动态血糖监测探讨2型糖尿病睡前血糖和夜间低血糖的关系

85例2型糖尿病使用CGMS监测48～72小时,有完整夜间血糖记录220天.以睡前血糖≤80mg/dl,≤90mg/dl,≤100mg/dl,≤110mg/dl,≤120mg/dl,≤130mg/dl,评估夜间低血糖≤50mg/dl的发生情况.结果夜间低血糖发生39例,其睡前血糖40～227mg/dl,平均79.9±46.8mg/dl,睡前血糖≤120mg/dl,其ROC曲线下面积为最大0.359±0.046,其阳性预测值25%,阴性预测值91.7%.结论夜间低血糖的发生是频繁的,当睡前血糖低于120mg/dl更多见,CGMS是诊断夜间无症状性低血糖的有用方法.     

甘精胰岛素联合格列美脲及阿卡波糖治疗2型糖尿病患者24小时动态血糖变化

26例继发性磺脲类失效(SFS)的2型糖尿病患者,改用甘精胰岛素加格列美脲及阿卡波糖治疗3个月后与联合治疗前比较,24．h总体血糖达标时段[(19．1±3．6)h vs(2．3±2．1)h]显著延长,24 h平均血糖[(6．8±1．4)mmoL／Lvs(15．2±3．2)mmol／L]、空腹血糖[(5．4±1．3)mmol／Lvs(11．6±5．2) mmol／L]、24h内最高血糖[(10．8±4．2)mmol／Lvs(20．3±5．6)mmoL／L]及HbAIC[(7．7±1．3)％vs(10．8±1．6％)]均有显著下降(均P<0．01)。提示甘精胰岛素联合格列美脲及阿卡波糖能有效改善SFS的2型糖尿病24h血糖控制。     

应用动态血糖监测系统评价双相门冬氨酸胰岛素30对老年2型糖尿病患者的疗效

目的应用动态血糖系统（CGMS）观察老年人2型糖尿病（T2DM）患者中性鱼精蛋白锌胰岛素NPH与双相门冬氨酸胰岛素30（BI-Asp30）治疗的疗效和安全性。方法T2DM患者22例，分别接受BIAsp30和NPH治疗12w，治疗结束即时进行72h CGMS观察。结果12w时BI-Asp30组糖化血红蛋白（HbAlC）显著低于NPH组（7．46&#177;0．94％vs 7．90&#177;0．93）。CGMS检查显示，BIAsp30组早餐后（9．3&#177;2．4mmol／L vs 10．3&#177;2．5mmol／L）和晚餐后2h血糖（PG）（9．1&#177;2．2mmol／L vs 10．1&#177;3．1mmol／L）降低更明显，血糖≥10mmol／L时间百分比明显降低（14．5&#177;10．1 vs 20．8&#177;11．4），凌晨3点PG不过低（5．2&#177;0．8mmol／L vs 4．1&#177;1．0mmol／L）。BIAsp30组夜间低血糖发生率（1例次）显著少于NPH组（3例次），夜间血糖≤3．0mmo／L时间百分比亦明显减少（1．93&#177;1．37 vs 5．03&#177;1．33）。结论BIAsp30治疗更接近生理胰岛素分泌模式，能更好地控制餐后PG，减少低血糖发生。     

