血糖四分体的新主角-血糖波动性

血糖波动性成为血糖四分体的一个组分.长期血糖波动可以增加氧化应激,促进糖尿病微血管病变的发生.血糖波动与糖尿病大血管病变的关系有待进一步研究.CGMS有助于监测血糖波动,适用于对脆性血糖的患者或对低血糖感知下降的患者调整治疗.在T2DM患者中即使总体血糖控制较为理想,也需要采取有效措施降低血糖波动.选择合适的治疗策略是控制血糖波动的关键.     

血糖波动的研究进展

随着对糖尿病病理生理机制的深入研究及临床研究的不断开展,血糖波动的危害性越来越受到重视.有学者提出,血糖波动是糖尿病慢性并发症的独立危险因素.基础研究已证实,血糖波动可加剧氧化应激.但临床研究中,血糖波动对糖尿病慢性并发症的影响仍有争论.因此,本文就血糖波动的损伤机制、危害、评估方法及干预措施的研究进展情况加以总结论述.     

动态血糖监测系统血糖波动评估参数及其临床应用

动态血糖监测系统(CGMS)是近年推出的新型血糖监测系统,它有很多反映血糖波动的指标,如血糖水平的标准差、曲线下面积或血糖的频数分布、平均血糖波动幅度、24 h平均血糖水平、日间血糖平均绝对差、平均每日风险范围等.各指标均有优势和缺陷,现回顾了CGMS常用的一些指标和近年来提出的新指标,为临床工作者和研究者提供评估血糖...     

肝炎后肝硬化患者血糖异常临床分析

对病毒性肝炎和肝炎后肝硬化病人的空腹血糖、餐后2h血糖进行检测,并与病毒性肝炎患者进行对比.结果肝炎后肝硬化病人可以出现糖代谢紊乱(69.4%),明显多于病毒性肝炎患者,空腹低血糖,空腹高血糖及餐后2h血糖升高均可能出现.结论对肝炎后肝硬化患者进行血糖监测有重要意义.     

血糖波动与糖尿病血管病变有无因果关系的讨论

高血糖是糖尿病的标志,也是导致糖尿病并发症的一个主要因素.血糖波动是糖代谢的重要指标.非循证医学研究显示,血糖波动与血管损伤和糖尿病并发症的发生有关,但尚无大型临床干预试验证明,因此血糖波动与血管损伤及糖尿病并发症之间的因果关系缺乏循证医学证据.实际工作中我们应重视血糖波动并进行相应的循证医学研究.     

血糖控制未达标2型糖尿病患者血糖波动与认知功能关系研究

目的 观察血糖控制未达标2型糖尿病患者血糖波动与认知功能的关系.方法 采用问卷调查的方法评定认知功能,比较不同血糖波动组间认知功能的差异,并对认知功能与问卷当日的血糖波动情况等进行相关性分析.结果 (1)日7次血糖的均数、标准差、血糖波动及总血糖在不同HbA1c组间有统计学差异(P＜0.01);(2)不同血糖波动组间认知功能有统计学差异(P＜0.05),但性别、年龄、受教育年限等方面却无统计学差异(P＞0.05);(3)认知功能与检查当日7次血糖的平均值、最高血糖水平、最低血糖水平、血糖波动幅度及总血糖水平等均呈负相关.结论 血糖控制未达标2型糖尿病患者认知功能与血糖波动密切相关.减少血糖波动对认知功能的保护有着重要的意义.     

