Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Data on dyslipidemia in type 1 diabetes is scarce. The authors aimed to evaluate the lipid profile in patients with type 1 diabetes and its correlation to glycemic control. Ninety-four subjects (53.2% males), aged 15.4+/-4.7 (3.6-21.9 years), with disease duration of 5.0+/-3.6 years (0.3-17 years) were evaluated for heart rate, blood pressure, height, and weight. Laboratory data included total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglycerides (TGs), glycemia, glycosylated hemoglobin (HbA1c), creatinine, thyroid-stimulating hormone, antithyroid antibodies, and 24-hour microalbuminuria. Correlations were performed by the Spearman rank correlation test, and the significance level was <0.05. Mean values were TC, 168.6+/-46.6 mg/d; HDL, 43.1+/-15.3 mg/dL; LDL, 110.9+/-40.6 mg/dL; TGs, 78.3+/-48.6 mg/dL; glycemia, 204.6+/-116.7 mg/dL; and HbA1c, 11.2%+/-2.9%. High TC (43.9% vs. 10.7%; p<0.002) and LDL (51.5% vs. 10.7%; p<0.01) were more prevalent in patients 19 years and younger (n=66). HbA1c correlated with TC (r=0.30; p=0.004), LDL (r=0.28; p=0.008), TG (r=0.31; p=0.003), and TG/HDL ratio (r=0.25; p=0.01). Duration of diabetes correlated with LDL (r=0.21; p=0.04) and insulin daily doses with TG (r=0.23; p=0.04) and body mass index expressed as z scores (r=-0.28; p=0.007). There was a high prevalence of hypercholesterolemia (54.6%) in these diabetic patients, and lipid fraction levels were correlated with HbA1c. Good management of diabetes seems to be of paramount importance in controlling dyslipidemia.
Prev Cardiol 2006
PMID:Lipid profile correlates with glycemic control in young patients with type 1 diabetes mellitus. 1660 26

Acute phase proteins have been suggested to be increased in patients with type 1 diabetes. The aim of this study was to evaluate the relationship between serum C-reactive protein (CRP) and intima-media thickness (IMT) and functions of the common carotid artery (CCA) in children and adolescents with type 1 diabetes. Serum CRP levels were measured in 65 children and adolescents with diabetes (33 girls and 32 boys; mean age, 12.7 +/- 3.8 years; range, 7-18; duration of diabetes, 6.9 +/- 3.6 years). Age and diabetes duration, as well as major cardiovascular risk factors including anthropometric and metabolic parameters, were matched between girls and boys. The relations of serum CRP levels to CCA structure and functions were measured by ultrasonography as IMT, cross-sectional compliance, cross-sectional distensibility, diastolic wall stress (DWS), and incremental elastic modulus (IEM). There was no significant difference for serum CRP levels between girls and boys (3.7 +/- 1.3 vs 3.2 +/- 0.4 mg/L; p > 0.05). CRP was positively correlated with IMT (r = 0.49, p = 0.001), IEM (r = 0.24, p = 0.05), DWS (r = 0.58, p < 0.001), and body mass index (BMI) (r = 0.28, p = 0.05). In a multivariate regression model, we included CRP and metabolic and anthropometric parameters such as duration of diabetes, HbA1c, BMI, waist:hip ratio, age, and systolic and diastolic blood pressure as independent variables in the model for CCA structure and functions. CRP emerged as an independent correlation for mean IMT (beta = 0.51, p < 0.001) and DWS (beta = 0.61, p < 0.001). According to our findings, CRP was associated with CCA structure and functions in children and adolescents with type 1 diabetes.
Pediatr Cardiol
PMID:Evidence for an association between type 1 diabetes and premature carotid atherosclerosis in childhood. 1663 45

