Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During percutaneous coronary intervention, the reference segment is assessed angiographically. This report described the discrepancy between angiographic and intravascular ultrasound (IVUS) assessment of reference segment size in patients with type 2 diabetes mellitus. Preintervention IVUS was used to study 62 de novo lesions in 41 patients with type 2 diabetes mellitus. The lesion site was the image slice with the smallest lumen cross-sectional area (CSA). The proximal and distal reference segments were the most normal-looking segments within 5 mm proximal and distal to the lesion. Plaque burden was measured as plaque CSA/external elastic membrane (EEM) CSA. Using IVUS, the reference lumen diameter was 2.80 +/- 0.42 mm and the reference EEM diameter was 4.17 +/- 0.56 mm. The angiographic reference diameter was 2.63 +/- 0.36 mm. Mean difference between the IVUS EEM diameter and angiographic reference diameter was 1.56 +/- 0.55 mm. The mean difference between the IVUS reference lumen diameter and angiographic reference lumen diameter was 0.18 +/- 0.44 mm. Plaque burden in the reference segment correlated inversely with the difference between IVUS and quantitative coronary angiographic reference lumen diameter (slope = -0.12, 95% confidence interval -0.17 to -0.07, p <0.001), but it was not related to the absolute angiographic reference lumen diameter. Thus, reference segment diameters in type 2 diabetic patients were larger using IVUS than angiography, especially in the setting of larger plaque burden. In conclusion, these findings combined with inadequate remodeling may explain the angiographic appearance of small arteries in diabetic patients.
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PMID:Comparison of intravascular ultrasound and angiographic assessment of coronary reference segment size in patients with type 2 diabetes mellitus. 1830 4

The aim of the study was to identify incremental values of carotid ultrasound measurements (carotid plaques and stenosis) on the prediction of future coronary revascularization among type 2 diabetic patients. The second objective was to determine the predictive value of the assessment of blood lipids, BMI, abdominal obesity and the ankle-brachial index (ABI). Three hundred and thirty three (333) patients with type 2 diabetes and manifested coronary artery disease were randomly selected in a cohort prospective study. Univariate and multivariate logistic regression analyses were conducted to identify variables predictive of the need for future revascularization: percutaneus coronary interventions (PCI) or coronary bypass surgery (CABG) followed 24 months after the study starting point. The presence of arterial hypertension, hyperlipidemia, physical inactivity, intermittent claudication, the value of systolic pressure, BMI, waist and hip measurement, glycemia and blood lipid fraction (total cholesterol, HDL, LDL, non-HDL, triglycerides) were entered in a model. Ultrasound measurements: carotid IMT, presence of carotid plaques and stenosis, and ABI were also included in the analysis. Based on the univariate and multivariate findings, the presence of internal carotid artery (ICA) stenosis (OR 4,562, 95% CI 1,327-15,687), carotid plaque (OR 1,465, 95% CI 0,829-2,591), and increased waist measurement (OR 1,371, 95% CI 0,757-2,483) were found as significant independent predictors of future PCI. LDL and non HDL cholesterol were found to be factors independently associated with the need for future CABG by univariate analysis, which was not confirmed by multivariate analysis. In conclusion, the current study has provided an identification of predisposing factors for the future need of coronary revascularization among type 2 diabetic patients that permits risk stratification and may facilitate improved patient selection or optimization.
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PMID:Carotid ultrasound, blood lipids and waist determination can predict a future coronary revascularisation in the type 2 diabetic cohort. 1835 84

