Impaired glucose tolerance in acute pancreatitis

Acute pancreatitis (AP) is an acute inflammatory disease of the exocrine pancreas. In spite of the pivotal role of the endocrine pancreas in glucose metabolism, the impact of impaired glucose tolerance on AP has not been fully elucidated. A meta-analysis of seven observational studies showed that type 2 diabetes mellitus (DM) was associated with an increased risk of AP. The increased risk of AP shown in the meta-analysis was independent of hyperlipidemia, alcohol use and gallstones. Anti-diabetic drugs including incretins might increase the risk of AP, but no intervention trials have confirmed this. Although a controversial finding, DM seems to be associated with severe attacks and organ failure in AP. We analyzed the results of a nationwide epidemiological survey of AP in Japan. We studied the impact of pre-existing DM on the clinical course of AP in 1954 cases for which information on DM status was available at the onset of AP. The prevalence of DM in AP patients (12.8%) was higher than that in the general population in Japan (10.5%). AP patients with DM had higher morbidity of cardiovascular and renal failure than those without DM. About 35% of the idiopathic AP patients with DM had renal failure. The mortality of AP patients with DM (4.0%) was higher than that of AP patients without DM (1.7%). If stratified by etiology, idiopathic, but not alcoholic or biliary, AP patients with DM were predisposed to increased mortality (9.7%). In conclusion, impaired glucose tolerance might have an impact on the development and clinical outcome of AP. However, the impact might depend on the cause of hyperglycemia, the condition of DM including severity, duration and treatment, and the characteristics of the AP patients including age, etiology and comorbidity.     

葡萄糖耐量低减与动脉粥样硬化

目的　观察葡萄糖耐量低减 (IGT)与动脉粥样硬化 (AS)的关系。方法　在曾经有血糖异常升高 (但未达糖尿病标准 )、患有心血管疾病 (如冠心病、中风或高血压 )或其危险因素 (如血脂异常 )的人群进行 75g口服葡萄糖耐量试验 (OGTT)筛查IGT病人 ,并同时记录病史、体检。空腹血脂指标由自动生化分析完成。同时用B型超声检查双侧颈总动脉 ,观察内膜连续性、内膜 中层厚度 (IMT)、斑块等指标。结果　IGT组 (n =5 1)的内膜连续性比正常糖耐量 (NGT)组 (n =97)明显差 (P <0 .0 5 ) ,IGT组双侧平均IMT和动脉粥样硬化 (AS)积分均显著高于NGT组 (均P <0 .0 5 ) ,IGT的平均IMT异常增高的发病率显著高于NGT。但以上指标IGT与糖尿病组 (n =73 )差异无显著性。多元分析发现 ,IGT的AS指标增加效应经同时校正甘油三酯、胆固醇、冠心病史、中风史、吸烟、性别、体重指数仍具有显著意义 ;但是分别校正年龄、腰臀围比值、高密度脂蛋白胆固醇和高血压病史 ,三种AS指标有不同程度的减弱。结论　与NGT人群相比 ,IGT人群已经存在明显的AS表现 ,其程度与糖尿病类似。IGT的动脉粥样硬化现象独立于部分心血管危险因子和已经存在的心血管疾病。     

空腹血糖受损患者糖耐量异常及影响因素分析

目的了解空腹血糖受损(IFG)患者糖耐量异常(IGT)情况及其影响因素。方法纳入空腹血糖为5.6~6.1 mmol/L的IFG患者337例,检测患者口服75克葡萄糖后2小时血糖等资料,分析患者IGT情况及其影响因素。结果纳入的337例IFG患者中46.6%(157/337)伴有IGT。口服葡萄糖耐量异常和正常组超重和肥胖率分别为75.0%和63.1%(P0.05);口服葡萄糖耐量异常组甘油三酯水平显著高于正常组,高密度脂蛋白胆固醇水平低于正常组,均有统计学差异(P0.05)。多因素Logistic回归分析结果显示,年龄、体重指数、甘油三酯水平是IFG患者葡萄糖耐量异常的影响因素,相对危险分别为:1.06(95%CI:1.03~1.08);1.11(95%CI:1.05~119);1.58(95%CI:1.23~2.09)。进一步对体重正常者发生糖耐量异常的影响因素进行分析,除年龄外,甘油三酯水平是空腹血糖受损患者糖耐量异常的影响因素,相对危险为2.10(95%CI:1.29~3.43)。结论空腹血糖受损患者约半数伴有糖耐量异常,体重指数和甘油三酯水平是空腹血糖受损患者糖耐量异常的影响因素。     

