高血糖对大鼠肝星状细胞活化及转化生长因子-β1和结缔组织生长因子表达的影响

目的探讨高血糖加重四氯化碳中毒大鼠肝纤维化进展的机制.方法24只SD大鼠分为对照组、高血糖组、正常血糖 四氯化碳组、高血糖 四氯化碳组,通过链脲佐菌素诱导高血糖,4周后用四氯化碳诱导肝纤维化,第9周处死.免疫组化法检测肝组织α-平滑肌肌动蛋白表达(反映肝星状细胞活化);实时RT-PCR及免疫印迹法测量肝组织转化生长因子-β1(TGF-β1)、结缔组织生长因子(CTGF)mRNA及蛋白表达.结果肝星状细胞活化、TGF-β1和CTGFmRNA和蛋白表达在对照组和高血糖组无明显改变,正常血糖 四氯化碳组、高血糖 四氯化碳组较对照组升高,后者较前者变化更为明显.这些改变与肝纤维化积分相平行.结论高血糖可通过诱导肝脏TGF-β1、CTGF表达以及星状细胞活化,加重四氯化碳中毒大鼠肝纤维化的程度.     

波动性高血糖、代谢记忆与糖尿病慢性并发症

糖尿病治疗的核心是防治糖尿病慢性并发症,波动性高血糖通过刺激氧化应激,会增加患者产生代谢记忆及诱发糖尿病并发症的机率.代谢记忆已逐渐成为糖尿病治疗中新的挑战.一、波动性高血糖和糖尿病并发症血糖紊乱分为持续性高血糖和血糖波动为特征的波动性高血糖[1].波动性高血糖是指间歇性或阵发性高血糖状态,亦称血糖飘移.早期的研究多关注于长期慢性高血糖与并发症的关系,随着血糖监测手段的发展,糖尿病患者血糖波动逐渐为人们所重视.近年来的研究表明,波动性高血糖相对于持续性高血糖更能增加糖尿病患者发生并发症的危险性.糖尿病慢性并发症的发生、发展不仅与整体血糖水平相关,而且与血糖的波动性密切相关[2].血糖波动通过活化氧化应激、炎症反应损失内皮细胞参与糖尿病并发症的进展,因此,对血糖波动的正确认识、评价和积极控制将有助于减缓糖尿病并发症的发生.波动性高血糖导致糖尿病慢性并发症,可能与血糖波动产生氧化应激产物激活血管损伤的4条途径有关[3].     

妊娠期高血糖患者血糖波动特点及其与妊娠结局的关系

妊娠期高血糖包括糖尿病合并妊娠与妊娠期间首次发现的高血糖.妊娠期高血糖患者整体血糖水平升高及血糖波动增加与围产期母婴不良结局密切相关.动态血糖监测(CGM)有助于全面了解血糖波动的变化特点,在妊娠期高血糖患者血糖管理、改善母婴预后等方面具有重要作用.利用CGM可以分析妊娠期高血糖患者的血糖波动特点,分析血糖波动与胰岛细胞功能的关系、对母婴结局的影响.     

肝病与血糖

肝病与血糖关系密切,肝病既可致高血糖症,又可致低血糖症。同时,高血糖也可引起肝脏组织学和功能的改变。本文主要从上述三个方面对肝病与血糖的关系研究作一综述。     

非糖尿病高血压合并脑梗死患者血糖水平与病情及预后的关系

目的 探讨非糖尿病高血压合并脑梗死患者血糖水平与病情及预后的关系.方法 选择本院120例非糖尿病高血压合并脑梗死患者检测其发病后72h内空腹血糖,并根据血糖水平的高低分为高血糖组和血糖正常组.其中高血糖组74例,血糖正常组46例,比较两组脑梗死面积、神经功能缺损程度及预后,同时对高血糖组大灶梗死和小灶梗死与血糖升高水平进行比较.结果 高血糖组脑梗死多为主干及大灶梗死,且神经功能缺损严重,预后差,与血糖正常组比较差异有统计学意义(P＜0.05);高血糖组大、小梗死灶与血糖水平比较差异有统计学意义(P＜0.05),血糖水平越高脑梗死灶越大.结论 非糖尿病高血压合并脑梗死患者的病情轻重及预后与发病后血糖水平有密切关系,积极监测和控制血糖水平对脑梗死的治疗及预后有重要的意义.     

