多发伤患者严重度与血糖、胰岛素、C肽相关性的临床研究

目的了解多发伤患者急性期血糖、胰岛素、C肽的变化及其临床意义。方法在患者入院后第1、3、7天测定血糖、胰岛素、C肽的水平,并观察急性生理和慢性健康评分Ⅱ(APACHEⅡ)及死亡率之间的关系。结果重创组血糖(15.61±2.21)mmol/L、胰岛素(29.47±7.58)m IU/L、C肽(3.19±1.47)ng/m l均高于对照组(P<0.05),且APACHEⅡ31分以上,死亡率明显增高(36.84%)。结论多发伤急性期血糖、胰岛素、C肽的变化对判断病情严重度有一定意义。     

血糖及血清胰岛素与急性脑血管病的相关性研究

 目的 探讨血糖及血清胰岛素水平与急性脑血管病(ACVD)之间的关系。方法 对连续入院的ACVD患者,排除肝肾损害及糖尿病后,于入院24h内清晨采空腹静脉血,测定血糖及血清胰岛素水平,并观察其与ACVD的关系。结果观察组患者血糖及血清胰岛素水平均较对照组增高(＜0.05);脑出血组较脑梗死组增高明显(P＜0.05);重症脑出血较轻症脑出血胰岛素水平增高明显(P＜0.01)。结论血糖及血清胰岛素水平增高与ACVD的发病及预后有关,其增高的水平与ACVD的程度呈正相关。     

急性脊髓损伤大鼠血糖和胰岛素浓度的变化

目的 探讨急性脊髓损伤大鼠血糖与血清胰岛素浓度的变化. 方法 192只雄性大鼠按随机对照法分为假手术组、轻度损伤组和重度损伤组.Allen法制作脊髓损伤模型.One-Touch(R) Ultra~(TM)微型血糖仪测定血糖浓度,放射免疫法测定血清胰岛素浓度.在伤前及伤后1 h、4 h、8 h、12 h、1 d、3 d、5 d,测定各组大鼠的血糖和血清胰岛素值,并计算血清胰岛素敏感指数(ISI).结果 急性脊髓损伤大鼠血糖和血清胰岛素浓度显著升高.脊髓损伤越重,血糖和血清胰岛素浓度升高越明显.轻度和重度脊髓损伤后大鼠的血清ISI均有下降,但重度损伤组大鼠血清IsI的下降更明显,且随脊髓损伤程度的增高而降低.结论 急性脊髓损伤后血糖浓度的升高可能与机体存在胰岛素不敏感有关.     

Effects of MDMA on blood glucose levels and brain glucose metabolism

Purpose This study was designed to assess changes in glucose metabolism in rats administered single or repeated doses of MDMA. Methods Two different experiments were performed: (1) A single-dose study with four groups receiving 20 mg/kg, 40 mg/kg, saline or heat, and (2) a repeated-dose study with two groups receiving three doses, at intervals of 2 h, of 5 mg/kg or saline. Rats were imaged using a dedicated small-animal PET scanner 1 h after single-dose administration or 7 days after repeated doses. Glucose metabolism was measured in 12 cerebral regions of interest. Rectal temperature and blood glucose were monitored. Results Peak body temperature was reached 1 h after MDMA administration. Blood glucose levels decreased significantly after MDMA administration. In the single-dose experiment, brain glucose metabolism showed hyperactivation in cerebellum and hypo-activation in the hippocampus, amygdala and auditory cortex. In the repeated-dose experiment, brain glucose metabolism did not show any significant change at day 7. Conclusion These results are the first to indicate that MDMA has the potential to produce significant hypoglycaemia. In addition, they show that MDMA alters glucose metabolism in components of the motor, limbic and somatosensory systems acutely but not on a long-term basis.     