Impaired glucose tolerance with late hypersecretion of insulin during oral glucose tolerance test in patients with vasospastic angina

Objectives.This study tested whether patients with vasospastic angina have impaired glucose tolerance or impaired insulin response.Background.Hyperinsulinemia has been demonstrated in patients with coronary artery disease and syndrome X.Methods.We performed an oral glucose tolerance test (75 g) in 30 patients with vasospastic angina in whom severe coronary vasospasm was induced by acetylcholine and in a matched group of 30 patients with atypical chest pain in whom no significant vasospasm was induced. The responses of insulin and glucose were compared between the two groups. No subjects had overt diabetes mellitus, hypertension, dyslipidemia, obesity or angiographically detected significant baseline coronary stenosis. Venous blood samples were taken during fasting and at 30, 60, 120 and 180 min after glucose load to obtain plasma glucose and immunoreactive insulin levels.Results.Impaired glucose tolerance was detected in the 19 (63%) of 30 patients with vasospastic angina and in none of 30 patients with atypical chest pain (p < 0.001). The immunoreactive insulin levels at 60 and 120 mins as well as the interval to peak insulin level were significantly greater in patients with vasospastic angina (p < 0.001). Among patients with vasospastic angina, those with acetylcholine-induced multivessel coronary vasospasm showed a significantly higher sum of insulin concentrations than those with single-vessel spasm (p < 0.01). During induction of coronary spasm, 10 patients with vasospastic angina presented ventricular arrhythmias. The sum of insulin concentrations was significantly greater in patients with than in those without ventricular arrhythmias.Conclusions.Patients with vasospastic angina exhibited a high incidence of impaired glucose tolerance and delayed and significantly higher insulin responses. These findings suggest that impaired glucose tolerance with late hypersecretion of insulin may contribute to the pathogenesis of severe coronary vasospasm.     

Long-term glucose tolerance in highly experienced HIV-infected patients receiving nucleoside analogue-sparing regimens

Thirty-nine HIV-1-infected patients treated for 156 weeks with a new nucleoside analogue-sparing regimen [raltegravir, etravirine and maraviroc (REM) or raltegravir, etravirine and darunavir/ritonavir (RED)] showed a uniform increase in fasting glucose levels and a uniform decrease in insulin secretory capacity. Diabetes mellitus occurred in one RED-treated and four REM-treated patients. A worsening glucose tolerance was observed in highly treatment-experienced HIV-infected patients receiving effective antiretroviral therapy after virological failure.     

葡萄糖耐量受损与冠心病

葡萄糖耐量受损（IGT）与冠心病关系密切,显著地影响冠心病的发病和转归。本文介绍餐后血糖定义及状态、监测及适应证、IGT的检出率与相关因素、对心血管系统的危害、干预措施和效果。     

Impaired glucose tolerance in the third trimester of pregnancy

When the methods and interpretation of glucose tolerance as recommended by the World Health Organisation were applied to 247 patients in the third trimester of pregnancy selected on account of glycosuria, previous large-for-dates offspring, diabetic family history, maternal obesity or a fetus large for gestational age, impaired glucose tolerance (IGT) was found in 20 (8.1%). Patients with IGT were older than those with normal tests: 30.5 +/- 4.8 years (mean +/- S.D.) vs 27.8 +/- 4.8 years (p less than 0.02) and more having IGT had a first degree family history of diabetes (25% vs 10%, p less than 0.05). The majority (15) of the IGT patients then received dietary advice to restrict refined carbohydrate. Post-prandial blood glucose and HbA1 concentrations in these subjects remained within the normal range except for one patient who was treated with insulin. Pregnancy outcome was satisfactory in the patients with impaired tolerance and further studies will be required to assess the clinical significance of IGT in pregnancy.     

Impaired glucose tolerance and insulin insensitivity in primary hyperparathyroidism