空腹血糖水平与肝硬化发病关系的前瞻性研究

目的 探讨中国人群中空腹血糖水平与肝硬化发病风险的关系.方法 基于河南省某县食管癌营养干预试验队列完成了一项巢式病例对照研究.利用全自动生物化学分析仪及酶联免疫法检测了310例肝硬化个体与620例对照者的基线空腹血糖以及3项肝炎病毒学标志物(HBsAg、抗-HBc与抗-HCV)水平,并从调查问卷收集了研究对象相关特征信息.使用两独立样本t检验比较了基线特征与研究因素中的连续性变量在病例组和对照组之间的分布差异,而分类变量的比较则使用了x2检验.使用多重线性回归模型对各项研究因素与血糖连续性变量的依存关系进行探索用于筛选潜在的混杂因素.在多重线性回归模型中提示与血糖浓度有关的因素以及考虑可疑的混杂因素均被纳入Logistic回归模型中作为调整以分析血糖水平与及肝硬化的联系,模型中血糖最低浓度组被定义为参考水平,对回归模型统计学意义的评价使用了似然比检验.结果 病例组与对照组血糖浓度分别为(4.5±1.8)mmol/L与(4.2±2.1)mmol/L,两者比较,差异有统计学意义(t=-2.414,P＜0.05);第5组中的研究对象与第1组即参考水平相比肝硬化发病风险升高,OR=1.672;并且血糖水平的升高与疾病发病风险的增加具有线性相关关系(P＜0.05).在对可能的混杂因素包括性别、年龄、HBsAg、抗-HCV以及饮酒情况进行调整之后,高浓度组肝硬化疾病风险的增加仍具有统计学意义(OR=1.96,P＜0.05).结论 提示较高的空腹血糖水平可能作为肝硬化一项独立的危险因素,与肝硬化发病风险升高相关.     

糖尿病血糖波动与氧化应激

糖尿病血糖波动与氧化应激对靶器官的损伤和并发症的影响正成为糖尿病防治研究的新热点.血糖波动产生的氧化应激与糖尿病及其并发症的发生、发展有着密切的联系,减少血糖波动对氧化应激的影响,逆转氧化应激对组织细胞的损伤,从而可能阻止或延缓糖尿病及其并发症的产生.本文就近年来发表的相关文献和相关进展综述如下.     

老年2型糖尿病患者血糖控制全面评估

目的对老年2型糖尿病患者血糖控制情况进行全面评估,并探讨糖化血红蛋白（HbAlc）与血糖波动的相关性;方法选取老年糖尿病患者共284名,测定空腹血糖（FPG）、餐后2h血糖（PPG）、HbAlc水平,进一步采用动态血糖监测系统（CGMS）评估血糖波动情况。按照HbAlc水平分为两组（HbAlc≤7％组和HbAlc〈7％组）,比较两组间血糖控制水平及血糖波动情况。结果本研究中老年糖尿病患者FPG达标率为67．6％,PPG为34．9％,HbAlc为42．9％,血糖波动正常范围内的患者占28．6％,血糖波动大的患者占71．4％。两组间比较,FPG、PPG、MBG差异有统计学意义（P〈0．01）;但两组间代表血糖波动的各参数平均血糖标准差（SDBG）、最大血糖波动幅度（LAGE）、平均血糖波动幅度（MAGE）、日间血糖波动幅度（MODD）相比,差异无统计学意义（P〉0．05）。相关性分析表明,MAGE及MODD均与HbAlc水平无关（P〉0．05）。结论大多数老年糖尿病患者的血糖控制未达标,且约70％的老年糖尿病患者血糖波动大。HbAlc与血糖波动无关,HbAlc和血糖波动是评价血糖控制的独立指标。     

血糖波动对急性冠状动脉综合征合并血糖代谢异常患者的影响

<正>血糖波动是指机体血糖在一定时间内变化的离散趋势,是评估糖尿病患者血糖控制的指标之一。随着动态血糖监测系统(continuous glucose monitoring system,CGMS)的应用,越来越多的研究人员及临床工作者逐渐认识到,血糖波动和     

Determination of plasma glucose during rapid glucose excursions with a subcutaneous glucose sensor

Continuous glucose monitoring has the potential to improve glucose management and reduce the risk of hypoglycemia in individuals with diabetes. Accurate sensors may also allow the development of a closed-loop insulin delivery system. The purpose of this work was to determine the delay time associated with a subcutaneous glucose sensor during rapidly changing glucose excursions. Subcutaneous glucose sensors (Medtronic MiniMed, Inc., Northridge, CA) were inserted in five healthy men. After a 2-h stabilization period, a 3-h hyperglycemic (approximately 11 mM) clamp was performed followed by a 90-min period in which plasma glucose was allowed to decline to as low as 2.8 mM. Sensors were calibrated using two points (basal and hyperglycemia), and the calibrated sensor glucose measurements were compared with those from a reference analyzer (Beckman Instruments, Fullerton, CA). Response time was estimated from a first-order kinetic model. Plasma glucose levels, determined with the subcutaneous sensor, were highly correlated with those obtained with the reference glucose analyzer (r(2) = 0.91, p < 0.001; mean absolute difference of approximately 8%). The half-time for the sensor response was estimated to be 4.0 +/- 1.0 min. The subcutaneous glucose sensor has the potential to facilitate the detection of hypoglycemia and improve overall glycemic control when used in a real-time monitor. The rapid response should be sufficient to allow a fully automated closed-loop insulin delivery system to be developed based on the subcutaneous sensing site.     

