Protective effect of DRB1 locus against type 2 diabetes mellitus in Mexican Mestizos

The aim of the study was to investigate the participation of human leukocyte antigen (HLA) class II alleles in the expression of type 2 diabetic and in nondiabetic subjects with and without family history of diabetes. The purpose was to evaluate any HLA association and to look for different patterns of insulin resistance and insulin secretion, comparing subjects with a low probability of developing diabetes, as a result of their family history. We recruited 87 healthy subjects without family history of diabetes, 48 healthy subjects with family history, and 47 type 2 diabetic patients. All of them were Mexican Mestizos of central Mexico. Using a standard 75-g oral glucose tolerance test, insulin resistance was determined and insulin secretion was assessed with the HOMA model. DRB1, DQA1 and DQB1 alleles were typed using polymerase chain reaction-sequence-specific oligonucleotide probe (PCR-SSOP) and sequence specific primers (PCR-SSP). Nondiabetic subjects had similar HOMA-IR and DeltaI 30/DeltaG 30 index (HOMA). A significant decreased frequency of DRB1*0403 (p = 0.01; odds ratio [OR] = 0.20) was demonstrated in type 2 diabetic patients, and DRB1*0701 (p = 0.02; OR = 0.17) in nondiabetics with family history of diabetes. These alleles associated with protection against type 2 diabetes, share glutamic acid at position-74 and were previously demonstrated to contribute to protection against type I diabetes.     

Intron 4 polymorphism of the endothelial nitric oxide synthase gene is associated with elevated blood pressure in type 2 diabetic patients with coronary heart disease

The endothelial nitric oxide synthase (eNOS) gene is responsible for constitutive nitric oxide synthesis and arterial vasodilatation. Recently two polymorphisms, the 27-bp repeat sequence in intron 4 and the Glu298Asp substitution in exon 7 of the eNOS gene have been reported to be related to coronary heart disease (CHD). We screened these polymorphisms of the eNOS gene in 308 unrelated nondiabetic subjects with CHD, in 251 unrelated patients with type 2 diabetes with CHD, and in 110 randomly selected healthy subjects without CHD. The 4a and Asp298 allele frequencies of the eNOS gene were 0.19 and 0.36 in nondiabetic patients with CHD, 0.21 and 0.27 in type 2 diabetic patients with CHD, and 0.16 and 0.31 in nondiabetic subjects without CHD (n.s. between the groups). The Asp298 allele in exon 7 of the eNOS gene was not associated with elevated blood pressure in any of the study groups. Among type 2 diabetic patients with CHD the 4a allele in intron 4 of the eNOS gene was associated with elevated levels of systolic (P=0.035) and mean arterial blood pressure (P=0.040). In nondiabetic subjects these associations were not statistically significant. When all study groups were pooled in statistical analysis the 4a allele of the eNOS gene was associated with elevated diastolic (P=0.032) and mean (P=0.030) arterial blood pressure even after adjustment for confounding factors. We conclude that the 4a allele of the eNOS gene is not associated with CHD or type 2 diabetes, but that it is related to elevated blood pressure levels particularly among type 2 diabetic patients with CHD.     

Risk factors for diabetes,but not for cardiovascular disease,are associated with family history of Type 2 diabetes in subjects from central Mexico

Background: Independent of obesity, family history of type 2 diabetes mellitus (FHT2DM) is another important risk factor for developing diabetes.

Aim: To establish the association among FHT2DM, risk factors for diabetes and cardiovascular disease in subjects from central Mexico.

Subjects and methods: Clinical and biochemical studies were performed in 383 first-degree relatives of patients with type 2 diabetes and 270 subjects unrelated to patients with type 2 diabetes—all subjects were from the city of Puebla in central Mexico. Logistic regressions were used to assess the association between FHT2DM and metabolic parameters. Cardiovascular risk was classified by dyslipidemia and the Framingham Risk Score (FRS).