067 在胰岛素强化治疗期间胰岛素类似物Lispro对减少夜间低血糖发作的作用

[英]/Heller sR…／／Diabetes Care．-1999．22．-1607～1611 评价了1型糖尿病(DM)患者在胰岛素强化治疗方案中，应用胰岛素Lispro降低夜间低血糖发生的作用。 对象及方法随机选取165例1型糖尿病患者，有2 a以上病史，使用基础治疗至少3月，糖化血红蛋白(HbA1c)<8％，同时愿意更严格地控制血糖(有活动视网膜病变，明显的糖尿病肾病或近12个月发生严重的低血糖的患者除外)。 病人先进入两个月的观察期，在此期间，三餐前用常规短效胰岛素，睡前用中效胰岛素控制血糖，血糖控制的目标为餐前4～7 mmol／L，餐后7～10 mmol／L，同时病人记录自己低血糖发作的症状和次数。另外，病人每隔两周收集一天7次血糖标本送实验室检测。血糖水平在控制范围内的次数<70％或HbA1c>8％的病人不被纳入分组。两月后合适的病人被随机分为两组，运用交叉试验，一组先用胰岛素Lispro4个月，再用常规胰岛素4个月，另一组则相反。记录病人低血糖发作的次数和程度，且每月检测一天七个时间点的血糖。 结果治疗一阶段低血糖的发生率用胰岛素Lis-pro比用常规胰岛素低(1 156次对775次)，且发生夜间低血糖的次数减少(181次对52次，P=0．01)，二阶段用胰岛素Lispro与用常规胰岛素低血糖的发生率为883次对702次。用常规胰岛素与用胰岛素Lispro的HbA1c水平分别为：一阶段开始为6．4％±0．9％对6．2％±1．1％，结束时为6．2％±0．8％对6．0％±0．9％；二阶段开始为6．0％±0．9％对6．2％±0．8％，结束时为6．4％±1．1％对6．4％±1．1％。用胰岛素Lispro的病人早餐后及午餐后的血糖都比用常规胰岛素的病人低[分别为(7．4±0．5)对(8．5±0．4)mmol／L，P=0．048；6．6±0．3对(7．2±0．3)mmol／L，P=0．043]，但睡前却高[(8．1±0．5)对(7．5±0．4)mmol／L，P=0．03]。用常规胰岛素的病人体重增加[从(73．5±10．1)至(75．5±10．2)]，而用胰岛素Lispro不增加。两组病人在研究开始或结束时使用的中效和短效胰岛素的用量都无明显变化 结论本试验显示达到同样良好血糖控制同时，用胰岛素Lispro比用常规胰岛素减少了低血糖的发作(12：00～6：00pm)，特别是减少了夜间低血糖的发作和严重低血糖的发作。 (苏白海摘 魏松全校)     

强化胰岛素治疗后2型糖尿病夜间低血糖及其与睡前血糖关系的研究

目的探讨2型糖尿病患者强化胰岛素治疗时发生夜间未察觉低血糖的情况及与睡前血糖或晚餐后血糖的关系。方法对中山大学附属第二医院内分泌科2007—2008年收治的2型糖尿病患者45例,采用强化胰岛素治疗方案,血糖达标后进行72 h动态血糖监测,分析低血糖发生情况。结果低血糖(血糖≤3.9 mmol/L)发生率为79.5%,较严重的低血糖(血糖≤2.8 mmol/L)发生率为52.3%,其中86.0%的低血糖发生在夜间,患者均无诉不适。睡前血糖与夜间低血糖发生率存在相关性(列联系数rp=0.26,P<0.05),晚餐后血糖与夜间低血糖的相关性无统计学意义(rp=0.15,P>0.05);当睡前血糖处于4.0～9.9 mmol/L时,夜间低血糖或较严重低血糖的持续时间百分比并无差异(P>0.05)。结论强化胰岛素治疗的2型糖尿病患者夜间未察觉低血糖的发生率较高;监测睡前血糖较晚餐后血糖更能反映夜间低血糖的发生;血糖4.0～9.9 mmol/L时,不主张通过刻意提高睡前血糖来降低低血糖的发生。     

应用动态血糖监测评估2型糖尿病患者的夜间低血糖

动态血糖监测系统(CGMS)监测1 147例2型糖尿病患者血糖变化.结果 显示,夜间低血糖多发生在22:00～2:00,与平均血糖及晚餐后3 h血糖负相关,晚餐后3 h血糖4.7 mmoL/L时发生夜间低血糖几率达50%.     