Until recently, atherosclerosis was thought to be a passive process of lipid deposition in the arterial wall, followed by progressive occlusion of the lumen, and finally plaque rupture and thrombosis. Recent data suggest the contrary-atherosclerosis is a dynamic process developing over many years, characterized by active uptake of lipids and smooth muscle proliferation, "molding" of plaque, and subject to the influence of many environmental and genetic factors. Central to these processes, both at initiation and propagation, are factors associated with inflammation. Insulin resistance (IR), the underlying cause of type 2 diabetes mellitus (DM), is also associated with elevated levels of inflammatory factors, such as C reactive protein (CRP), plasminogen activator inhibitor-1 (PAI-1), and fibrinogen. Recent studies indicate that these same factors precede and predict DM. These findings have led to the notion that the strong association of IR/DM with cardiovascular disease (CVD) may be through inflammation pathways. In this article, we review what is known about the association of inflammation with IR and atherosclerosis. We show that many of the same inflammatory factors associated with IR are present in atherosclerosis. We also discuss the underlying determinants of inflammation in these conditions.
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PMID:Inflammation, insulin resistance, and atherosclerosis. 1837 Jun 41

Hyperuricemia has been reported to be associated with increased risk of renal insufficiency as well as cardiovascular events. The aim of this study was to evaluate the relationships between serum uric acid concentration and degree of urinary albumin excretion as well as markers of subclinical atherosclerosis in men with type 2 diabetes mellitus. Serum uric acid concentrations were measured in 343 men with type 2 diabetes mellitus. We then evaluated relationships of serum uric acid concentrations to degree of urinary albumin excretion as well as to major cardiovascular risk factors, including age, blood pressure, serum lipid concentration, and glycemic control (hemoglobin A1c). The relationships between serum uric acid concentration and pulse wave velocity or ankle-brachial index (n=236) and between serum uric acid concentration and carotid intima-media thickness or plaque score (n=125) were investigated additionally in a subgroup of patients. Serum uric acid concentration correlated positively with logarithm of urinary albumin excretion (r=0.302, P<.0001). Positive correlation was found between serum uric acid concentration and intima-media thickness (r=0.233, P=.0087), whereas inverse correlation was found between serum uric acid concentration and ankle-brachial index (r=-0.150, P=.0207). Multiple regression analysis demonstrated that serum uric acid concentration (beta=.281, P<.0001), duration of diabetes (beta=.253, P<.0001), hemoglobin A1c (beta=.166, P=.0034), serum triglyceride concentration (beta=.125, P=.0472), and systolic blood pressure (beta=.275, P=.0013) were independent determinants of logarithm of urinary albumin excretion. In conclusion, serum uric acid concentration is associated with microalbuminuria and subclinical atherosclerosis in men with type 2 diabetes mellitus.
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PMID:Serum uric acid is associated with microalbuminuria and subclinical atherosclerosis in men with type 2 diabetes mellitus. 1844 24

A genome-wide linkage scan of 357 European American (EA) and 72 African American (AA) pedigrees multiplex for type 2 diabetes mellitus (T2DM) was performed with multipoint nonparametric QTL linkage analysis. Four subclinical measures of cardiovascular disease (CVD): coronary artery (CCP), carotid artery (CarCP), and abdominal aortic calcified plaque (AACP) and carotid artery intima-media thickness (IMT) were mapped. Analyses were adjusted for age, gender, body mass index, and (if appropriate) ethnicity and diabetes status. Evidence for linkage was observed in EA T2DM subjects to CarCP near 16p13 (LOD=4.39 at 8.4 cM; P = 0.00001). When all EA subjects were included, the LOD score was 2.52, suggesting an amplification of the linkage by diabetes. Linkage analysis of a principal components measure of vascular calcium (LOD = 3.85 at 9.3 cM on 16p in EA T2DM subjects) and bivariate analysis of CarCP X IMT (LOD = 3.77 at 9.3 cM on 16p in EA T2DM subjects) were consistent with this linkage. In addition, evidence for linkage was observed with CCP near D15S1515 (LOD = 2.34) in EAs. Additional loci on chromosomes 1, 2, 7, 10, 13, and 21 had LODs > 2.0. The identification of trait-determining polymorphisms underlying these linkages will help delineate risk factors for CVD in T2DM and the general population.
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PMID:Genetic epidemiology of subclinical cardiovascular disease in the diabetes heart study. 1846 48