Results: FHT2DM was associated with risk factors for diabetes, such as increased fasting insulin levels (OR = 1.731, 95% CI = 1.041–2.877), decreased insulin sensitivity (OR = 1.951, 95% CI = 1.236–3.080) and pre-diabetes (OR = 1.63, 95% CI = 1.14–2.33). FHT2DH was not associated with risk factors for cardiovascular disease, such as dyslipidemia (OR = 1.12, 95% CI = 0.70–1.79) and FRS (OR = 0.74, 95% CI = 0.40–1.36) when adjusted for gender, age, smoking and obesity.

Conclusion: Diabetic risk factors, but not cardiovascular disease risk factors, are associated with a positive family history of diabetes in subjects from central Mexico, independent of the presence of obesity.     

血清糖化血红蛋白及脂蛋白-(a)水平变化与糖尿病并发冠心病的关系

目的:探讨血清糖化血红蛋白(HbAlc)及脂蛋白-a[Lp(a)]水平变化与糖尿病并发冠心病的关系。方法:单纯2型糖尿病患者54例(糖尿病组)和2型糖尿病并发冠心病患者128例(糖尿病并发冠心病组),测定各组血清HbAlc和Lp(a)水平,通过Logistic回归和ROC曲线分析血清HbAlc和Lp(a)水平变化对糖尿病并发冠心病的相对危险性预测价值。结果:糖尿病合并冠心病组HbAlc(7.5±1.4)%和Lp(a)(0.25±0.19)g/L明显高于单纯糖尿病组[(6.9±1.4)%和(0.19±0.16)g/L,均P<0.05]。Logistic回归分析显示,血清高水平HbAlc和Lp(a)分别是糖尿病并发冠心病的独立危险因素(OR值2.28,95%CI1.12～4.63,P<0.05)及(OR值2.3,95%CI1.11～4.79,P<0.05)。Logistic回归模型的ROC曲线下面积为0.73(P<0.01)。最佳切点0.7对判断糖尿病患者并发冠心病的敏感性和特异性分别为70%和65%。结论:血清HbAlc和Lp-(a)水平是糖尿病患者并发冠心病的独立危险因素,对评估糖尿病并发冠心病的相对危险性具有临床价值。     

Colonic transit time in diabetic patients--comparison with healthy subjects and the effect of autonomic neuropathy

Constipation and the use of laxatives are relatively common in patients with diabetes mellitus. However, the mechanisms responsible for the constipation are unclear. Even though autonomic neuropathy is regarded as one of the important mechanisms of constipation, it requires further clarification. In addition, the colonic function in diabetic patients requires further investigation. The aim of this study was to compare the colonic transit time between patients with diabetes mellitus and healthy subjects, and correlate it to the presence of cardiovascular autonomic neuropathy. The colonic transit time was measured by a noninvasive, radio-opaque marker method, and the presence of cardiovascular autonomic neuropathy was evaluated by the beat-to-beat variation and the orthostatic hypotension. Constipation was defined by the Rome II criteria. The mean total colonic transit time of the 28 diabetic patients (34.9 +/- 29.6 h, mean +/- S.D.) was significantly longer than that of the 28 healthy subjects (20.4 +/- 15.6 h, p < 0.05). Among the diabetic patients, 9/28 (32%) had constipation and 14/28 (50%) had cardiovascular autonomic neuropathy. The diabetic patients with constipation showed longer total, left and recto-sigmoid colonic transit times than those without constipation. However, the mean colonic transit time of diabetic patients with and those without cardiovascular autonomic neuropathy was similar. In conclusion, other mechanisms than the mere presence of cardiovascular autonomic neuropathy might be more relevant to the development of constipation in patients with diabetes mellitus.     

Cardiovascular risk factors in type I (insulin-dependent) diabetic patients with and without proteinuria

In diabetes mellitus cardiovascular mortality among patients with increased urinary albumin excretion seems to be higher than in patients with normal urinary albumin excretion. Therefore we investigated blood pressure, total cholesterol, fibrinogen and in vivo platelet adhesion in 61 patients with type I (insulin-dependent) diabetes, 39 without complications, such as retinopathy or proteinuria and 22 with proteinuria and slightly elevated serum creatinine. The two groups had similar age, sex, diabetes duration and glucose control. Blood pressure, total cholesterol, fibrinogen and in vivo platelet adhesion were all significantly elevated in patients with proteinuria (p less than 0.01), whereas these parameters were normal in the uncomplicated diabetic patients, independent of diabetes duration. The mortality of cardiovascular disease during 20 years' follow-up was significantly higher among patients with proteinuria compared with patients without proteinuria (p less than 0.001), indicating that these risk factors contribute to the increased cardiovascular mortality in patients with clinical nephropathy.     