餐后血糖调节与血管并发症

来自美国,欧洲和亚洲的流行病学资料均证实在自然人群中,已诊糖尿病患者与尚未被诊断的无症状糖尿病患者数量相当.在这些人群中有一部分人是通过筛查空腹血糖确诊的,而更多的人是通过OGTT试验或测试餐后血糖确诊的.这是因为葡萄糖刺激后2小时血糖随着年龄的增加而升高,空腹血糖则无这种改变.大多数无症状的老年糖尿病患者仅表现为负荷后高血糖.现在有越来越多的证据表明餐后高血糖可预测心血管疾病的发生发展.     

维吾尔族MODY家系的脂代谢特点

目的 研究不同糖代谢状态下维吾尔族MODY家系脂代谢变化的特点. 方法 收集新疆喀什地区维吾尔族四代健在的2个MODY家系共44名成员,测量其家系成员的一般资料及血糖、血脂.按1999年WHO关于糖尿病的诊断标准将所有家系成员分为2个组:正常血糖组,包括正常空腹血糖组和正常OGTT组.高血糖组,包括空腹血糖受损(IFG)组、糖耐量减低(IGT)组和糖尿病组.比较两组血糖、血脂的变化并分析其相关性. 结果 正常血糖组年龄明显低于高血糖组(P<0.01);正常血糖组空腹血糖、餐后2h血糖均明显低于高血糖组(P<0.01);正常血糖组LDL-C低于高血糖组(P<0.05).高血糖组TC、TG、HDL-C较正常血糖组高,但差异无统计学意义(P>0.05).正常血糖组和高血糖组间血糖、血脂升高无明显差异(P>0.05).收缩压与TC间呈正相关(r=0.482, P<0.05),与LDL-C呈正相关(r=0.486, P<0.05);舒张压与TC呈正相关(r=0.432, P<0.05),与LDL-C呈正相关(r=0.464, P<0.05).其余各指标间无明显相关性. 结论 MODY家系成员在正常糖代谢状态下存在血脂紊乱表现,其收缩压、舒张压与TC、LDL-C呈正相关.     

冠状动脉搭桥术后患者血糖水平的变化

目的 探讨冠状动脉搭桥术（CABG）后患者的血糖变化规律.方法 138例接受CABG的患者,按术前有无糖尿病分为糖尿病组和非糖尿病组,术后观察其血糖水平.结果 138例患者中有101例术后发生高血糖,其中非糖尿病组53例、糖尿病组48例,两组相比,P＞0.05.术前血糖水平与术后高血糖的发生有关（P＜0.01）,术后高血糖患者99.0%血糖升高出现在术后24 h以内,血糖峰值的出现时间为术后16 h.结论 CABG后高血糖的发生率较高,且绝大多数出现在术后 24 h以内,术后高血糖发生率与术前血糖水平有关.     

一文读懂TIR

临床发现,即使糖化血红蛋白达标,患者仍有低血糖、高血糖、血糖波动过大等风险. 现己知道,血糖显著波动与糖尿病慢性并发症的发生和发展密切相关,其危害甚至比持续性高血糖更为严重.因此,关于血糖监测,我们不仅要关注患者的血糖水平,还要注意血糖波动大小,显然这是糖化血红蛋白难以胜任的.     