Using biochemical/pharmacological approaches, we previously showed that type 2 ryanodine receptors (RyR2) become dysfunctional in hearts of streptozotocin-induced type 1 diabetic rats. However, the functional consequence of this observation remains incompletely understood. Here we use laser confocal microscopy to investigate whether RyR2 dysfunction during diabetes alters evoked and spontaneous Ca(2+) release from the sarcoplasmic reticulum (SR). After 7-8 weeks of diabetes, steady-state levels of RyR2 remain unchanged in hearts of male Sprague-Dawley rats, but the number of functional receptors decreased by >37%. Interestingly, residual functional RyR2 from diabetic rat hearts exhibited increased sensitivity to Ca(2+) activation (EC(50activation) decreased from 80 microM to 40 microM, peak Ca(2+) activation decreased from 425 microM to 160 microM). When field stimulated, intracellular Ca(2+) release in diabetic ventricular myocytes was dyssynchronous (non-uniform) and this was independent of L-type Ca(2+) currents. Time to peak Ca(2+) increased 3.7-fold. Diabetic myocytes also exhibited diastolic Ca(2+) release and 2-fold higher frequency of spontaneous Ca(2+) sparks, albeit at a lower amplitude. The amplitude of caffeine-releasable Ca(2+) was also lower in diabetic myocytes. RyR2 from diabetic rat hearts exhibited increased phosphorylation at Ser2809 and contained reduced levels of FKBP12.6 (calstablin2). Collectively, these data suggest that RyR2 becomes leaky during diabetes and this defect may be responsible to the reduced SR Ca(2+) load. Diastolic Ca(2+) release could also serve as a substrate for delayed after-depolarizations, contributing to the increased incidence of arrhythmias and sudden cardiac death in type 1 diabetes.
J Mol Cell Cardiol 2007 Jan
PMID:Dyssynchronous (non-uniform) Ca2+ release in myocytes from streptozotocin-induced diabetic rats. 1702 51

Type 2 diabetes (DM-2) has become a major global health problem that has been fueled mainly by increasing obesity and aging of the population. Most studies show that arterial stiffening occurs across all age groups in both type 1 diabetes and DM-2, and among those with impaired fasting glucose, impaired glucose tolerance, and the metabolic syndrome. Arterial stiffening in DM-2 results, in part, from the clustering of hyperglycemia, dyslipidemia and hypertension, all of which may promote insulin resistance, oxidative stress, endothelial dysfunction, and the formation of pro-inflammatory cytokines and advanced glycosylation end-products. Likewise, aging may increase arterial stiffening by altering the proportions of elastin and collagen in the aorta. The consequences of arterial stiffening are increased pulse pressure, hypertension, and a greater risk of cardiovascular disease. Treatment strategies to reduce or prevent arterial stiffening include pharmacologic agents that block the renin-angiotensin-aldosterone system, relax vascular smooth muscle, enhance release of nitric oxide from endothelial cells, and break glycosylation end-product cross-links, and fish oil supplementation.
Adv Cardiol 2007
PMID:Diabetes and arterial stiffening. 1707 13

We report about a 41-year old male patient who presented to the emergency room with acute chest pain, exertion dyspnoea, muscle stiffness, myalgia and adynamia. There was no history of coronary artery disease but known arterial hypertension and insulin dependent diabetes mellitus. Four weeks before submission the patient had been thyroidectomized after he had been diagnosed with papillary thyroid carcinoma and was now awaiting further radioiodine therapy. The thyroid-stimulating hormone level was markedly elevated to 67 mU/l (normal range 0.27-4.20 mU/l) and fT4 significantly reduced to 0.19 ng/ml (normal range 0.9-1.9 ng/ml). CK was elevated to 328 U/l, cardiac Troponin I (Stratus CS) above the threshold with 0.13 microg/l and Elecsys third generation troponin T above the threshold with 0.04 microg/l. The electrocardiogram showed a normal sinus rhythm and did not reveal any signs of ST-elevation or -depression. During follow-up a cardiac MRI was performed, showing normal dimensions and function but a very small area of diffuse myocardial damage, atypical of ischemic injury. In coronary angiography normal coronary arteries were found. We conclude that cardiac troponins I and T may be elevated in severe hypothyroidism without coronary artery disease due to diffuse myocardial injury which can be imaged by MRI.
Int J Cardiol 2007 Feb 07
PMID:Positive cardiac troponin I and T and chest pain in a patient with iatrogenic hypothyroidism and no coronary artery disease. 1708 20