Taq1B polymorphism of CETP gene on lipid abnormalities in patients with type II diabetes mellitus

The most common alterations in lipid and lipoprotein metabolism in type 2 diabetes involve an elevation in both plasma triglyceride and VLDL concentrations, a dense LDL phenotype and low levels of HDL cholesterol. The inverse relationship between the level of HDL cholesterol and the risk of cardiovascular disease is commonly explained by the crucial role of HDL in reverse cholesterol transport. Cholesterol ester transfer protein (CETP) has a central role in the metabolism of HDL and may therefore alter the susceptibility to atherosclerotic vascular disease. To evaluate the effect of Taq1B polymorphism of intron 1 of CETP gene on serum lipid concentrations in Turkish type 2 diabetic patients, we investigated Taq1B polymorphism and serum lipid levels in 116 controls and in 164 diabetic patients. Polymerase chain reaction (PCR), restriction fragment length polymorphism (RFLP), and agarose gel electrophoresis techniques were used to determine the CETP Taq1B polymorphism. Serum lipid levels were measured enzymatically. Statistical analyses was performed by SPSS. In control group: subjects with B2B2 genotype have high HDL-cholesterol levels (p=0.029) and B1B1 genotypes have high triglyceride levels (p=0.07). Diabetic patients with and without MI with B2B2 genotype have high HDL-cholesterol levels. Taq B1B1 genotype has higher in diabetic patients with myocardial infarction (MI) than diabetic patients without myocardial infarction (42.1% and 32.7%; chi2=1.42, p=0.23). The present study demonstrates that the CETP Taq1B gene polymorphism is an association with low HDL cholesterol levels in patients with type II diabetes mellitus and healthy controls in Turkey. We also showed that CATE Taq1B gene polymorphism may be related to myocardial infarction in type II diabetic patients.     

Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes

The incidence of end-stage renal disease in patients with diabetes mellitus is reportedly higher among blacks than among whites. This finding may be explained by the greater prevalence of diabetes among blacks. The relation of the type of diabetes to the risk of diabetic end-stage renal disease is largely unstudied. We addressed these issues in a study of all the black and white diabetic patients with end-stage renal disease (470 blacks and 861 whites) reported to the Michigan Kidney Registry who began treatment during 1974 through 1983. We also reviewed the medical records of a subpopulation of such patients (284 blacks and 310 whites) who were less than 65 years of age at the start of treatment for end-stage renal disease to determine what type of diabetes they had. In this study, we made use of national data on the prevalence of diabetes. We found that the incidence of diabetic end-stage renal disease was 2.6-fold higher (P less than or equal to 0.0001) among blacks after we adjusted for the higher prevalence of diabetes among blacks, with the excess risk occurring predominantly among blacks with non-insulin-dependent diabetes mellitus (NIDDM). Most black patients with diabetic end-stage renal disease had NIDDM (77 percent), whereas most white patients with diabetic end-stage renal disease had insulin-dependent diabetes mellitus (IDDM) (58 percent) (P less than or equal to 0.0005 for the difference between the races). For both races combined, the risk of diabetic end-stage renal disease during the 10-year period we studied was markedly greater for patients with IDDM (5.8 percent) than for those with NIDDM (0.5 percent). Our results indicate an increased risk of diabetic end-stage renal disease among blacks as compared with whites, particularly blacks with NIDDM. Although the risk of diabetic end-stage renal disease is higher in patients with IDDM, the majority of patients with diabetic end-stage renal disease in the population we studied had NIDDM.     

