44 research outputs found
Riboflavin alleviates cardiac failure in Type I diabetic cardiomyopathy
Heart failure (HF) is a common and serious comorbidity of diabetes. Oxidative stress has been associated with the pathogenesis of chronic diabetic complications including cardiomyopathy. The ability of antioxidants to inhibit injury has raised the possibility of new therapeutic treatment for diabetic heart diseases. Riboflavin constitutes an essential nutrient for humans and animals and it is an important food additive. Riboflavin, a precursor of flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), enhances the oxidative folding and subsequent secretion of proteins. The objective of this study was to investigate the cardioprotective effect of riboflavin in diabetic rats. Diabetes was induced in 30 rats by a single injection of streptozotocin (STZ) (70 mg /kg). Riboflavin (20 mg/kg) was orally administered to animals immediately after induction of diabetes and was continued for eight weeks. Rats were examined for diabetic cardiomyopathy by left ventricular (LV) remadynamic function. Myocardial oxidative stress was assessed by measuring the activity of superoxide dismutase (SOD), the level of malondialdehyde (MDA) as well as heme oxygenase-1 (HO-1) protein level. Myocardial connective tissue growth factor (CTGF) level was measured by Western blot in all rats at the end of the study. In the untreated diabetic rats, left ventricular systolic pressure (LVSP) rate of pressure rose (+dp/dt), and rate of pressure decay (−dp/dt) were depressed while left ventricular end-diastolic pressure (LVEDP) was increased, which indicated the reduced left ventricular contractility and slowing of left ventricular relaxation. The level of SOD decreased, CTGF and HO-1 protein expression and MDA content rose. Riboflavin treatment significantly improved left ventricular systolic and diastolic function in diabetic rats, there were persistent increases in significant activation of SOD and the level of HO-1 protein, and a decrease in the level of CTGF. These results suggest that riboflavin treatment ameliorates myocardial function and improves heart oxidant status, whereas raising myocardial HO-1 and decreasing myocardial CTGF levels have beneficial effects on diabetic cardiomyopathy
Poorly controlled type 2 diabetes is accompanied by significant morphological and ultrastructural changes in both erythrocytes and in thrombin-generated fibrin: implications for diagnostics
We have noted in previous work, in a variety of inflammatory diseases, where iron dysregulation occurs, a strong
tendency for erythrocytes to lose their normal discoid shape and to adopt a skewed morphology (as judged by
their axial ratios in the light microscope and by their ultrastructure in the SEM). Similarly, the polymerization of
fibrinogen, as induced in vitro by added thrombin, leads not to the common ‘spaghetti-like’ structures but to dense
matted deposits. Type 2 diabetes is a known inflammatory disease. In the present work, we found that the axial
ratio of the erythrocytes of poorly controlled (as suggested by increased HbA1c levels) type 2 diabetics was
significantly increased, and that their fibrin morphologies were again highly aberrant. As judged by scanning
electron microscopy and in the atomic force microscope, these could be reversed, to some degree, by the addition
of the iron chelators deferoxamine (DFO) or deferasirox (DFX). As well as their demonstrated diagnostic significance,
these morphological indicators may have prognostic value.Biotechnology and Biological Sciences Research Council (grant
BB/L025752/1) as well as the National Research Foundation (NRF) of South
Africa.http://www.cardiab.com/hb201
Waist circumference reduction after insulin Detemir therapy in type 2 diabetes patients previously treated with NPH.
Background 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
The metabolic sindrome is not a risk factor for reduced kidney function in obese non diabetic subjects.
Atorvastatin downregulates monocyte CD36 scavenger receptor expression and nuclear NF kappa B levels in type 2 diabetic patients
Atorvastatin; Type 2 diabete