OBJECTIVE A high prevalence of diabetes mellitus has been shown in patients with primary hyperparathyroidism (PHPT). However, it is unclear whether this is related to the metabolic abnormalities in PHPT or to the presence of other risk factors for glucose intolerance in these patients. The aim of our study was to determine whether glucose intolerance and insulin insensitivity occur in subjects with PHPT who do not have other risk factors for diabetes mellitus. DESIGN Cross-sectional study of glucose metabolism in PHPT patients without other risk factors for diabetes mellitus, compared to age and body mass index (BMI) matched healthy subjects. SUBJECTS Nineteen non-obese, non-diabetic, normotensive patients with PHPT and 11 age and BMI matched healthy subjects. MEASUREMENTS The continuous infusion of glucose test was used to assess glucose tolerance. Plasma glucose and insulin were measured during a 1-hour continuous infusion of glucose (5 mg/kg ideal body weight/min); insulin sensitivity and beta-cell function were derived from the glucose and insulin data by mathematical modelling. Fasting serum concentrations of parathyroid hormone, ionized calcium and 1,25-dihydroxyvitamin D (1,25(OH)₂D) were measured in all subjects. RESULTS PHPT patients attained higher plasma glucose levels at the end of the glucose infusion (median 9.0 (interquartile range 8.1–9.8) mmol/l) than did controls (7.9 (7.1–8.9) mmol/l, P<0.05), and 8 (42%) PHPT patients had impaired glucose tolerance. Insulin sensitivity was lower in PHPT (60.3% (49.8–85.4)) than in controls (113.7% (89.3–149.2), P<0.001); beta-cell function was not different in PHPT subjects. PHPT subjects with impaired glucose tolerance had reduced beta-cell function compared to PHPT subjects with normal glucose tolerance (89.9% (70.5–106.4) vs 120% (98.8–156.6) respectively, P<0.05). No significant correlations were found between insulin sensitivity and PTH (r_s=?0.21), 1,25(OH)₂D (r_s=?0.14), ionized calcium (r_s=–0.11) and inorganic phosphate (r_s= 0.34). Beta-cell function did not correlate with PTH (r_s= 0.15), 1,25(OH)₂D (r_s= 0.04), ionized calcium (r_s= 0.23) or inorganic phosphate (r,=? 0.35). CONCLUSION Insulin insensitivity is present in PHPT even in the absence of hypertension and obesity, and may be the cause of glucose intolerance and diabetes. PHPT subjects with reduced beta-cell function are more likely to develop glucose intolerance.     

Impaired glucose tolerance after autologous bone marrow transplantation

In this study we investigated glucose tolerance in relation to autologous bone marrow transplantation (ABMT). In 13 adult patients with acute myeloblastic (AML) or lymphoblastic (ALL) leukaemia in complete remission (CR), intravenous glucose tolerance test (IVGTT) was performed 1 month before and 6 months after ABMT. Patients with AML in CR received, as myeloablative therapy, cyclophosphamide combined with busulphan or total body irradiation (TBI). ALL patients received total body irradiation in combination with vincristine, daunorubicin, Ara-C, cyclophosphamide and prednisone. Before ABMT all patients, in spite of the intensive chemotherapy given for remission induction and consolidation, had a normal glucose tolerance. However, 6 months after the transplantation the k-value (rate of glucose elimination) for this group of patients had decreased (p less than 0.01). The trend towards impaired glucose tolerance was correlated with lower peak insulin values during IVGTT (p less than 0.05). Thus, the myeloablative therapy in connection with ABMT caused an impairment of pancreatic beta-cell function. No patient has hitherto developed clinical diabetes mellitus.     

Impaired fasting glucose and impaired glucose tolerance in urban population in India.

AIMS: To study prevalence of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) in urban Indians and their demographic and anthropometric characteristics. METHODS: Data on capillary blood glucose (OGTT), anthropometric and demography details were available in 10 025 subjects (M : F 4711 : 5314) aged > or = 20 years. Glucose tolerance was categorized as normal, isolated IFG, isolated IGT, IFG + IGT and diabetes using the fasting and 2-h blood glucose (2hBG; 75-g glucose load) values. Subjects with known diabetes were excluded. RESULTS: Age-standardized prevalences of IFG, IGT and newly detected diabetes were 8.7%, 8.1% and 13.9%, respectively. IFG was more prevalent in women (9.8%) than in men (7.4%) (chi2 = 13.62, P = 0.0002), while the gender differences in IGT (men 8.4%, women 7.9%) and diabetes (men 13.3%, women 14.3%) were not significant. Body mass index and waist circumference were higher in glucose-intolerant groups than in normal glucose tolerance (NGT). Prevalence of diabetes, IGT and IFG + IGT increased with age. Among the IFG, 4% had diabetes and 27.1% had IGT using 2hBG criteria. In IFG, the fasting and 2hBG values were not correlated. CONCLUSIONS: Prevalences of IFG and IGT were similar in urban Indians and an overlap occurred in only less than half of these subjects. IFG was more common in women. Subjects with IFG were older and had more adverse anthropometric characteristics in comparison with NGT. IFG did not show an increasing trend with age.     