糖尿病合并冠心病患者红细胞膜脂肪酸成分改变与胰岛素抵抗

我们采用高效液相色谱（PHLC）和荧光偏振技术测定了2型糖尿病合并冠心病病人红细胞膜脂肪酸成分和膜微粘度,并分析了脂肪酸成分、膜流动性和胰岛素敏感指数（ISI）与冠心病发生的关系。结果表明糖尿病人红细胞膜花生四烯酸（AA,C20：4）含量及组成明显低于对照组,而伴冠心病组AA含量又低于单纯糖尿病组,且其总脂肪酸含量明显低于对照组。两组病人膜微粘度明显高于对照,而冠心病组又明显高于单纯糖尿病组。糖尿病人红细胞膜AA含量与膜微粘度呈负相关,与ISI呈正相关,膜微粘度与ISI呈负相关。AA含量,微粘度和ISI均与冠心病的发生有关。提示糖尿病人冠心病的发生、发展与其脂肪酸代谢紊乱有关。     

Risk Factors for Long-term Outcome of Drug-eluting Stenting in Adults with Early-onset Coronary Artery Disease

Objective We lack data on the long-term outcome of drug-eluting stenting in patients with early-onset coronary artery disease (CAD). Here, we investigated the association of traditional risk factors and major adverse cardiovascular events (MACEs) after drug-eluting stenting in patients with CAD who were < 50 years old. Methods We enrolled 437 consecutive CAD patients < 50 years old who underwent drug-eluting stenting and 132 subjects who were age- and sex-matched and angiographically shown to be disease free as controls. MACEs were analyzed in CAD patients for a median of 24 months [interquartile range 14-34 months]. Results Male patients accounted for 90.4% of cases. As compared with controls, patients with early-onset CAD had higher body mass index and rates of smoking, family history of CAD, and diabetes and hypercholesterolemia. During the hospital stay, 1 patient died, and the incidence of MACEs was 1.1%. At the end of follow-up, the overall death rate was 0.7%. MACEs were observed in 54 patients (12.4%). On Cox proportional hazard analyses, positive family history and diabetes were independent risk factors of MACEs (HR 2.61, 95% confidence interval 1.29-4.00, p = 0.002; and HR 2.48, 95% confidence interval 0.86-3.14, p = 0.004, respectively). Conclusions Drug-eluting stenting is a reliable treatment for patients with early-onset CAD. Positive family history of CAD and diabetes are independent risk factors of adverse cardiovascular events in this subgroup of patients after drug-eluting stent implantation.     

超声多普勒检测糖尿病患者心功能的研究

目的检测糖尿病患者心功能。方法采用脉冲多普勒彩色超声心动图检测糖尿病、糖尿病合并冠心病患者各33例的心室结构和功能，并与健康组对照。结果糖尿病组的左心室舒张功能较健康组减退，而合并症组较糖尿病组减退更显著。结论糖尿病组的收缩功能与健康组间无统计学意义（P〉0．05），而三组问舒张功能有统计学意义（P〈0．01）。提示心室舒张功能较收缩功能变化更早、更显著。糖尿病组及合并症组左右心室均存在舒张功能障碍，表现为舒张早期心室充盈减低及房缩充盈代偿增强等（E峰流速减慢，A峰流速增快）。糖尿病的心室舒张功能减退与糖尿病的心脏病变和代谢紊乱均有关系，纠正代谢紊乱可避免心功能进一步恶化。     

Increased insulin concentrations in nondiabetic offspring of diabetic parents

Insulin resistance is thought by many to be the primary defect that results in non-insulin-dependent diabetes mellitus (NIDDM). An implication of this theory is that prediabetic persons have higher serum insulin levels than normal subjects. We assessed serum insulin concentrations in a cohort of 1497 nondiabetic Mexican Americans, a population at high risk for NIDDM, according to whether their parents or siblings had diabetes. It was assumed that prediabetic persons would be more likely to have strong family histories of diabetes. We found a stepwise increase in fasting insulin levels in nondiabetics with neither, one, or both parents with diabetes (69.8, 77.8, and 94.6 pmol per liter, respectively; P = 0.002). Similar results were observed for insulin sum (the total of insulin concentrations in the fasting state and at 30, 60, and 120 minutes after a 75-g oral glucose load). The differences in insulin sums according to family history remained statistically significant in analyses of covariance, which controlled for variations in body-mass index, body-fat distribution, and level of blood glucose. Subjects without diabetes who had a diabetic sibling had higher fasting concentrations of insulin than subjects without a diabetic sibling (83.2 vs. 69.6 pmol per liter), but the difference was not statistically significant. We conclude that prediabetic persons, who would be expected to be more numerous in kindreds with progressively stronger family histories of diabetes, have hyperinsulinemia. This supports the insulin-resistance hypothesis.     