空腹高血糖的2型糖尿病患者加用甘精胰岛素或中性鱼精蛋白锌胰岛素的比较研究

单用口服降糖药血糖控制不佳的2型糖尿病患者分别加用甘精胰岛素或中性鱼精蛋白锌胰岛素(NPH)联合治疗3个月,然后停止胰岛素治疗,恢复原口服治疗方案,共观察6个月。结果甘精胰岛素组的HbAIC和餐后血糖低于NPH组[治疗3个月(6．1±0．5)％vs(6．9±0．8)％和(7．2±2．1)mmol／L vs(9．3±3．1)mmol／L,治疗6个月(6．6±0．7)％vs(7．4±1．1)％和(8．8±2．8)mmol／Lvs(10．3±3．1) mmoL／L,P<0．01或P<0．05],两指标的下降值甘精胰岛素组大于NPH组[治疗3个月(4．0±0．7)％vs (3．7±0．6)％和(7．1 4-2．0)mmol／Lvs(5．9±1．8)mmol／L,治疗6个月(3．5±0．5)％vs(3．2±0．3)％和(5．5±1．4)mmol／Lvs(4．9±1．3)mmol／L,P<0．01或P<0．05],提示使用甘精胰岛素可以在不增加不良反应的情况下比NPH更加全面而有效地控制血糖。     

床边血糖监测系统监测睡前血糖预测住院2型糖尿病患者夜间低血糖发生情况的观察

目的 利用床边血糖监测系统回顾性分析住院T2DM患者睡前血糖与夜间低血糖的主要特点及危险因素. 方法 收集2008年1月至2011年12月接受稳步医院用（SureStep Flexx）床边血糖管理系统连续监测睡前及夜间血糖的2505例T2DM患者共14827次血糖数据行回顾性分析,探讨睡前血糖与夜间低血糖的关系. 结果 （1）夜间低血糖发生率10.8％（271/2505）,总夜间低血糖事件393次,其中严重低血糖发生率15.3％（60/393）,轻度低血糖84.7％（333/393）.（2）睡前血糖＜9.0 mmol/L时,预测夜间低血糖敏感性57.7％,特异性62.3％.（3）男性、≥60岁、胰岛素治疗且睡前血糖＜9.0mmol/L的住院T2DM患者,夜间低血糖发生风险升高（P＜0.05）. 结论 住院T2DM患者睡前血糖＜9.0 mmol/L时,夜间低血糖发生风险升高,应重视睡前血糖监测,预防夜间低血糖发生.     

无症状低血糖和行急诊冠脉介入的ST段抬高型心肌梗死患者围手术期室性心律失常相关性研究

【】目的：评价对于行急诊冠脉介入治疗的急性ST段抬高型心肌梗死患者无症状低血糖和室性心律失常的关系。方法：所有患者使用动态血糖监测系统(continuous glucose monitoring system ,CGMS)及动态心电监测(Holter)系统,进行动态血糖及心电的同步监测,观察无症状低血糖和室性心律失常的关系。结果：根据入选标准和排除标准,入选了237例行急诊冠脉介入治疗的STEMI患者,CGMS共记录了477次无症状低血糖(血糖<3.9mmol/l)发作,糖尿病组患者平均血糖(10.6±2.3mmol/l vs. 6.7±1.1 mmol/l)、血糖最高值(15.9±3.5mmol/l vs.10.9±3.1 mmol/l)、MAGE(3.9±1.1mmol/l vs.2.8±1.6 mmol/l)、SDBG(2.5±1.3mmol/l vs. 1.3±0.7 mmol/l)、平均低血糖发作次数(2.7±3.2mmol/l vs. 1.7±1.8mmol/l)均高于非糖尿病组患者(P<0.05)。此外,无论是糖尿病还是非糖尿病患者,低血糖发作均好发于夜间。与非低血糖组患者相比,无症状低血糖组患者室性早搏、室早二联律及非持续性室速发生次数更多(P<0.05)。结论：行急诊冠脉介入治疗的STEMI患者,无症状低血糖发作是普遍存在的,且好发于夜间。无症状性低血糖和室性心律失常相关。     