GBP影响Ⅱ型糖尿病大鼠空腹血糖及胰岛素的Meta分析

目的研究糖尿病胃转流手术（gastric bypass,GBP）对Ⅱ型糖尿病大鼠空腹血糖（FBG）和空腹胰岛素（FINS）调控的效果。方法计算机检索中文期刊全文数据库、维普中文科技期刊数据库、万方数据库收录的1979年1月～2010年12月发表的关于GBP降低Ⅱ型糖尿病大鼠血糖和胰岛素相关的对照研究,并辅以手工检索,对照纳入标准筛选文献。对符合纳入标准的研究的质量进行评价,用RevMan5．1软件进行Meta分析。结果共收集到相关文献37篇,其中符合纳入标准的有14篇,总的有效量合并RR值为0．79[95％CI（0．66,0．94）]。其中符合术后1、2、4W空腹血糖研究纳入标准的有9篇,其空腹血糖浓度合并RR值0．81[95％CI（0．76—0．86）],WMD为-0．21mmol／L[95％CI（-0．37～-0．04）];符合空腹胰岛素研究纳入标准的有6篇,术后2w空腹胰岛素合并RR值0．93[95％CI（0．84～1．02）],WMD为-0．083mmol／L[95％CI（-0．266～0．099）]。发表偏倚估计t=0．332,P〉0．05。结论GBP手术对降低Ⅱ型糖尿病大鼠空腹血糖和空腹胰岛素有显著的效果,并且具有一定的长效性。     

hGLP-1类似物基因转染对糖尿病大鼠血糖、血清胰岛素水平及胰岛细胞的影响

目的 研究尾静脉注射人胰高血糖素样肽-1(hGLP-1)类似物基因(2×Val~2-hGLP-1)重组表达质粒对糖尿病模型大鼠血糖、血清胰岛素水平及胰岛细胞的影响.方法 建立链脲佐黹素(STZ)诱导SD糖尿病大鼠模型,随机分为含有hGLP-1类似物基因的重组质粒(plRFLS2-FGFP/Val~2-hGLP-1)转染组、空质粒(pIRES2-EGFP)转染组、糖尿病模型对照组,每组8只.另取8只未经处理的SD大鼠作为正常对照组.重组质粒转染组和空质粒转染组分别通过尾静脉注射含相应质粒(110μg/只)的溶液,糖尿病模型对照组和正常对照组给予等量的生理盐水.实验动物共干预30d,实验结束后,观察各组大鼠血糖及血清胰岛素水半的变化,采用糖耐量及胰岛素耐量实验检测大鼠胰岛素敏感性然后处死动物,HE染色观察胰岛细胞病变情况,免疫组化法分析胰岛素分泌情况.结果 与正常对照组、糖尿病模型对照组和空质粒转染组比较,重组质粒转染组血糖水平明显降低(P<0.01),血清胰岛素水平显著升高(P<0.01).基因治疗改善了糖尿病大鼠的糖耐量,降低了胰岛素抵抗,提高了机体对胰岛素的敏感性(P<0.01).空质粒转染组与糖尿病模型对照组比较,以上指标的差异均无统计学意义(P>0.05).同时,重组质粒转染组的胰岛素分泌水平提高,与糖尿病模型对照组比较,胰岛细胞病变程度明显改善.结论 hGLP-1类似物基因转染可促进胰岛细胞增殖,提高胰岛素敏感性,从而显著降低糖尿病大鼠的血糖水平,并改善胰岛组织病变程度.     

18F-FDG assessment of glucose disposal and production rates during fasting and insulin stimulation: a validation study.

