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Prevalenza di bassi livelli di colesterolo HDL e correlazione con il grado di controllo glicometabolico in pazienti con diabete di tipo 2.
No full textThe SNP rs9677 of VPAC1 gene is associated with glycolipid control and heart function in female patients with type 2 diabetes: A follow-up study
No full textBACKGROUND AND AIMS:
In a previous study, the single-nucleotide polymorphism (SNP) rs9677, mapped in the 3'-UTR of vasoactive intestinal peptide receptor 1 (VPAC1) gene, was found to be associated with type 2 diabetes (T2D) in Caucasian women. Moreover, the CC genotype correlated with a worse glycolipid profile. The objectives of this study were to confirm this correlation and assess the prevalence of coronary artery disease (CAD) in the previously investigated diabetic women after a follow-up of 4.6 years.
METHODS AND RESULTS:
A total of 143 women with T2D, with 53 carrying the CC genotype (age: 71.7 ± 7.4 years, diabetes duration: 17.2 ± 9.9 years) and 90 carrying the CT + TT genotypes (age: 69.4 ± 8.8 years, diabetes duration: 14.3 ± 8.2 years), were followed up for 4.6 ± 1.8 years. At follow-up, the clinical and haematochemical parameters were analysed. Twelve-lead electrocardiography, Doppler echocardiography and the percentage of patients with acute myocardial infarction (AMI) or of those subjected to coronary angioplasty and coronary artery bypass surgery were evaluated. At follow-up, there was no significant difference in terms of the clinical and haematochemical parameters between the two groups. However, despite a significantly increased use of statin therapy, no significant improvement in the LDL cholesterol levels was observed in CC female patients unlike those with CT + TT (P = 0.02). Moreover, the CC female patients presented a significantly higher percentage of echocardiographic abnormalities (P = 0.035), especially left ventricular (LV) diastolic dysfunction (P = 0.04).
CONCLUSIONS:
The rs9677 CC genotype could be correlated with a reduced response to statin therapy and seems to be involved in diabetes cardiomyopathy in female patients with T2D
Waist circumference reduction after insulin Detemir therapy in type 2 diabetes patients previously treated with NPH.
No full textBackground and aims: Abdominal weight may increase vascular complication risk. Insulin detemir reduces weight gain in comparison with NPH and insulin glargine. We studied the weight-sparing effect of detemir and assessed glycemic control and treatment satisfaction when switching from NPH to detemir, to improve metabolic control.
Methods and Results: Twenty type 2 diabetes (T2D) patients (mean age 59.4 years, BMI 7.5%, diabetes duration ≥12 months, previously treated with NPH) were recruited to this 20-week study. Patients received once-daily detemir (0.1 U/kg) at bedtime and OAD dose remained unchanged. HbA1c was measured at baseline and end-of-trial and DTSQ completed. Mean HbA1c (8.5±1.3 vs. 7.9±1.2%, P<0.05) and waist circumference (107.0±13.4 vs. 102.2±10.5 cm, P<0.05) were significantly reduced with detemir. Treatment satisfaction significantly improved (38.9±7.0 vs. 30.3±9.5, P<0.03). No weight gain was observed after treatment with insulin detemir (from 88.9±16.7 to 85.1±15.0 kg).
Conclusions: Detemir improves glycemic control for T2D patients previously on NPH, increases treatment satisfaction, and may provide additional weight-sparing benefits
Poor Glycemic Control Is an Independent Risk Factor for Low HDL Cholesterol in Patients With Type 2 Diabetes
No full textOBJECTIVE— To determine whether the association observed between poor glycemic control and low HDL cholesterol in type 2 diabetes is dependent on obesity and/or hypertriglyceridemia. RESEARCH DESIGN AND METHODS— We performed a cross-sectional study of 1,819 patients with type 2 diabetes and triglycerides <400 mg/dl enrolled at three diabetes centers in Italy. The risk for low HDL cholesterol was analyzed as a function of A1C levels. Odds ratios (ORs) were calculated after adjustment for confounding factors. RESULTS— A 1% increase in A1C significantly increased the risk for low HDL cholesterol (OR 1.17 [95% CI 1.1–1.2], P = 0.00072); no changes were observed when age, sex, smoking, and lipid-lowering therapy were included in the model (1.17 [1.1–1.2], P = 0.00044). The association remained strong after adjustments for obesity and hypertriglyceridemia in multivariate analysis (1.12 [1.05–1.18], P = 0.00017). CONCLUSIONS— Poor glycemic control appears to be an independent risk factor for low HDL cholesterol in type 2 diabetes
Effetti del trattamento con atorvastatina sull'espressione del CD36 e sui livelli di NFkB nucleare in monociti circolanti di pazienti con diabete di tipo 2.