Increased glucose turnover and glucose cycling in acromegalic patients with normal glucose tolerance

Summary To characterize the diabetogenic effects of growth hormone, we simultaneously measured glucose turnover with 2-³H- and 6-³H-glucose in six acromegalic patients with normal fasting blood glucose and oral glucose tolerance tests. Eight healthy volunteers served as controls. All subjects were studied under both basal conditions and during glucose infusion (2 mg · kg^–1 · min^–1). We determined true glucose production and irreversible glucose uptake using 6-³H-glucose and glucose cycling (difference between 2-³H- and 6-³H-glucose). After an overnight fast, glucose production was higher than normal in the acromegalic patients (2.18±0.15 vs 1.85±0.03 mg · kg^–1 · min^–1,p < 0.05) despite hyperinsulinaemia. The metabolic clearance rate was normal. During the glucose infusion, glucose production was not suppressed as effectively in the acromegalic patients as in controls nor was glucose uptake augmented, while metabolic clearance rate was decreased. In acromegaly, basal glucose cycling was increased (0.44 ± 0.08 vs 0.25 ± 0.07 mg · kg^–1 · min^–1, p < 0.05). Furthermore cycling of endogenous glucose measured during glucose infusion was also augmented (0.41 ± 0.05 vs 0.24 ± 0.05 mg · kg^–1 · min^–1, p < 0.05). Hence the increase of glucose cycling (70%) was much more pronounced than that of glucose production (17%). In conclusion, small defects in glucose metabolism in acromegaly can be detected with sensitive tracer methods. These derangements are confined to the liver under fasting conditions, but are of both hepatic and extrahepatic origin during glucose loading.     

Effect of intravenous glucose on serum glucose determinations

Hyperglycemia is frequently seen in hospitalized nondiabetic patients receiving intravenous glucose solutions. As no standard method of interpreting the serum glucose value has been defined in patients receiving intravenous glucose, we have attempted to determine if any correlation can be made. It was found that with a 5% dextrose in water infusion at 100 ml/hr, the mean change in serum glucose was $\text{9}\text{mg}\text{100}\text{ml}$ above the fasting serum glucose; with a 5% dextrose in water at 200 ml/hr, the mean serum glucose rose $\text{24}\text{mg}\text{100}\text{ml}$ above the fasting serum glucose obtained in the arm opposite the intravenous infusion. It was thus determined that a serum glucose level greater than $\text{20}\text{mg}\text{100}\text{ml}$ above the fasting serum glucose level in an individual with a 5% glucose in water infusion at 100 ml/hr, or $\text{42}\text{mg}\text{100}\text{ml}$ above the fasting serum glucose in an individual with a 5% glucose in water infusion at 200 ml/hr, which are 3 SD above the mean glucose, should be early evidence for mild subclinical glucose intolerance.     

Immobilized glucose oxidase in implantable glucose sensor technology

Glucose oxidase has had a central role in previous glucose sensing methods and is key to the development of certain new glucose sensors. The immobilized enzyme is specific for glucose and sufficiently long-lived for many sensor applications, but new glucose sensing applications may place increased demands on the enzyme.     

Regulation of hepatic glucose output by glucose in vivo

The effect of infusing glucose at a rate estimated to equal hepatic glucose production (2 mg/kg BW X min) was investigated in postabsorptive unrestrained miniature pigs. Glucose turnover was estimated by the use of 3-H-glucose before and during glucose infusion where the contribution of the glucose-induced hormonal changes were estimated by infusing glucose plus somatostatin with or without insulin and/or glucagon substitution. Our data give evidence for an inhibitory effect of glucose on endogenous glucose production in the postabsorptive state. This effect seems to be independent of the hormonal changes induced by glucose infusion.     