The dysregulation of the insulin-glucose axis represents the crucial event in insulin resistance syndrome. Insulin resistance increases atherogenesis and atherosclerotic plaque instability by inducing proinflammatory activities on vascular and immune cells. This condition characterizes several diseases, such as type 2 diabetes, impaired glucose tolerance (IGT), impaired fasting glucose (IFG), obesity, hypertension, dyslipidemia, and other endocrinopathies, but also cancer. Recent studies suggest that the pathophysiology of insulin resistance is closely related to interferences with insulin-mediated intracellular signaling on skeletal muscle cells, hepatocytes, and adipocytes. Strong evidence supports the role of free fatty acids (FFAs) in promoting insulin resistance. The FFA-induced activation of protein kinase C (PKC) delta, inhibitor kappaB kinase (IKK), or c-Jun N-terminal kinase (JNK) modulates insulin-triggered intracellular pathway (classically known as PI3-K-dependent). Therefore, reduction of FFA levels represents a selective target for modulating insulin resistance.
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PMID:Insulin resistance: a proinflammatory state mediated by lipid-induced signaling dysfunction and involved in atherosclerotic plaque instability. 1860 3

Statins lower cardiovascular risk in patients with diabetes; however, as these patients are at higher risk than other cardiovascular patients, statins merely decrease coronary event rates to the level seen in untreated nondiabetic individuals at risk for cardiovascular disease, indicating the existence of substantial residual risk. One reasonable explanation resides in the fact that statins have only limited effectiveness on hypertriglyceridemia and low HDL cholesterol, and they do not normalize the LDL size-distribution pattern. Peroxisome proliferator-activated receptor (PPAR)alpha agonists, which include fibrates, normalize this atherogenic lipid profile, as well as several cardiovascular risk markers associated with the metabolic syndrome and type 2 diabetes. In particular, hypertriglyceridemia and the ratio of small dense:large buoyant LDL particles are significantly improved. Outcome trials of PPARalpha agonists have demonstrated reductions in cardiovascular morbidity in patients with diabetes and in those with the metabolic syndrome; plaque progression is diminished, diabetic nephropathy and retinopathy are counteracted and amputation-risk decreased. The combination of fibrates with statins improves overall lipoprotein profile further. PPARalpha agonists seem particularly indicated in patients with diabetes who have residual dyslipidemia (high triglyceride and/or low HDL) despite receiving statin therapy, and patients who are nondiabetic, overweight, insulin-resistant and who have hypertriglyceridemia and/or low HDL cholesterol and chronic inflammation.
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PMID:Fibrates and future PPARalpha agonists in the treatment of cardiovascular disease. 1862 76