2型糖尿病人微血管舒张功能测定及其影响因素分析

目的： 用毛细血管恢复试验测定2型糖尿病人和糖耐量正常人的微血管舒张功能并分析其影响因素。方法： 2型糖尿病患者共276人按性别（男/女）、病程（<5年，5-10年，≥10年）、家族史（有/无）及体型（体重指数≥25 kg/m2/<25 kg/m2）分组，比较毛细血管恢复率（%）的差异。同时，对20名糖耐量正常人进行微血管舒张功能的测定。结果： 20名［平均年龄为（60.56±6.73）岁］口服糖耐量试验正常者的平均毛细血管恢复率为（36.50±9.48）%。2型糖尿病人平均年龄为(64.94±10.72)岁，平均毛细血管恢复率为（27.68±12.48）%，明显低于正常人（P<0.05）。随着糖尿病病程延长，毛细血管恢复率呈递减趋势，分别为（29.63±13.85）%、（27.45±12.23）%、（25.75±10.90）%（P<0.05）。有糖尿病家族史和体型肥胖者比对照组的毛细血管恢复率明显降低（P<0.05），但不同性别之间毛细血管恢复率没有显著差异。结论： 2型糖尿病人毛细血管恢复率比糖耐量正常人明显降低，提示2型糖尿病人有明显的微血管舒张功能障碍，肥胖、病程和糖尿病家族史与微血管舒张功能的障碍密切相关。     

Hemostasis and fibrinolysis factors in first-degree relatives of patients with Type 2 diabetes without hypertension

First-degree relatives of type 2 diabetic patients with or without a family history of hypertension are at increased risk for cardiovascular diseases. The aim of this study was to verify some possible hemostatic alterations in first-degree relatives of type 2 diabetic, normotensive and hypertensive patients. In 78 non-diabetic, normotensive first-degree relatives of type 2 diabetic patients (47 without a family history of hypertension and 31 with a family history of hypertension) and in 36 normoglycemic, normotensive subjects with no family history of hypertension, we evaluated plasma levels of fasting glucose and insulin, tissue-type plasminogen activator (t-PA), plasminogen activator-inhibitor (PAI-1), D-dimer (DD) and prothrombin fragment 1 + 2 (F1+2). Insulin resistance, calculated by the HOMA model, and plasma levels of t-PA and PAI-1 were significantly higher in relatives of diabetics compared to controls. As far as the thrombin activation indexes are concerned, we detected a significant increase in DD and F1+2 in relatives of diabetics with hypertension compared to other study subjects. In conclusion, our data indicate that familial predisposition may influence the hemostatic system in first-degree relatives of diabetic and/or hypertensive patients.     

Family History is a Coronary Heart Disease Risk Factor in the Second Northwick Park Heart Study

We have estimated the risk of coronary heart disease (CHD) from family history of CHD (FHCHD) in 2827 healthy European middle‐aged men, and explored the extent to which this can be explained by classical and genetic risk factors. Men with FHCHD (obtained by questionnaire) had a hazard ratio of CHD of 1.73 (95% confidence interval: 1.30, 2.31) compared to those without FHCHD; after adjusting for classical risk factors this did not change substantially. Those with FHCHD had 2.3% lower Factor VIIc (p = 0.03) and 1.14% higher systolic and 1.21% higher diastolic blood pressure (p = 0.04 and p = 0.02 ), with evidence of interaction between blood pressure and FHCHD status on risk (p = 0.01) . The risk for those with a positive family history who were also current smokers was 3.01 compared to non‐smokers without FHCHD, which is greater than the risk posed by smoking or FHCHD alone (1.96 and 2.05 respectively compared to non‐smokers without FHCHD), but not significantly different from a multiplicative model (p‐value for interaction 0.33). Allele frequencies for 13 candidate gene variants were not significantly different between those with and without FHCHD. In those with FHCHD, current smokers who carried the APOE4 allele (e4+) had a hazard ratio of 5.66 compared to non‐smokers who had no FHCHD and were not APOE4+, with a significant interaction between smoking and APOE4 in those with FHCHD p = 0.001 . These data demonstrate the complex interaction between genetic and environmental factors in determining CHD risk, and suggest that the causes of the familial clustering of CHD remain largely unexplained.     