慢性阻塞性肺疾病急性加重期患者血糖血脂的表达特征

目的探讨慢性阻塞性肺疾病急性加重期(AECOPD)患者血糖、血脂的表达特征及其与病情的相关性。方法检测66例AECOPD患者,(其中34例为轻中度,32例为重度、极重度),及同期住院32例非COPD患者的空腹血清甘油三酯(TG)、胆固醇(CH)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白A1(APoA1)、载脂蛋白B(APoB)、糖化血红蛋白(HbAlc)、空腹血糖(FBG)、餐后2h血糖(P2hBG)、空腹及餐后2h胰岛素(IRI)的水平。结果 COPD组中的HbAlc、FBG、P2hBG、空腹IRI、餐后2hIRI水平均较非COPD组明显升高(P<0.01),其中COPD患者中重度、极重度组餐后2hIRI水平又高于轻中度组(P<0.05);COPD患者的TG、ApoB水平均比非COPD组降低(P<0.05),COPD重度、极重度组LDL-C水平比非COPD组及轻中度组升高(P<0.05)。结论 AECOPD患者尤其是重度、极重度阶段存在血糖、血脂紊乱,主要表现为高血糖、胰岛素抵抗、血脂异常。COPD组中LDL-C升高,提示COPD与冠心病(CHD)可能存在一定的相关性。     

Gastrointestinal motor mechanisms in hyperglycaemia induced delayed gastric emptying in type I diabetes mellitus.

BACKGROUND: Hyperglycaemia delays gastric emptying, both in healthy controls and in patients with diabetes mellitus. The effect of hyperglycaemia on antroduodenal motility in diabetes has not yet been studied. AIM: To investigate the gastrointestinal motor mechanisms involved in the hyperglycaemia induced retardation of gastric emptying in patients with type I diabetes mellitus and autonomic neuropathy. In eight diabetic patients antroduodenal manometry was performed simultaneously with scintigraphic measurement of emptying of a mixed solid-liquid meal, during euglycaemia (5-8 mmol/l glucose) and hyperglycaemia (16-19 mmol/l glucose), on separate days, in random order. RESULTS: Hyperglycaemia decreased the cumulative antral motility index from 38.3 (range 24.2-47.6) to 30.8 (range 17.3-38.1) (p = 0.025) and reduced the number of antral pressure waves propagated over > or = 4.5 cm (p = 0.04). Duodenal phase III-like activity was seen irrespective of the glycaemic state (in three patients during euglycaemia and in four patients during hyperglycaemia). Hyperglycaemia significantly affected gastric emptying of the solid meal: it prolonged the lag phase from 20.0 minutes to 28.5 minutes (P = 0.02), increased the 50% emptying time from 73.5 minutes to 104.5 minutes (p = 0.03), and increased the percentage of isotope remaining in the stomach after 120 minutes from 33.5% to 46.5% (p = 0.02). The cumulative antral motility index was correlated with the 50% emptying time (r = 0.75, p = 0.02) during euglycaemia, but not during hyperglycaemia (r = 0.28, P = 0.31). Liquid emptying was not influenced by the blood glucose concentration. CONCLUSIONS: Hyperglycaemia reduces postprandial antral contractile activity and its organisation in patients with type I diabetes and autonomic neuropathy. These changes in antroduodenal motility are likely to constitute the mechanism through which gastric emptying of solids is delayed during high blood glucose concentrations in these diabetic patients.     

Insulin resistance and inflammation - A further systemic complication of COPD

Chronic obstructive pulmonary disease (COPD) is associated with a continuous systemic inflammatory response. Furthermore, COPD is associated with an excess risk for cardiovascular disease and type II diabetes. Systemic inflammation in other populations is a factor in atherogenesis and has been associated with insulin resistance. We assessed the association between systemic inflammation and insulin resistance in non-hypoxaemic patients with COPD. Fasting plasma glucose, insulin and inflammatory mediators were measured in 56 patients and 29 healthy subjects. Body mass index (BMI) and height squared fat- and fat-free-mass index were similar between subject groups. Using homeostatic modelling techniques, mean (SD) insulin resistance was greater in the patients, 1.68 (2.58) and 1.13 (2.02) in healthy subjects, p=0.032. Fasting plasma insulin was increased in patients while glucose was similar to that in healthy subjects. Patients had increased circulating inflammatory mediators. Insulin resistance was related to interleukin-6 (IL-6), r=0.276, p=0.039, and tumour necrosis factor alpha soluble receptor I, r=0.351, p=0.008. Both IL-6 and BMI were predictive variables of insulin resistance r(2)=0.288, p<0.05. We demonstrated greater insulin resistance in non-hypoxaemic patients with COPD compared with healthy subjects, which was related to systemic inflammation. This relationship may indicate a contributory factor in the excess risk of cardiovascular disease and type II diabetes in COPD.     