动态血糖参数正常参考值的建立及临床应用

目的建立动态血糖评估参数的正常参考值,为临床应用提供依据。方法采用动态血糖监测系统（CGMS）对48例正常糖调节者进行连续3d的血糖监测,并分析24h的平均血糖水平（MBG）及其标准差（SDBG）、餐前1h及餐后3h的MBG、血糖的时间百分比（PT）、血糖的曲线下面积（AUC）、最大血糖波动幅度（LAGE）、平均血糖波动幅度（MAGE）及日间血糖平均绝对差（MODD）。各参数非正态分布者以百分位数法估计95％的正常参考值范围,呈正态分布者按x±1.96s计算。结果（1）除血糖的frr及AUC呈非正态分布外（P〈0．05）,其余参数均呈正态分布（P〉0．05）,各参数在不同性别间的差异无统计学意义（P〉0．05）。（2）动态血糖参数的正常参考值上限：24hMBG〈6．5mmol／L,早、中及晚餐前1hMBG分别〈6．0mmol／L、〈6．3mmol／L和〈6．0mmol／L,早、中及晚餐后3hMBG分别〈7．0mmol／L、〈6．7mmol／L和〈7．0mmol／L,血糖≥7．8mmol／L及≤3．9mmol／L的PT分别〈9％和〈20％,血糖≥5．6mmol／L的AUC〈0．9d·mmol·L^-1,SDBG〈1．4mmol／L,LAGE〈5．7mmol／L,MAGE〈3．4mmol／L,MODD〈1．4mmol／L。（3）24hMBG与MAGE、MODD及SDBG均不相关（P〉0．05）,MAGE与SDBG显著正相关（r=0．93,P〈0．01）。结论初步建立了CGMS各血糖参数的正常参考值,应用上述参数能较全面地反映受试者整体血糖水平和血糖稳定性的特征。     

The effect of hyperglycemia, hyperinsulinemia, and route of glucose administration on glucose oxidation and glucose storage

The separate effects of hyperinsulinemia, hyperglycemia, and the route of glucose administration on total glucose metabolism, glucose oxidation, and glucose storage were examined in 19 healthy young volunteers by employing the glucose clamp technique in combination with indirect calorimetry. Following 2 hr of euglycemic hyperinsulinemia (plasma insulin ～97μU/ml) created by intravenous insulin/glucose infusion, total glucose metabolism (6.08 ± 0.56 mg/kg. min), glucose oxidation ($\text{2.63 ± 0.26 mg}\text{0.26 mg kg · min}$), and glucose storage (3.46 ± 0.42 mg/kg · min) all increased 2 to 3-fold over basal rates. When additional hyperinsulinemia (163 ± 19 μU/ml) was created while maintaining euglycemia, total glucose metabolism (8.87 ± 0.69) and glucose storage (6.06 ± 0.51) both increased significantly (p < 0.005 and 0.02, respectively), but the rise in glucose oxidation (2.96 ± 0.17) was small and insignificant. During combined hyperglycemia (214 mg/dl) and hyperinsulinemia (217 μU/ml), total glucose metabolism (16.21 ± 0.58 mg/kg · min) and glucose storage (13.05 ± 0.57 mg/kg · min) both increased significantly (p < 0.001) compared to the euglycemic hyperinsulinemic conditions but glucose oxidation (3.04 ± 0.16 mg/kg · min) failed to increase further. These results indicate that the body's ability to oxidize glucose becomes saturated within the physiologic range of plasma insulin and glucose concentrations. With further increases in plasma glucose and insulin levels, the increase in glucose metabolism is primarily accounted for by an increase in glucose storage. The route of glucose administration, oral versus intravenous, had no effect on glucose oxidation. Under conditions of prolonged (6 hrs) euglycemic hyperinsulinemia, glucose oxidation was not significantly different whether the glucose was given intravenously (3.14 ± 0.11 mg/kg · min) or orally (3.63 ± 0.17). Similarly, under comparable conditios of hyperglycemic hyperinsulinemia, glucose oxidation was not different in subjects receiving intravenous (3.60 ± 0.28 mg/kg · min) and oral (4.03 ± 0.13) glucose. However, under conditions of hyperglycemic hyperinsulinemia both total body glucose metabolism (22.91 ± 0.42 versus 19.66 ± 1.10 mg/kg · min, p < 0.02) and glucose storage (18.76 ± 0.47 versus 15.95 ± 1.17, p < 0.02) were significantly greater during oral versus intravenous glucose. The site of the increased glucose storage observed with oral glucose could not be located since hepatic and femoral venous catheterization was not performed.     