Oxidative damage indices for the assessment of subclinical diabetic macrovascular complications

Subclinical cardiovascular disease (SCVD), including complications in diabetes, is associated with oxidative damage and precedes future cardiovascular disease (CVD). Hence, assessment and management of oxidative damage is imperative. This study investigates biomarkers associated with CVD, diabetes and oxidative stress in order to determine a set of indices that could be useful to assess oxidative damage in diabetic macrovascular pathogenesis. A total of 266 participants were selected and divided into seven groups (control, family history of diabetes, prediabetes, prediabetes with CVD, diabetes mellitus [DM], DM+CVD and CVD) based on clinical history/status. Blood glucose (BG) level, erythrocyte glutathione (GSH), malondialdehyde, methaemoglobin, D-dimer, homocysteine, blood viscosity and cholesterol profile were determined. Factorial MANOVA and independent univariate analyses were performed. Prevalence of significant biomarkers was assessed following a 3.5-year retrospective study. Multivariate analysis showed statistically significant differences between groups (P < 0.0001) with post hoc tests identifying a statistically significant association for BG level (P < 0.0001), GSH (P < 0.0001), D-dimer (P < 0.02) and total cholesterol (P < 0.0001). Of the subjects who showed hyperglycaemia-associated progression in clinical and biochemistry status, 89% had low-level GSH and 44% had high-level D-dimer. Four individuals exhibited prediabetic status at some stage and would qualify for macrovascular disease intervention. The results of this study suggest that BG level, D-dimer, GSH and total cholesterol contribute significantly to a diabetic oxidative damage panel of markers that could assist in evidence-based pharmacological intervention with anti-aggregation and/or antioxidant agents against future CVD in diabetes.     

2型糖尿病一级亲属不同糖耐量者第一时相胰岛素分泌功能的变化

目的：探讨胰岛素分泌功能和胰岛素抵抗（IR）在2型糖尿病（T2DM）发生、发展中的作用。 方法： T2DM一级亲属正常糖耐量（NGT+）组32例，T2DM一级亲属糖耐量异常（IGT+）组36例，新诊断的T2DM组35例，计算各组的第一时相胰岛素分泌功能指数（AIR3-5）及胰岛素敏感性指数（SIM），与无糖尿病家族史的正常糖耐量（NGT-）组（38例）比较。 结果： T2DM一级亲属T2DM组、IGT+和NGT+组AIR3-5均低于NGT-组（P值分别为<0.01、<0.01、＜0.05）；T2DM组和IGT+组SIM均低于NGT-组（均P<0.01），而NGT+组SIM值与NGT-组比较无统计学差异（P>0.05）。结论： 胰岛素分泌功能缺陷可能是T2DM发病的始动因素。当发展为IGT及T2DM时，胰岛素分泌功能进一步降低，并伴有胰岛素敏感性的降低。     