The glucose analog (18)F-FDG is commonly used to quantify regional glucose uptake in vivo. The aim of this study was to test whether the analysis of plasma (18)F-FDG kinetics could be used to estimate endogenous glucose production (EGP) and the total rate of appearance (Ra), total rate of disappearance (Rd), and the metabolic clearance rate (MCR) of glucose. METHODS: Fourteen pigs were coinjected with (18)F-FDG and 6,6-(2)H-glucose ((2)H-G) during fasting (n = 6) and during physiologic (1.0 mU.kg(-1).min(-1), n = 4) and supraphysiologic (5.0 mU.kg(-1).min(-1), n = 4) euglycemic hyperinsulinemia. Arterial plasma was sampled for 180 min to quantify the parameters for the 2 tracers. RESULTS: Fasting Rd((2))(H-G) and Rd(FDG) were 12.3 +/- 2.1 and 13.3 +/- 1.3 micromol.kg(-1).min(-1) (difference not statistically significant [NS]). M values were more than doubled between the 2 clamp studies (P < 0.0001). Rd((2))(H-G) and Rd(FDG) were dose-dependently higher during the hyperinsulinemic state (19.8 +/- 3.7 vs. 18.9 +/- 1.1 and 31.4 +/- 4.1 vs. 31.9 +/- 2.3 in 1.0 and 5.0 mU.kg(-1).min(-1) studies, respectively; difference between tracers NS) than during the fasting state, with a parallel suppression of EGP((2))(H-G) and EGP(FDG). Parameters estimated by (18)F-FDG and (2)H-G were equivalent in all groups; their agreement was confirmed by Bland-Altman examination. Total Rd(FDG) correlated with Rd((2))(H-G) (r = 0.74; P = 0.003), M (r = 0.92; P = 0.001), MCR((2))(H-G) (r = 0.52; P = 0.037), and EGP((2))(H-G) (r = -0.71; P = 0.004). EGP(FDG) correlated with EGP((2))(H-G) (r = 0.62; P = 0.018), Rd((2))(H-G) (r = -0.78; P = 0.001), and MCR((2))(H-G) (r = -0.67; P = 0.008). The (18)F-FDG mean transit time correlated inversely with the M and Rd values and positively with EGP. CONCLUSION: The glucose analog (18)F-FDG can be used in the simultaneous estimation of whole-body glucose turnover and production and regional (18)F-FDG PET measurements under both fasting and insulin-stimulated conditions.     

Effects of exercise training on insulin response to intravenous glucose in pubertal rats.

This study was undertaken to evaluate the effects of exercise training on glucose tolerance and glucose-stimulated insulin response (GSIR) in 55- and 90-day-old peripubertal female rats. Intravenous glucose tolerance tests (0.5 g/kg) were done in: 1) 90-day-old rats exercised in swimming sessions for either 5 or 10 weeks and evaluated 48 h after the last exercise bout; 2) 55-day-old rats exercised for 5 weeks and evaluated either 24 h or 48 h after the last exercise bout and; 3) unexercised 55- and 90-day-old rats. The total area under the GSIR curve was suppressed in 55- and 90-day-old rats exercised since the age of 21 days. However, this decrease was observed 48 and only 24 h after the last exercise bout in the 90- and 55-day-old rats respectively. Exercise did not affect the GSIR curve for the 90-day-old rats subjected to 5 weeks of exercise training (started at 55 days of age) when evaluated 48 h after the last exercise bout. Nor did one single bout of swimming exercise (2 h) in the last 24 h affect the GSIR in unexercised 55-day-old rats. These results suggest that the shorter duration of the residual effects of exercise in the younger rats (55 days) was related to the shorter length of the training programme. Body weight was not significantly reduced with exercise in 55-day-old rats, whereas the same amount of exercise in 90-day-old rats caused body weight reduction of approximately 35 g (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

血糖变异性对急性冠脉综合征患者近期预后的影响

目的 回顾性分析血糖变异性对急性冠脉综合征(ACS)近期预后的相关性.方法 选择878例ACS患者,其中有糖尿病史者298例,无糖病史者580例.将所有患者按住院期间血糖变异性(以血糖变异系数CV为指标)和平均血糖水平按照四分位法分为4组,记录所有患者基线资料、住院期间血糖变异性、平均血糖水平及不良事件发生情况并进行回顾性分析.结果 878例ACS患者,按照血糖变异性以四分位法分为4组,随着血糖变异性增大,住院期间心衰、心源性休克、死亡率增加,组间差异明显(p＜0.001).将有糖尿病史者、无糖尿病史者各自按同样方法分为4组,亦见随血糖变异性增大,住院期间死亡率增加,且组间差异明显(P＜0.05);按平均血糖水平分组时,结果类似.多元回归分析显示患者基线时各指标、住院期间血糖变异性、住院期间平均血糖水平中有5种因素与死亡呈显著相关,依次为糖尿病、高血压、高密度脂蛋白胆固醇、平均血糖、血糖CV.结论 无论是否合并糖尿病,ACS患者住院期间的血糖变异性均与近期预后不良相联系.临床工作中应加强对ACS患者的血糖监测和对血糖稳定性的控制.     