Special considerations for the diabetic patient in the ICU; targets for treatment and risks of hypoglycaemia

Due to the diabetes pandemic the number of diabetic patients admitted to the intensive care unit (ICU) increases. Diabetic patients admitted to the ICU are more vulnerable for developing complications as compared to non-diabetic patients, but this does not directly translate into higher mortality rates. However, mortality might differ per admission diagnosis. Hyperglycaemia is common in diabetic as well as non-diabetic critically ill patients, but probably chronic hyperglycaemia is pathophysiologically different from acute hyperglycaemia. As opposed to non-diabetic patients, there is discussion about the association between hyperglycaemia and mortality in diabetic patients. They do not seem to benefit from strict glycaemic control and also glucose variability appears less harmful, although clinical trials in diabetic populations have not been performed yet. Diabetes is a risk factor for hypoglycaemia and evidence suggests that even near-normal glucose levels are associated with worse outcome. Taking this together, it is suggested to strive for moderate targets when treating hyperglycaemia in critically ill diabetic patients.     

Prognostic value of erythrocyte sedimentation rate in ST segment elevation myocardial infarction: interaction with hyperglycaemia

OBJECTIVES: Many inflammatory markers are associated with an adverse prognosis after ST segment elevation myocardial infarction (STEMI). Hyperglycaemia may exacerbate this inflammatory response. We investigated whether the erythrocyte sedimentation rate (ESR) was associated with an adverse prognosis and whether this was mediated by glucose levels. RESEARCH DESIGN AND METHODS: It concerns a post hoc analysis of a prospective randomised trial. In 346 patients with STEMI treated with reperfusion therapy, we investigated long-term outcome. Patients with ESR in the upper quartile (>14 mm h(-1)) were compared to patients with a normal ESR. Hyperglycaemia was defined as admission glucose >or=7.8 mmol L(-1). Median follow up was 7.4 years (range: 5.7-8.3). MAIN OUTCOME MEASURES: All cause mortality, cardiovascular mortality, sudden death, death as a result of heart failure. RESULTS: Both elevated ESR and hyperglycaemia were associated with a worse prognosis and increased mortality. Elevated ESR was particularly associated with an increased risk of sudden death (OR: 3.3, 17% vs. 6%, P < 0.01) whereas hyperglycaemia was especially associated with an increased risk of death because of heart failure (OR: 6.5, 8% vs. 1%, P < 0.01). There was no association between increased ESR and elevated glucose levels. Multivariate analysis did reveal that both elevated ESR and admission glucose were independent predictors of long-term mortality. CONCLUSIONS: Elevated ESR and admission glucose are independent predictors of mortality in STEMI patients treated with reperfusion therapy. There is no association or interaction between glucose levels and the inflammatory response as reflected by ESR.     

Neurological and endocrinological disorders: orphans in chronic obstructive pulmonary disease

Patients with chronic obstructive pulmonary disease (COPD) are often characterised by a range of characteristic co-morbidities that interfere with their pulmonary disease. In addition to a mere association with co-morbidities, a complex pathophysiological interaction and mutual augmentation occurs between COPD and its co-morbidities that may result in disease progression and increased morbidity and mortality. An interdisciplinary approach is required both for diagnosis and treatment to target co-morbidities early in the course of the disease. This review summarizes the current knowledge of the interaction with cerebrovascular disease and endocrinological co-morbidities in COPD patients. There is growing evidence that COPD is an independent risk factor for ischemic stroke, increasing the risk about twofold. Stroke risk in COPD patients increases with the severity of the disease as measured by the degree of airflow limitation. The presence of cardiovascular risk factors is of particular importance for stroke prevention in COPD patients. Endocrinological co-morbidities are also important and many are associated with increased cardiovascular risk. Impaired glucose metabolism ranges from insulin resistance to overt diabetes mellitus, which is a frequent finding and is associated with worse outcome.     