Exercise-induced hepatic glucose output is precisely sensitive to the rate of systemic glucose supply

It has previously been established that a glucose infusion causing hyperglycemia and alterations in the levels of glucoregulatory hormones suppresses the exercise-induced increment in systemic glucose appearance (Ra). In an attempt to define the mechanisms responsible for this suppression of Ra, five normal subjects were exercised for 60 minutes on a bicycle ergometer at 60% Vo2 max on two occasions. On both occasions Ra was measured by a nonsteady state technique using a constant infusion of 3-3H-glucose. On the second occasion, an IV infusion of glucose was administered in a stepwise fashion to simulate in timing and magnitude the measured Ra response from the first study. Endogenous glucose production in the second study, estimated by subtracting the amount of glucose infused from the measured Ra response, did not increase above basal (endogenous glucose output response = 0.5 +/- 8.4 mmol/60 min v control study 60.2 +/- 6.6 mmol/60 min, P less than 0.01). The suppression of Ra was associated with a small but significant effect on venous plasma glucose (increment above basal less than 0.3 mmol/L, P less than 0.05) and a significant change in glucose metabolic clearance rate during the second 30 minutes of exercise. Serum insulin, C-peptide, cortisol, growth hormone, and plasma glucagon responses to exercise were not significantly affected by glucose infusion and the ratio of circulating insulin to glucagon was also not affected. These results indicate that hepatic glucose output during exercise is precisely sensitive to glucose supply. The feedback inhibition is presumably mediated by a small increase in plasma glucose but cannot readily be accounted for by changes in glucoregulatory hormones.(ABSTRACT TRUNCATED AT 250 WORDS)     

The glucoregulatory response to intravenous glucose infusion in normal man: Roles of insulin and glucose

In order to differentiate the roles of hyperinsulinemia and hyperglycemia per se in the homeostatic response to i.v. glucose administration, two groups of normal subjects were given either glucose alone (3.5 mg kg^?1 min^?1) or glucose (3 mg kg^?1 min^?1) in conjunction with somatostatin (500 μg hr^?1), insulin (0.15 mU kg^?1 min^?1) and glucagon (1 ng kg^?1 min^?1). Glucose kinetics were measured by the primed-constant infusion of 3-³H-glucose. During the infusion of glucose alone, plasma glucose stabilized at levels 45–50 mg/dl above the fasting values. Endogenous glucose output was markedly suppressed by 85%–90% while glucose uptake rose to values very close to the infusion rate of exogenous glucose. Glucose clearance remained unchanged. Plasma insulin rose three-fourfold while plasma glucagon fell by 25%–30%. When glucose was infused with somatostatin, insulin, and glucagon, plasma insulin was maintained at levels 50% above baseline while glucagon remained at preinfusion levels. Under these conditions, the infusion of exogenous glucose resulted in a progressive increase of plasma glucose which did not stabilize until the end of the study period (190 mg/dl at 120 min). Endogenous glucose production was consistently suppressed (52%) but significantly less than observed with the infusion of glucose alone (p < 0.01). Glucose uptake increased to the same extent as with glucose alone, despite the more pronounced hyperglycemia. Thus, glucose clearance fell significantly below baseline (25%–30%; p < 0.01). These data demonstrate that hyperglycemia per se (fixed, near basal levels of insulin and glucagon) certainly contributes to the glucoregulatory response to i.v. glucose administration by both inhibiting endogenous glucose output and increasing tissue glucose uptake. However, the extra-insulin evoked by hyperglycemia is necessary for the glucoregulatory system to respond to the glucose load with maximal effectiveness.     

The physiologic action of insulin on glucose uptake and its relevance to the interpretation of the metabolic clearance rate of glucose

Glucose uptake (Ru) is dependent upon the concentrations of both glucose and insulin. The metabolic clearance rate of glucose (MCRG), has been used as an in vivo measure of insulin action, because it was said to be independent of the prevailing glucose concentration. The validity of this assumption has recently been challenged. In this study, the effect of insulin concentration on the rate of glucose uptake (Ru) and on the MCRG was studied during euglycemia (5.1 +/- 0.3 mmol/L) and moderate hyperglycemia (10.4 +/- 0.5 mmol/L) in 17 experiments on nine normal ambulant volunteers. Stable plasma insulin levels were maintained with fixed infusion rates of insulin (0-300 mU/kg/h) and somatostatin (7.5 micrograms/min). At low insulin concentrations (less than 5 microU/mL) the increase in glucose uptake in response to hyperglycemia was small (5.3 +/- 2.3 mumol/kg/min). In contrast, with insulin levels more than 25 microU/mL, there was a steep rise in glucose uptake with hyperglycemia (55 +/- 3 mumol/kg/min; range: 44-74 mumol/kg/min). The metabolic clearance rate of glucose fell by an average of 32% with hyperglycemia in the studies at the lowest insulin levels (2.2 +/- 0.6 v 1.5 +/- 0.1 mL/kg/min; 0.15 greater than P greater than 0.1). There was no change in the MCRG in the subjects studied at higher insulin levels. It is concluded that (1) low concentrations of insulin are essential for the increase in glucose disposal during hyperglycemia; and (2) provided insulin levels are more than 25 microU/mL and plasma glucose less than 11 mmol/L, MCRG is independent of the plasma glucose concentration and is therefore a valid measure of insulin-mediated glucose uptake.     