The aim of this study was to determine whether early myocardial structural and functional systolic and diastolic alterations in asymptomatic and uncomplicated patients with type 1 diabetes mellitus (DM) could be detected using the new highly sensitive echocardiographic techniques of integrated backscatter and color Doppler myocardial imaging. Forty asymptomatic and uncomplicated patients with type 1 DM and 40 gender- and age-matched normal controls were studied. All patients were analyzed by conventional and new echocardiographic techniques (integrated backscatter and color Doppler myocardial imaging). Patients with DM showed reduced systolic function compared with controls, evidenced by significantly lower peak strain, strain rates, and cyclic variation indexes at the septum (p <0.0001, <0.01, and <0.001, respectively) and at the posterior wall level (p <0.0001, <0.0001, and <0.001, respectively). On receiver-operating characteristic curve analysis, systolic strain and the cyclic variation index showed the highest discriminating power for separating patients with DM and control subjects. Neither structural or ultrastructural nor diastolic functional abnormalities were detected. On univariate regression analysis, a significant inverse correlation was found for DM duration with conventional (E/A ratio) and unconventional (tissue Doppler imaging E/A ratio) indexes of diastolic function, in the absence of any correlation for systolic function. In conclusion, highly sensitive ultrasonic techniques demonstrate evidence of left ventricular systolic dysfunction in the early stage of type 1 DM, in the absence of ultrastructural and left ventricular diastolic functional abnormalities.
Am J Cardiol 2007 Jan 01
PMID:Left ventricular function in normotensive young adults with well-controlled type 1 diabetes mellitus. 1719 68

Diabetic cardiomyopathy has been documented as an underlying etiology of heart failure (HF) among diabetics. Although oxidative stress has been proposed to contribute to diabetic cardiomyopathy, much of the evidence lacks specificity. Furthermore, whether alterations occur at the cardiac proteome level in diabetic cardiac complications with attendant oxidative stress remains unknown. Therefore, we sought to identify cardiac protein changes in relation to myocardial oxidative stress that are specific to diabetic cardiomyopathy. Diabetes was induced in rats by a single injection of streptozotocin (STZ). STZ-treated rats were examined for diabetic cardiomyopathy at 8 weeks post-STZ by left ventricular (LV) hemodynamic analysis. LV systolic pressure (LVSP), rate of pressure rise (+dP/dt), and rate of pressure decay (-dP/dt) were depressed while LV end-diastolic pressure (LVEDP) was increased. Myocardial oxidative stress was increased in STZ-diabetic rats, as indexed by significant increases in myocardial formation of 8-iso PGF(2alpha) and oxidized glutathione (GSSG). In-depth mining of the diabetic myocardial proteome by proteomic analysis utilizing two-dimensional difference gel electrophoresis and mass spectrometry (DIGE/MS) techniques revealed that a high proportion (12 of 24) of the altered proteins that could be identified by mass spectrometry were localized to the mitochondria. Down-regulation of antioxidant and anti-apoptotic proteins was also observed in STZ-diabetic hearts. These results characterize a specific 'type I diabetic' pattern of cardiac proteome changes indicative of diabetic cardiomyopathy presenting with higher oxidative stress, supporting the idea that analysis of isoprostane biosynthesis and protein expression profiles may be useful diagnostically to assess the efficacy of antioxidant therapies as prophylactic treatments against type I diabetes mellitus complications involving the heart.
J Mol Cell Cardiol 2007 Apr
PMID:Alterations in the diabetic myocardial proteome coupled with increased myocardial oxidative stress underlies diabetic cardiomyopathy. 1732 Jan