L-arginine ingestion after rest and exercise: effects on glucose disposal

PURPOSE: There is considerable interest, both in health and disease, in enhancing postexercise glucose uptake and glycogen resynthesis in skeletal muscle. The amino acid, arginine, is known to stimulate insulin release and enhance glucose-stimulated insulin release. METHODS: The present investigation examined whether an oral dose of L-arginine (10 g), when given with 70 g carbohydrate (CHO, in the form of simple sugars) improved factors associated with glucose disposal in previously exercised and nonexercised healthy males. The effects of different modes of activity (resistance or cycling exercise) upon these factors were also examined. RESULTS: Whole-blood glucose and serum insulin concentrations after L-arginine + CHO ingestion were not significantly different from the placebo condition (glycine + CHO ingestion) in all experimental treatments (nonexercised, resistance exercise, and cycling exercise). Similarly, CHO oxidation, forearm blood flow, blood pressure, and heart rate during the postingestion period were unaffected by L-arginine + CHO consumption in all three experimental treatments. CONCLUSION: A 10-g oral dose of L-arginine was found to have no effect on blood glucose disposal in human subjects after oral CHO ingestion, either when rested or after different modes of exercise known to differentially affect glucose disposal. These results suggest that the addition of L-arginine to a CHO beverage would not augment postexercise CHO replenishment in healthy human subjects.     

The effects of exercise training intensification on glucose disposal in elite cyclists

To assess the effect of training on glucose disposal, we performed a longitudinal study of 11 elite cyclists before and after 4 months of intensive training compared to 11 sedentary subjects. Insulin sensitivity (SI) and glucose effectiveness (Sg) were measured using Bergman's minimal model. Sg includes basal insulin effectiveness (BIE) and a parameter termed glucose effectiveness at zero insulin (GEZI). After overnight fasting glucose was administered intravenously (0.5 g x kg(-1), 30% solution given over 3 min), and insulin (0.02 U x kg(-1), 1 -2U) was injected immediately after 19 min. Sg, SI and BIE, were significantly higher in elite cyclists both before and after training than in sedentary subjects (P < 0.01). However, the non-insulin-dependent component of Sg (GEZI) was higher only after the intensive training in the cyclists (3.31 +/- 0.67% x min(-1)) than in sedentary subjects (1.7 +/- 0.2% x min(-1), P < 0.02). We conclude that insulin sensitivity (SI) and glucose effectiveness (Sg) are higher in elite cyclists than in sedentary subjects and that these high and almost optimal values are not further improved by additional training. However, the improvement in GEZI, as reflected by the difference between post-training GEZI and sedentary control values, raises the possibility of an increase of the non-insulin-mediated mobilization of glucose transporters.     

地黄寡糖对妊娠期糖尿病大鼠血糖和胰岛素水平的影响

目的：研究地黄寡糖对妊娠糖尿病大鼠血糖和血浆胰岛素水平的影响。方法：以四氧嘧啶（150 mg/kg,ip）诱发妊娠大鼠糖尿病模型,灌胃给予地黄寡糖200 mg/（kg/d）,检测给药前、给药7 d及给药14 d后大鼠血糖和血浆胰岛素的变化。结果：地黄寡糖口服可降低四氧嘧啶诱发之妊娠糖尿病模型大鼠的空腹血糖,增加血浆胰岛素水平。结论：地黄寡糖具有降低妊娠糖尿病大鼠血糖和改善胰岛素释放的作用。     

急性脑卒中血糖变化对预后影响的临床分析

目的观察急性脑血管病时非糖尿病病人血糖变化与临床的关系及对预后影响。方法对我院152例既往无糖尿病的急性脑卒中住院患者起病时急性高血糖进行回顾分析。全部病例经头颅cT或MRI证实为急性脑卒中,其中脑出血84例,脑梗死68例,两组患者性别、年龄等一般情况无显著差别。结果出血性脑卒中组血糖值为（17．7±3．5）mmol／L,缺血性脑卒中组血糖值为（9．3±2．8）mmol／L,出血性脑卒中组血糖值明显高于缺血组（P〈0．05）;两组死亡病人中,血糖增高组65例（病死率77％）,血糖正常组5例（病死率7％）,前者明显高于后者;病人神经功能缺损,血糖增高组较血糖正常组严重,而且恢复时间长。结论急性脑卒中患者血糖水平的高低与预后有密切关系。因此,对急性脑卒中患者应及时了解和监测血糖情况,以估计疾病严重程度和预后。发病早期采用慎重的措施控制高血糖,以期减轻不良预后。     

Effect of an acute beta-adrenergic blockade on the blood glucose response during lactate minimum test.