Hepatic glucose production and splanchnic glucose exchange in hyperthyroidism

Hepatic glucose production (HGP) and net splanchnic glucose balance (NSGB) were simultaneously determined in the basal state in 8 hyperthyroid patients and 10 normal subjects using iv infusion of [3H]3-glucose and the hepatic venous catheter technique. Splanchnic glucose uptake (SGU) was calculated as the difference between the HGP and NSGB. SGU was also measured by determining the splanchnic extraction ratio of [3H]3-glucose across the splanchnic bed. In 5 hyperthyroid patients and 5 normal subjects a renal vein was also catheterized in the basal state. The influence of increased endogenous insulin secretion [stimulated by a low rate iv infusion of glucose (2 mg/kg . min)] on splanchnic and hepatic glucose exchange was also examined. Basal HGP (measured with [3H]3-glucose) was increased by 20% in the hyperthyroid patients [14.2 +/- 0.6 (SEM) mumol/kg . min] as compared to normal subjects (11.9 +/- 0.6, P less than 0.02). In marked contrast, NSGB output was slightly but not significantly decreased in the hyperthyroid group. SGU in the hyperthyroid patients, as determined with both techniques, was more than 2-fold higher than in the normal group (P less than 0.02-P less than 0.005). Splanchnic uptake of gluconeogenic precursors (lactate, pyruvate, glycerol) was increased by 20-120% in the patient group. During iv infusion of glucose, plasma insulin levels increased more in the hyperthyroid group (66% vs. 37%, P less than 0.05). Nevertheless, HGP and NSGB were less markedly suppressed in the patients as compared to the normal subjects (P less than 0.01), whereas the augmented SGU in the hyperthyroid patients reverted to normal. Splanchnic uptake of gluconeogenic precursors was unchanged in both groups. No net renal glucose production could be demonstrated in either group in the basal state. We conclude that in hyperthyroidism, increased HGP occurs in the face of an unchanged or slightly reduced rate of net glucose delivery to extrasplanchnic tissue. This discrepancy can be ascribed to augmented splanchnic uptake of glucose. These findings raise the possibility of futile cycling of glucose in the liver as a mechanism of increased oxygen consumption in hyperthyroidism. The data also demonstrate a diminished inhibitory effect of endogenous insulin on splanchnic glucose production, suggesting the presence of hepatic resistance to insulin in hyperthyroidism.     

Relationship between glucose oxidation and glucose tolerance in man

The study was performed to determine the influence of peripheral glucose utilization on glucose tolerance. Glucose oxidation was measured in a group of 6 normal subjects by means of continuous indirect calorimetry during a 100 g oral glucose tolerance test for 3 hr, comparing the control state with experimental inhibition or stimulation of glucose oxidation. Suprabasal oxidation, corresponding to oxidation in response to the load, mainly by insulin-dependent tissue, was obtained by subtracting basal oxidation (essentially by non-insulin dependent tissues) from total oxidation. Suprabasal oxidation of glucose was inhibited by a neutral fat infusion, and stimulated by means of dichloracetate. In the control test, from the 100 g glucose administered, 18 g participated to suprabasal oxidation during the 3 hr of the test. A neutral fat infusion, started 2 hr before the glucose load and lasting throughout the test, decreased suprabasal oxidation to 7.5 g, i.e. to 42% of the control value. With the fat infusion, a larger fraction of the energy consumption was shown to originate from lipid oxidation (37% versus 25% in controls, p < 0.05) at the expense of carbohydrate (CHO) oxidation (44% versus 60% in controls, p < 0.05). However, these major changes in peripheral glucose oxidation were accompanied by only a moderate decrease in glucose tolerance. Dichloracetate administered prior to the test increased suprabasal oxidation to 25 g glucose oxidized in the 3 hours following the glucose load, i.e. an increment of 39% above the control value. A larger fraction of energy consumption was derived from carbohydrates (77% versus 60% in controls, p < 0.05). However, no significant change was observed in glucose tolerance. These results indicate that marked changes of peripheral glucose oxidation have little influence on glucose tolerance and suggest that another mechanism, i.e. glucose storage, plays a larger role in regulating plasma glucose levels during oral glucose tolerance tests.