Vitamin D deficiency is a risk factor for osteoporosis and other chronic diseases, including type 1 diabetes, hypertension, metabolic syndrome, and ischemic heart disease. Cholesterol and vitamin D share the 7-dehydrocholesterol metabolic pathway. This study evaluated the possible effect of atorvastatin on vitamin D levels in patients with acute ischemic heart disease. Eighty-three patients (52 men and 31 women) with an acute coronary syndrome (75 with acute myocardial infarction and 8 with unstable angina) were included. After diagnosis, patients received atorvastatin as secondary prevention. Serum vitamin D was measured by high-performance liquid chromatography at baseline and at 12 months. Atorvastatin treatment produced a statistically significant decrease in cholesterol and triglyceride levels and an increase in vitamin D levels (41+/-19 vs 47+/-19 nmol/L, p=0.003). Vitamin D deficiency was decreased by 75% to 57% at 12 months. In conclusion, atorvastatin increases vitamin D levels. This increase could explain some of the beneficial effects of atorvastatin at the cardiovascular level that are unrelated to cholesterol levels.
Am J Cardiol 2007 Apr 01
PMID:Effects of Atorvastatin on vitamin D levels in patients with acute ischemic heart disease. 1792 Mar 83

We read with great interest the study by Karamitsos et al. the methods and interpretation of the results, however, raise several concerns: 1. Are the LVMI higher in patients with type 1 diabetes mellitus than controls? If yes, do patients with type 1 diabetes mellitus and normal LVMI have impaired diastolic function? 2. Is the significant alteration of left and right ventricular diastolic function by tissue Doppler echocardiography in patients with type 1 diabetes mellitus in this study caused by the higher level of glycemia, or is tissue Doppler echocardiography sensitive enough to evaluate early alteration of cardiac function in patients with type 1 diabetes? Therefore, we think that further studies about left and right ventricular systolic and diastolic functions when glycemic control improves and aggravates are needed.
Int J Cardiol 2008 May 07
PMID:Early diastolic impairment of diabetic heart: the significance of right ventricle. 1677 48

Coronary artery calcium (CAC) has been previously associated with atherosclerotic plaque disease and coronary events. Thus, identifying predictors of CAC progression may provide new insights for early risk-factor intervention and subsequent reduction of the rates of more severe atherosclerotic disease. The aim of this study was to identify risk factors for CAC progression and evaluate whether risk-factor change was related to CAC progression in a cohort of patients with type 1 diabetes mellitus (DM). Participants in the Pittsburgh EDC Study, a prospective investigation of childhood-onset type 1 DM, who underwent 2 electron beam tomographic screenings 4 years apart were selected for study (n = 222). CAC was calculated using the Agatston method of scoring, and progression was defined as an increase >2.5 in the square root-transformed CAC score. Adjusting for DM duration and initial CAC score, body mass index (BMI; odds ratio [OR] 1.13, 95% confidence interval [CI] 1.01 to 1.26), non-high-density lipoprotein cholesterol (OR 1.01, 95% CI 1.003 to 1.03), and albumin excretion rate (OR 1.30, 95% CI 1.03 to 1.63) were associated with CAC progression. When considering change in risk factors, an increase in BMI (OR 1.38, 95% CI 1.10 to 1.72) was also associated with CAC progression after adjustment. In conclusion, in this cohort with type 1 DM, in addition to baseline BMI, non-high-density lipoprotein cholesterol, albumin excretion rate, and all known coronary artery disease risk factors, weight gain further added to the prediction of CAC progression. Thus, weight control, in addition to lipid and renal management, may help retard atherosclerosis progression in persons with type 1 DM.
Am J Cardiol 2007 Nov 15
PMID:Progression of coronary artery calcium in type 1 diabetes mellitus. 1799 16


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