甲状腺功能亢进症与妊娠期糖代谢异常

目的分析甲状腺功能亢进症（甲亢）与妊娠糖代谢异常的关系。方法对1983年1月1日-2007年12月31日在本院分娩的、孕期患有甲亢的134例孕妇（孕期甲亢组）和74例孕前有甲亢病史、孕期甲状腺功能（甲功）正常的孕妇（孕前甲亢史组）,孕期糖代谢异常的情况及影响因素进行分析;并与我院同期妊娠分娩的、非甲亢的31581名孕妇（非甲亢组）进行比较。结果208例甲亢孕妇（包括孕期甲亢组和孕前甲亢史组）糖代谢异常的患病率为30．8％[包括GDM7．2％,IGT3．4％和单独50g葡萄糖筛查（GCT）阳性20．2％],显著高于非甲亢孕妇的患病率（9．4％,其中包括GDM2．8％,IGT3．0％和50gGCT阳性3．7％）（P〈0．01）。孕期甲亢组和孕前甲亢史组妇女糖代谢异常率、GDM和单独50gGCT阳性率均无统计学差异（P均〉0．05）。孕期甲亢组妇女的分娩年龄（30±4岁）和分娩前BMI（27．1±3．1）均显著低于孕前甲亢史组（分别为32±4岁,P＝0．022;28．1±3．1,P＝0．041）。结论甲亢可能是导致妊娠糖代谢异常的危险因素之一。     

Opiate modulation of glucose turnover in dogs

We examined the effect of opiate infusion and of opiate blockage on glucose turnover in the basal state, using isotope dilution techniques in trained conscious dogs (n = 5). After a primed-continuous infusion of 3-3H glucose to steady state specific activity (90 minutes), infusion of one of the following was given: D-met2 pro5 enkephalinamide (DMPE), a potent morphine-like opiate, 0.5 mus g/kg/min; naloxone, an opiate antagonist, 1.25 mg followed by 10 mus g/min; or saline control. Infusion of DMPE led to a fall in glucose from 92 +/- 3 to 87 +/- 3 mg/dL by 60 minutes (P less than 0.05), associated with a rise in glucose utilization (Rd) from 3.0 +/- 0.4 to 3.9 +/- 0.6 mg/kg/min by 30 minutes (P less than 0.05); a transient rise in glucose production (Ra; from 3.2 +/- 0.4 to 4.3 +/- 0.4 mg/kg/min; P less than 0.05). Changes in counterregulatory hormones did not account for these findings; insulin was unchanged during all infusions; glucagon showed small late rises at 75 minutes during both DMPE and naloxone infusion; cortisol rose by 30 and 15 minutes, respectively, of DMPE and naloxone infusion; epinephrine rose transiently after 5 minutes of naloxone but was unchanged during DMPE, and norepinephrine was unchanged throughout. Saline infusion had no effects on any of these indices. We conclude that a potent opiate with morphine-like effects (DMPE) can lower glucose in dogs by enhancing peripheral glucose utilization independently of hormonal changes.     