Metabolic syndrome in subjects with type-2 diabetes mellitus

BACKGROUND: Each component of metabolic syndrome (MS) conveys increased cardiovascular disease risk, but as a combination they become much more powerful. Vigorous early management of the syndrome may have a significant impact on the prevention of both diabetes and cardiovascular disease. AIM: This study aims to determine the frequency of occurrence of MS and its relation to cardiovascular events among patients with type-2 diabetic mellitus. METHODS: The study group consisted of 218 type-2 diabetic patients. These were screened for hypertension, hyperlipidemia, obesity, microalbuminuria, and cardiovascular events. RESULTS: There were 128 (58.7%) males and 90 (41.3%) females. The mean age was 53.4 +/- 6.3 years and a mean body mass index (BMI) of 25.5 +/- 5.4 (males-23.4 +/- 4.2; females-26.2 +/- 5.7). MS was present in 55 (25.2%) of the study population. Systemic hypertension was the most common component of MS seen in 84 (38.5%) patients. The mean serum total cholesterol was 168.6 +/- 25.8 mg% (men 153 +/- 23; women 169 +/- 19; p > 0.05). Eight female and 12 male patients had serum total cholesterol > or = 200 mg%. Dyslipidemia occurs more commonly in males than females. Obesity was more common in female patients than in males. Out of 128 male type-2 patients with diabetes seen, 111 (86.7%) were without microalbuminuria. The corresponding figure among the females was 90% (81 out of 90 patients). CONCLUSIONS: The study demonstrated that MS was present in 25.2% of the study population. The syndrome and its different components were positively associated with a higher risk of stroke, peripheral vascular disease, and occurrence of microalbuminuria, p < 0.001. Ischemic heart disease occurs rarely in the population. A long-term, targeted, intensive intervention involving multiple cardiovascular risk factors is recommended to reduce the risk of both cardiovascular and microvascular events among patients with type-2 diabetic mellitus.     

Conduite à tenir devant une glycémie « limite supérieure »

Type 2 diabetes is preceded by a long preclinical period with progressively glucose tolerance abnormalities. Beside diabetes defined by a venous fasting glucose superior to 7 mmol/l (1.26 g/l), American Diabetes Association identified two others abnormalities of glucose tolerance: the impaired glucose tolerance (IGT) defined by a two hours glycaemia between 7.8 and 11 mmol/l (1.4 and 1.9 g/l) at the oral glucose tolerance test (OGTT) and the impaired fasting glycaemia (IFG) with a fasting glycaemia between 6.1 and 6.9 mmol/L (1.1 and 1.25 g/l). Prevalence of IGF is between 2 and 10% in non diabetic adult subjects. IFG concerns mainly subjects aged 40–50 years and is 1.5 to 3 fold more frequent in man. Most of the well-known risk factors for developing type 2 such us overweight, abdominal obesity, familial history of diabetes, over –consumption of fat and alcohol are present in subjects having IFG. Hypertension is present in more than 50% of the subjects with IFG. Fifty percents of subjects with IFG are also an impaired glucose tolerance. IFG is associated with a high diabetes risk because 10 to 30% of subjects with IFG will develop type 2 diabetes after five years. Both IFG and IGT are associated with an increase of risk of cardiovascular mortality while the two hours glycaemia of OGTT is more predictive than IFG. Microalbuminuria and carotid intima media-thickness are significantly increased in subjects having both IGT and IFG compared to subjects with only IGT. Subjects with IFG are associated with an increase risk of developing diabetes and cardiovascular disease. IFG requires the realization of an OGTT to search IGT or diabetes.     

肝脂酶基因启动子-250G/A多态性与2型糖尿病合并冠心病易感性的相关研究

目的 探讨汉族人群肝脂酶(hepatic lipase,HL)基因启动子-250G/A多态性与2型糖尿病(type 2 diabetes mellitus,T2DM)合并冠心病(coronary heart disease,CHD)的相关性.方法 采用聚合酶链反应-限制性片段长度多态性方法(polymerase chain reaction-restricted fragment length polymorphism,PCR-RFLP)检测364例T2DM+CHD组、357例T2DM组患者和356名健康对照者HL基因启动子-250G/A多态性,并分析其对脂类的影响.结果 T2DM组与对照组HL基因启动子-250G/A多态性基因型和等位基因频率差异无统计学意义(P>0.05);T2DM+CHD组GA+AA基因型频率低于对照组(0.431 vs 0.618,P=0.031);等位基因频率差异无统计学意义(P>0.05).调整混杂因素后,Spearman相关及线性回归分析,糖尿病患者(T2DM组和T2DM+CHD组),A等位基因与高密度脂蛋白胆固醇、载脂蛋白A1呈正相关;Logistic回归分析显示,A等位基因是冠心病发生的一个危险因素.结论 HL基因启动子-250G/A多态性与2型糖尿病合并冠心病的发生有关,并影响脂类代谢.