强化血糖控制对慢性阻塞性肺疾病急性加重期合并高血糖肺功能的影响

目的：观察强化血糖控制对慢性阻塞性肺疾病急性加重期合并高血糖肺功能的影响,为慢性阻塞性肺疾病急性加重期合并高血糖的治疗提供理论依据和实践指导。方法：采用同期、平行、随机对照试验的方法对研究对象的肺功能进行分析。结果：治疗后两组的肺功能均有明显改善,第14d后实验组FEV1／FVC及FEV1实测／预计值较对照组比较有统计学差异,P〈0．05。结论：强化血糖控制利于患者肺功能恢复,改善患者生活质量。     

What glucose target should we aim for in myocardial infarction?

Hyperglycaemia in the period following myocardial infarction is associated with increased mortality and there is some evidence that its treatment can improve survival. However, it remains unclear as to what the ideal glucose targets might be. This study examined observational data taken from a previously reported randomised controlled trial of insulin therapy for myocardial infarction (The Hyperglycaemia: Intensive Insulin Infusion In Infarction Study), to determine optimal glucose levels for this period. Capillary glucose readings were recorded at 8 standard time points for 234 subjects in first 24 h after myocardial infarction. Survival over 6 months was analysed according to whether 80% of each subject's glucose readings were below specified glucose thresholds (Achievers) or not (Non-Achievers). We found that the glucose threshold at which there was greatest separation in mortality between Achievers and Non-Achievers was at 8 mmol/L [144 mg/dL] (6 month mortality 1.6% vs. 9.1%, p = 0.05). Therefore subjects who maintained the majority of their blood glucose levels below 8 mmol/L following myocardial infarction had optimal survival outcomes. We suggest that this might be an appropriate glucose target to aim for in the peri-infarct period.     

Exercise capacity in subjects with type 1 diabetes mellitus in eu- and hyperglycaemia

BACKGROUND: Circumstantial evidence suggests that an increase in plasma glucose availability improves exercise capacity in subjects with type 1 diabetes mellitus. The aim of this study was to assess exercise capacity in eu- and hyperglycaemic conditions in subjects with type 1 diabetes. METHODS: Eight moderately exercise-trained male subjects with type 1 diabetes on continuous subcutaneous insulin infusion were studied. Using identical insulin infusion rates, the patients were randomly allocated to perform two stepwise ergometer tests in eu- and hyperglycaemic clamp conditions. The primary endpoint was the peak power output; the secondary endpoints comprised the rate of perceived exertion, lactate levels, heart rate, and respiratory exchange ratio. RESULTS: Eu- and hyperglycaemic clamp conditions were observed at a plasma glucose concentration of 5.3 +/- 0.6 mmol/L and 12.4 +/- 2.1 mmol/L, respectively (mean +/- SD), and remained stable throughout the physical exercise. Insulin levels were similar in both conditions. Hyperglycaemia did not result in a significant increase in the peak power output compared to euglycaemia (mean paired difference of 4.96 W, 95% CI - 11.3 to 21.2, p = 0.49). Hyperglycaemia did not have a significant impact on the secondary endpoints compared to euglycaemia. Sensitivity analyses confirmed these results. CONCLUSIONS: In subjects with type 1 diabetes, exercise capacity is not influenced by hyperglycaemia. Comparable levels of lactate and similar respiratory exchange ratio suggest that an increase in extracellular glucose availability did not translate into increased intracellular glucose oxidation.