The metabolic syndrome is a common and complex disorder combining obesity, dyslipidemia, hypertension, and insulin resistance. It is a primary risk factor for diabetes and cardiovascular disease. We showed for the first time that the metabolic syndrome is associated with a higher fraction of oxidized LDL and thus with higher levels of circulating oxidized LDL. Hyperinsulinemia and impaired glycaemic control, independent of lipid levels, were associated with increased in vivo LDL oxidation, as reflected by the higher prevalence of high oxidized LDL. High levels of oxidized LDL were associated with increased risk of future myocardial infarction, even after adjustment for LDL-cholesterol and other established cardiovascular risk factors. This association is in agreement with the finding that accumulation of oxidized LDL, which activates/induces subsets of smooth muscle cells and macrophages to gelatinase production, was associated with upstream localization of a vulnerable plaque phenotype. Dyslipidemia and insulin resistance in obese LDL receptor-deficient mice were associated with increased oxidative stress and impaired HDL-associated antioxidant defence associated with accelerated atherosclerosis due to increased macrophage infiltration and accumulation of oxidized LDL in the aorta. The accumulation of oxidized LDL was partly due to an impaired HDL-associated antioxidant defence due to a decrease in PON. Our data in this experimental model are thus the more relevant because a decrease in PON activity was found to be associated with a defective metabolism of oxidized phospholipids by HDL from patients with type 2 diabetes. Weight loss in leptin-deficient, obese, and insulin-resistant mice was associated with expressional changes of key genes regulating adipocyte differentiation, glucose transport and insulin sensitivity, lipid metabolism, oxidative stress and inflammation, most of which are under the transcriptional control of PPARs. We established an important relationship between PPAR-gamma and SOD1 for the prevention of the oxidation of LDL in the arterial wall. For example we showed that rosuvastatin decreased the oxidized LDL accumulation by increasing the expression of PPAR-gamma and SOD1. In addition, we established a relation between increased PPAR-alpha expression in the adipose tissue and a change in the gene expression pattern, which explains the decrease of free fatty acids, triglycerides and the increase in insulin sensitivity. We demonstrated that plaque oxidized LDL correlated with coronary plaque complexity in a swine atherosclerosis model. Oxidized LDL correlated positively with the expression of IRF1 and TLR2 suggesting a relation between oxidative stress and inflammation in coronary atherosclerotic plaques. Oxidized LDL induced further the expression of TLR2 and IRF1 in macrophages in vitro suggesting a causative link. As in the mouse model described above, plaque oxidized LDL correlated negatively with SOD1 expression and ox-LDL inhibited the expression of SOD1 in macrophages in vitro. We showed that TLR2, CXCR4 and MYC are overexpressed in monocytes of obese women at high cardiovascular risk and that weight loss was associated with a concomitant decrease of their expression. This suggests that the transcription factor cMYC has an atherogenic effect by inducing pro-inflammatory genes. The increased expression of TLR2 and CXCR4 were observed in the absence of an increase in ox-LDL but in the presence of an increase in SOD1. Interestingly, the expression of SOD1 correlated also with that of MYC, suggesting that it has an atherogenic effect by inducing the expression of an anti-oxidant enzyme. How ox-LDL prevents this increase remains to be determined. How we plan to do this is explained in the next part. In aggregate, our studies contributed to a better understanding of the relationships between metabolic syndrome, insulin signalling, oxidative stress and inflammation and atherosclerosis. We identified paraoxonase, interferon regulatory factor-1, toll-like receptors, CXCR4 and SOD1 as possible targets for intervention.
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PMID:Relations between metabolic syndrome, oxidative stress and inflammation and cardiovascular disease. 1866 60

The periodontal status of 106 type 2 diabetic patients was assessed and compared with that of 106 age-matched nondiabetics. Patients older than 20 years with type 2 diabetes mellitus were recruited from the outpatient internal medicine clinics at the 2 main hospitals in Irbid governorate, Jordan. Periodontal disease was more severe in type 2 diabetic patients than in nondiabetics, as indicated by significantly mean higher gingival index, periodontal pocket depth, clinical attachment level and tooth mobility. There was no significant difference in the mean plaque index between diabetics and nondiabetics. The severity of periodontal disease was significantly higher in patients with diabetes > 5 years than those with duration < 5 years.
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PMID:Periodontal status of type 2 diabetics compared with nondiabetics in north Jordan. 1872 Jun 30

We report a patient with type 2 diabetes mellitus who, while treated with the antitumor necrosis factor-alpha blocking agent etanercept for severe plaque psoriasis, experienced persistent hypoglycemia requiring the lowering and eventual elimination of his previous insulin regimen. After 20 months of therapy on etanercept, his plaque psoriasis markedly improved, whereas both his fasting blood sugars and glycosylated hemoglobin A(1c) decreased. Hypoglycemia can be a serious side effect of etanercept in patients already on antidiabetic medications known to cause hypoglycemia, such as sulfonylureas, meglitinides, and insulin. Thus, it is important for dermatologists treating patients with diabetes and antitumor necrosis factor-alpha agents for psoriasis to be aware of potential hypoglycemia and to adjust antidiabetes therapy accordingly.
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PMID:Persistent hypoglycemia in a patient with diabetes taking etanercept for the treatment of psoriasis. 1921 93


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