Plasma glucagon suppressibility after oral glucose in obese subjects with normal and impaired glucose tolerance

Blood glucose, plasma insulin, and glucagon responses after a 75 g oral glucose-tolerance test were assessed in 9 normal controls, 5 obese nondiabetics (ON), 5 obese nondiabetics with fasting hyperinsulinemia (obese “resistant” nondiabetics—OR), 9 obese with impaired glucose tolerance (O-IGT), and 9 nonobese insulin-dependent diabetics (IDD). Fasting plasma glucagon concentrations were significantly higher in all groups of patients in comparison to the normal controls. Insulin secretion, evaluated in all but the IDD, was similar to normal in the ON and increased in the OR and O-IGT. Normal glucagon suppression was observed in the lean controls and ON but not in OR, O-IGT, and IDD. We suggested that the resistance to glucagon suppression after glucose load in the OR and O-IGT in the presence of increased insulin response could be an indication that the A cell participates in the relative insulin insensitivity of these subjects.     

Decreased plasma epinephrine concentrations after glucose ingestion in humans

Plasma levels of norepinephrine (NE), epinephrine (E), immunoreactive insulin (IRI), and glucose were measured in six healthy volunteers after glucose consumption and in six volunteers after a water solution. Ingestion of the glucose (100 g) solution significantly decreased E levels from 46.7 +/- 8.0 to 20.8 +/- 1.9 pg/mL (P less than 0.01). Three hours after the glucose ingestion, plasma E levels nearly returned to basal values. Plasma IRI and glucose levels peaked at 45 minutes after glucose consumption (P less than 0.01), then declined toward basal values. Plasma NE levels were unaffected by glucose consumption. There were no changes in glucose, IRI, NE, or E levels in the control group. These results suggest that E behaves as a counter-regulatory hormone to insulin under stimulation by glucose.     

Oral glucose tolerance test: Effect of different glucose loads on splanchnic carbohydrate and substrate metabolism in healthy man

To evaluate the role of splanchnic metabolism in the disposal of orally ingested glucose and thereby to define the optimal glucose load for glucose tolerance testing, splanchnic glucose output (SGO), as determined by the hepatic-venous catheter technique, was estimated in 16 healthy male volunteers in the basal state and after different glucose loads. Following glucose ingestion of 12.5, 25, 50, 75, and 100 g glucose, mean SGO over 2 hours was 9, 10, 12.3, 20, and 24.7 g above basal hepatic glucose production or 72, 40, 25, 26, and 25 percent of the respective glucose load. Increasing glucose doses represented a greater and more prolonged insulinogenic stimulus as determined by insulin concentrations in hepatic venous plasma. Splanchnic lactate uptake decreased and finally reverted to a net output in most of the subjects studied, whereas pyruvate production increased with rising glucose loads. It is concluded that (1) maximal stimulation of insulin release by administration of 50 to 100 g glucose results in maximal splanchnic extraction (75%) of an ingested glucose load, whereas smaller amounts of glucose are retained to a lesser extent; (2) 100 g of glucose provide optimal conditions for performing an oral glucose tolerance test (OGTT), thereby provoking a relative as well as an absolute maximum of splanchnic glucose extraction; and (3) splanchnic uptake of pyruvate and lactate following ingestion of small amounts of glucose revert to a net output with utilization of increasing glucose loads.     

Insulin and glucose levels during CPR in the canine model

Cardiopulmonary arrest and resuscitation produces tremendous physiological stress with resultant biochemical derangements. We undertook this study to determine insulin and glucose levels during cardiopulmonary arrest in the canine model. Baseline insulin and glucose levels were obtained from an ascending aortic arch catheter in six mongrel dogs. Ventricular fibrillation was induced by an electrical stimulus and ventilation was terminated. After five minutes of fibrillation, cardiopulmonary resuscitation (CPR) was initiated using external, mechanical CPR and a continuous epinephrine infusion at 5 micrograms/kg/min. Serum insulin and glucose levels were repeated 15 minutes after beginning CPR. Mean blood glucose 15 minutes after initiation of resuscitation (379 +/- 114 mg/dL) was significantly increased from prearrest levels (124 +/- 29 mg/dL, P less than .01). Mean serum insulin 15 minutes after initiation of resuscitation (11.3 +/- 3.3 microU/mL) was significantly decreased compared to prearrest levels (16.2 +/- 6.0 microU/mL, P less than .05). During ischemia, the myocardium becomes dependent primarily on glucose as a source of energy. Inappropriately low insulin levels during CPR may adversely affect an already compromised myocardial glucose metabolism. Further investigation is needed to determine the utility of insulin infusion during CPR.