The aim of this study was to determine the relationship between blood lactate and glucose during an incremental test after exercise induced lactic acidosis, under normal and acute beta-adrenergic blockade. Eight fit males (cyclists or triathletes) performed a protocol to determine the intensity corresponding to the individual equilibrium point between lactate entry and removal from the blood (incremental test after exercise induced lactic acidosis), determined from the blood lactate (Lacmin) and glucose (Glucmin) response. This protocol was performed twice in a double-blind randomized order by ingesting either propranolol (80 mg) or a placebo (dextrose), 120 min prior to the test. The blood lactate and glucose concentration obtained 7 minutes after anaerobic exercise (Wingate test) was significantly lower (p < 0.01) with the acute beta-adrenergic blockade (9.1 +/- 1.5 mM; 3.9 +/- 0.1 mM), respectively than in the placebo condition (12.4 +/- 1.8 mM; 5.0 +/- 0.1 mM). There was no difference (p > 0.05) between the exercise intensity determined by Lacmin (212.1 +/- 17.4 W) and Glucmin (218.2 +/- 22.1 W) during exercise performed without acute beta-adrenergic blockade. The exercise intensity at Lacmin was lowered (p < 0.05) from 212.1 +/- 17.4 to 181.0 +/- 15.6 W and heart rate at Lacmin was reduced (p < 0 .01) from 161.2 +/- 8.4 to 129.3 +/- 6.2 beats min(-1) as a result of the blockade. It was not possible to determine the exercise intensity corresponding to Glucmin with beta-adrenergic blockade, since the blood glucose concentration presented a continuous decrease during the incremental test. We concluded that the similar pattern response of blood lactate and glucose during an incremental test after exercise induced lactic acidosis, is not present during beta-adrenergic blockade suggesting that, at least in part, this behavior depends upon adrenergic stimulation.     

Effects of insulin and glucose loading on FDG uptake in experimental malignant tumours and inflammatory lesions.

Fluorine-18 2-deoxy-2-fluoro-D-glucose (FDG) accumulation in tumours has been well investigated, but much less is known regarding FDG accumulation in inflammatory lesions. In this study, we determined the effects of hypo- and hyperglycaemia on FDG uptake in inflammatory lesions of infectious and non-infectious origin and compared them with those in malignant tumours in rats, to provide a biological basis for differentiating malignant lesions from benign lesions by means of FDG-PET. Rats were inoculated with a suspension of allogenic hepatoma cells (KDH-8) or Staphylococcus aureus, or with turpentine oil into the left calf muscle. Two weeks after KDH-8 inoculation and 1 week after S. aureus and turpentine oil inoculations, the rats were divided into three subgroups: insulin-loaded (2 U/kg body weight, i.p.), glucose-loaded (1.2 g/kg body weight, p.o.) and control groups. Radioactivity in tissues was determined 1 h after i.v. injection of FDG. Intraperitoneal injection of insulin and oral administration of glucose induced hypoglycaemia and hyperglycaemia, respectively. In the control animals, tumours showed a level of FDG uptake which was 2.2 and 3.0 times higher than the levels in the inflammatory lesions induced by S. aureus and turpentine oil, respectively (P<0.0001). There was no significant difference in the level of FDG uptake between the two inflammatory lesions of infectious and non-infectious origin. Insulin loading significantly decreased the level of FDG uptake in tumours and in both types of inflammatory lesion to approximately one-half of the control values (P=0.001 in the tumour group and P<0.0001 in the two inflammatory lesion groups). In the glucose-loaded group, the level of FDG uptake in both types of inflammatory lesion decreased significantly to 50%-61% of the control value (P=0.0002 in the S. aureus group and P<0.0001 in the turpetine group), while the tumour uptake did not decrease significantly (86% of the control value) (P=NS). It is concluded that FDG uptake in both types of inflammatory lesion was significantly impaired in rats with hyperglycaemia induced by glucose loading, while tumour uptake of FDG was not significantly affected. These results indicate that glucose loading has greater effects on FDG uptake in inflammatory lesions than in tumours, providing a biological basis for differentiation of malignant lesions from benign lesions by FDG-PET in a clinical setting.     