No full textAtorvastatin downregulates monocyte CD36 scavenger receptor expression and nuclear NFkB levels in type 2 diabetic patients.
No full textMetabolic syndrome is not a risk factor for kidney dysfunction in obese non-diabetic subjects
No full textObjective: To investigate whether insulin resistance (IR) and the metabolic syndrome (MS) are associated with kidney
dysfunction in obese non-diabetic (OND) subjects.
Methods and Procedures: Three-hundred and eighty (113M/267F; age = 41 ± 14 years) OND subjects (BMI ≥ 30 kg/m2;
range = 43 ± 8 kg/m2) were studied. Anthropometric measures, blood pressure, fasting glucose, insulin, lipid profile, and
serum creatinine were evaluated. Glomerular filtration rate (GFR) was estimated (e-GFR) with the Modification of Diet in
Renal Disease equation. Chronic kidney disease (CKD) was defined as e-GFR <60 ml/min/1.73 m2.
Results: e-GFR was associated with gender (being lower in women) (P = 0.001) and age (P < 0.0001). CKD was
present in 32 subjects (8.4%), who were older (P < 0.0001) and more frequently affected by hypertension (P = 0.04) as
compared to subjects without CKD. MS was present in 212 (55.8%) subjects. They were older (P < 0.001), had lower
e-GFR (P = 0.02) and were more frequently affected by CKD (odds ratio (OR), 95% confidence interval (CI) = 2.3,
1.1–5.1) than those without MS. However, differences in e-GFR values and in the risk of CKD were no longer
statistically significant after adjusting for age (P = 0.99 for e-GFR and OR, 95% CI = 1.2, 0.5–2.8 for the risk of CKD,
respectively). Homeostasis model assessment of IR (HOMAIR) index was neither higher in subject with CKD (P = 0.1)
nor inversely correlated with e-GFR (r = 0.1, P = 0.1).
Discussion: In OND individuals the risk of CKD is independent of the MS and related abnormalities. This suggests
that these individuals are not susceptible to a further deleterious role on kidney function on the top of that played by
obesity itsel
The 3'-UTR C>T polymorphism of the oxidized LDL-receptor 1 (OLR1) gene does not associate with coronary artery disease in Italian CAD patients or with the severity of coronary disease
No full textBackground and aim: Oxidized low-density tipoproteins (OxLDLs) play a critical rote in endothetiat dysfunction, which is implicated in the pathogenesis of atherosclerosis. Vascular enclothelial cells internalize and degrade oxLDL through the endothelial lectin-like oxidized LDL receptor 1 (OLR1). OLR1 is up-regulated in several pathological conditions, including hypertension, hyperlipidernia, diabetes, atherosclerosis and inflammation, and represents therefore a good candidate for coronary artery disease (CAD). Recently, a 3'-UTR (188 C > T) SNP in the OLR1 gene has been reported to be associated with coronary artery stenosis and myocardial infarction. In the present study we investigated whether the OLRI gene 188 C > T SNP is a genetic risk marker for CAD in Italian patients with angiographically defined coronary atherosclerosis, and assessed its relation with clinical and metabolic abnormalities, including severity of disease (classified as restenosis, single- or multiple coronary vessels disease, and MI).
Methods: The 3'-UTR C > T SNP was detected in real-time PCR in 351 subjects with CAD and in 215 control subjects.
Results: The OLR1-T allele frequencies were 48.9% in the CAD subjects and 47.7% in controls, with no significant difference between the two groups. Also, the 3'-UTR C > T SNP did not associate with any of the parameters of severity of disease. Furthermore, none of the other clinical and metabolic parameters were associated with the OLR1 gene SNP. Conclusions: Our observations suggest that, in our population, the 3'-UTR C > T polymorphism of the OLR1 gene is unlikely to play a role in the pathogenesis of coronary artery disease
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