(t=3.98,P<0.01);实验中给予大鼠自由饮食,糖尿病大鼠血浆总ghrelin水平显著增加(t=7.53,P<0.01),nesfatin-1水平显著降低(t=5.46,P<0.01)。糖尿病大鼠注射胰岛素后,可使增加的ghrelin水平(t=1.76,P=0.11)和降低的nesfatin-1水平接近正常(t=1.96,P=0.06);且胰岛素可显著反转糖尿病大鼠胃总ghrelin(t=8.54,P<0.01)和nesfatin-1水平(t=2.42,P<0.05);以及注射胰岛素后,糖尿病大鼠胃底ghrelin细胞显著增加,nesfatin-1细胞明显减少(t=3.21,t=2.59,P<0.05)。结论:Ghrelin或nesfatin-1参与糖尿病大鼠能量平衡调控。