高糖对外周血内皮祖细胞数量和功能的影响

目的　观察高糖对外周血内皮祖细胞(EPCs)数量和功能的影响。方法　密度梯度离心法获取外周血单个核细胞 ,培养 7天后 ,收集贴壁细胞并加入不同浓度葡萄糖使培养液终浓度分别为 1 5、2 5、35和 4 5mmol/L ,并干预一定时间 (6、1 2、2 4和 4 8h)。多波长激光共聚焦显微镜鉴定FITC UEA Ⅰ和DiI acLDL双染色细胞为正在分化的EPCs,流式细胞仪检测其表面标志进一步鉴定EPCs,倒置荧光显微镜下计数。然后 ,分别采用MTT比色法、改良的Boyden小室、黏附能力测定实验和体外血管生成试剂盒分别观察EPCs的增殖、迁移、黏附和体外血管生成能力。结果　高糖呈量效和时效地减少外周血EPCs数量 ,4 5mmol/L浓度高糖作用 2 4h对EPCs数量的影响最为显著 (较对照组减少了近 1 / 2 ,P <0 0 1 )。高糖也显著抑制外周血EPCs的黏附、迁移、增殖和体外血管生成能力。结论　高糖可减少EPCs数量、抑制其功能 ,并呈浓度和时间依赖性     

大黄素对Ⅰ型糖尿病大鼠血糖及体重的影响

目的 揭示Ⅰ型糖尿病大鼠血糖、体重改变及大黄素对其影响.方法健康SD大鼠适应性喂养1 w,选择血糖正常者40只,随机选取10只作为对照组,其余大鼠腹腔注射链脲佐菌素（STZ）65 mg/kg制作糖尿病模型（对照组注射等量柠檬酸缓冲液）.3 d后禁食不禁水6 h,采尾血测空腹血糖,STZ注射后第10 d（成模初期）再测血糖,以血糖≥16.9 mmol/L为造模成功.成模大鼠随机分为糖尿病组（10只）与大黄素组（10只）.成模2 w后,对照组与糖尿病组以PBS 5 ml/kg灌胃,大黄素组用8 g/L大黄素混悬液灌胃,5 ml/kg,1次/d,直至成模后第10 w.STZ注射后第3 d、第10 d（成模初期）及成模后第10 w,检测各组血糖及体重变化.结果 （1）成模初期,3组体重无差异;与对照组相比,糖尿病组与大黄素组血糖均升高,但两组间无显著差异.（2）成模后第10 w,与对照组相比,糖尿病组与大黄素组体重均减轻,血糖均升高;与糖尿病组相比,大黄素组体重无差异,血糖降低.（3）成模后期与初期相比,对照组体重增加,血糖无改变;糖尿病组体重减少,血糖升高;大黄素组体重减少,血糖无改变.结论 大黄素可降低Ⅰ型糖尿病大鼠血糖浓度,对体重无影响.     

大黄多糖对糖尿病动脉粥样硬化大鼠血糖、血脂、肝脂酶活性的影响

目的观察大黄多糖对糖尿病动脉粥样硬化大鼠血糖、血脂、肝脂酶活性的影响。方法将Wistar大鼠分为正常组和建模组，建模成功的糖尿病动脉粥样硬化大鼠随机分为模型组（糖尿病AS组）、大黄高、中、低剂量组，测定血脂生化指标及血浆中HL活性并制备主动脉病理切片。结果在高剂量大黄多糖的作用下，糖尿病动脉粥样硬化大鼠的血糖、总胆固醇、甘油三酯、低密度脂蛋白胆固醇明显降低，血浆肝脂酶活性增加。结论大黄其有效成分大黄多糖能降糖、降血脂、增加糖尿病动脉粥样硬化大鼠血浆中HL活性，防止糖尿病大血管并发症的发生发展。