Impaired proinsulin secretion before and during oral glucose stimulation in HIV-infected patients who display fat redistribution

The beta-cell function of HIV-infected patients on highly active antiretroviral therapy who display lipodystrophy may be impaired. An early defect in beta-cell function may be characterized by an increase in secretion of 32-33 split proinsulin (SP) and intact proinsulin (IP). To address this issue, the secretion patterns of SP and IP of 16 HIV-infected men with lipodystrophy (LIPO) and 15 HIV-infected men without lipodystrophy (NONLIPO) were studied during an oral glucose tolerance test (OGTT). All patients received highly active antiretroviral therapy. Insulin secretion rates were determined by deconvolution of plasma C-peptide concentrations. More LIPO than NONLIPO patients displayed diabetes mellitus and impaired glucose tolerance than normal glucose tolerance (LIPO 2/8/6 vs NONLIPO 1/2/12, P = .05). LIPO patients had increased fasting levels of SP and IP, ratio of SP/IP, and area under the curve of SP and IP during the early phase (0, 10, and 20 minutes) and during the late phase (45, 75, and 105 minutes) of the OGTT compared with NONLIPO patients (Ps < .05). LIPO patients exhibited significantly increased fasting SP/IP ratio, fasting SP/insulin ratio, and total proinsulin to C-peptide ratio during the OGTT. LIPO patients displayed increased incremental secretion of IP during the first 10 minutes of the OGTT (P < .05), although the incremental insulin secretion during this period did not differ between LIPO and NONLIPO patients. These data suggest that HIV-infected patients with lipodystrophy display major perturbations of proinsulin secretion in the fasting state and during an OGTT, which is compatible with the notion of a beta-cell dysfunction of such patients.     

葡萄糖耐量减低的研究进展及面临的挑战

葡萄糖耐量减低的研究进展及面临的挑战潘长玉葡萄糖耐量减低（ＩＧＴ）是指患者的血糖介于正常人血糖值与糖尿病者血糖值之间的一种中间状态。诊断标准为口服７５ｇ葡萄糖耐量试验（ＯＧＴＴ）后，２小时测血浆血糖处于７．８～１１．０ｍｍｏｌ／Ｌ之间。这一诊断标准系...     

Impaired glucose tolerance in pancreas grafted diabetic patients is due to insulin secretory defects.

INTRODUCTION: Pancreas transplantation in diabetic patients can sustain insulin independence for years. The aim of the study was to measure the incidence of an impaired or diabetic glucose tolerance in patients after successful transplantation and analyse insulin resistance and insulin secretion. METHODS: 174 Type 1 diabetic recipients of simultaneous pancreas/kidney (SPK) transplants were investigated early (three months) and 95 patients late (five years) after transplantation using an oral glucose tolerance test combined with an iv arginine load. RESULTS: Although mean fasting blood glucose and HbA1c levels were within the normal range, only 65% of the patients displayed a normal glucose tolerance (NGT), whereas 25% had an impaired (IGT) and 10% showed a diabetic glucose tolerance (DGT). Fasting blood glucose and HbA1c values were significantly lower in patients with NGT compared to graft recipients with IGT or DGT, either three months or five years after SPK. Indicators of insulin resistance (fasting insulin, HOMA-IR, Matsuda/de Fronzo Index) were elevated in all graft recipients, but no differences were found between groups. In contrast insulin secretion was significantly reduced in patients with IGT and DGT early and late after transplantation. SUMMARY: Insulin resistance is a common feature after pancreas transplantation. However, either three months or five years after SPK abnormal glucose tolerance was mainly due to a reduced glucose- and arginine-induced secretory response of insulin.     

Impaired glucose tolerance and growth hormone in chronic liver disease.

Of 30 patients with chronic liver disease 16 showed some degree of impairment of glucose tolerance, and 16 patients had lack of suppression of raised fasting growth hormone levels or showed an anomalous rise after oral glucose. No relationship, however, existed between the state of glucose tolerance and the presence of abnormal growth hormone levels. Plasma glucose in those with normal growth hormone response at 0, 1/2, 1, 1-1/2, and 2 hours, after 50 g glucose were 5.55 +/- 0.41 mmol/l, 8.71 +/- 0.59, 10.66 +/- 0.99, 10.28 +/- 1.37, 8.90 +/- 1.40 (mean +/- SEM; n = 14). Under the same conditions those with abnormal growth hormone responses showed values of 5.32 +/- 0.59, 7.83 +/- 0.81, 9.41 +/- 0.95, 9.46 +/- 0.99, 8.69 +/- 0.98. At no time were the differences significantly different as judged by Student's t test. Measurement of serum insulin indicated a relative deficiency in patients with impaired tolerance. It is concluded that the abnormal growth hormone is not directly responsible for the impaired glucose tolerance.