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Rosiglitazone Treatment (rosiglitazone + treatment)

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Medical Sciences	100%

Selected Abstracts

Effects of physical exercise versus rosiglitazone on endothelial function in coronary artery disease patients with prediabetes

DIABETES OBESITY & METABOLISM, Issue 9 2010
S. Desch
We conducted a three-arm, parallel-group, randomized, controlled trial to compare the effects of rosiglitazone and physical exercise on endothelial function in patients with coronary artery disease and impaired fasting glucose or impaired glucose tolerance over a 6-month period. Group A received rosiglitazone tablets 8 mg daily (n = 16), group B underwent a structured physical exercise programme (n = 15) and group C served as a control group (n = 12). At baseline and after 6 months, brachial artery ultrasound imaging was performed to assess reactive flow-mediated dilation (FMD). Rosiglitazone treatment and exercise both led to significant improvements in insulin resistance at 6 months, whereas no change was observed in control patients. FMD improved significantly in physical exercise patients, whereas no change could be observed in patients receiving rosiglitazone or in the control group. Between-group comparisons also showed a significant relative improvement in FMD in exercise patients compared with rosiglitazone. [source]

Rosiglitazone treatment attenuates renal tissue inflammation generated by urinary tract obstruction

NEPHROLOGY, Issue 2 2009
SHAI EFRATI
SUMMARY Aim: Peroxisome proliferator-activated receptor (PPAR)-, activation by rosiglitazone decreases manifestation of intrarenal inflammatory hallmarks. Inflammation significantly aggravates renal injury following urinary tract obstruction. The effect of rosiglitazone on renal inflammation following unilateral ureteral obstruction was investigated. Methods: Ninety-six Srague,Dawley rats were subjected to unilateral ureteral ligation, or to sham operation. Half of each group received rosiglitazone, 5 mg/kg bodyweight per day. The animals were killed and their kidneys allocated following 1 h, 24 h or 2 weeks, for pathological examination or for intrarenal transforming growth factor (TGF)-,, interleukin (IL)-4, IL-6, IL-10 and nitric oxide (NO) assessment by specific enzyme-linked immunosorbent assays. Apoptosis rates, extracellular matrix deposition, PPAR-,, ,-smooth muscle actin (,-SMA) expression and macrophage infiltration were assessed by specific immunohistological stainings. Results: PPAR-, receptor expression was downregulated, and infiltration of macrophages decreased, in all rosiglitazone-treated kidneys. Rosiglitazone significantly decreased apoptosis, TGF-,, IL-6, ,-SMA expression and NO availability in obstructed kidneys. Synthesis of IL-10 was unaltered, while IL-4 augmented by Rosiglitazone. Rosiglitazone also affected NO and IL-4 production in sham-operated controls. Conclusion: (i) Rosiglitazone attenuates profibrotic and pro-inflammatory responses in a rat model of ureteral obstruction-induced renal inflammation; (ii) rosiglitazone stimulates counteractive anti-inflammatory responses in the damaged kidneys; (iii) in part, rosiglitazone exerts comparable anti-inflammatory effects on obstructed kidneys and unobstructed healthy controls. Taken together, this ascertains the importance of the anti-inflammatory role of rosiglitazone treatment in amelioration of ureteral obstruction-induced renal damage. [source]

Rosiglitazone improves insulin sensitivity and glucose tolerance in subjects with impaired glucose tolerance

CLINICAL ENDOCRINOLOGY, Issue 1 2005
Yi-Jen Hung
Summary Objective, This study was designed to evaluate the effects of rosiglitazone (ROS) on insulin sensitivity, ,-cell function, and glycaemic response to glucose challenge and meal in subjects with impaired glucose tolerance (IGT). Methods, Thirty patients with IGT (ages between 30 and 75 years and BMI (body mass index) , 27 kg/m2) were randomly assigned to receive either placebo (n = 15) or ROS (4 mg/day) (n = 15). All participants underwent a 75-g oral glucose tolerance test (OGTT), meal test, and frequently sampled intravenous glucose tolerance test (FSIGT) before and after the 12-week treatment. Results, After 12 weeks of ROS treatment, there were significant increases in total cholesterol (TC) (4·25 ± 0·22 vs 4·80 ± 0·17 mmol/l, P < 0·001), high-density lipoprotein cholesterol (HDL-C) (1·25 ± 0·07 vs 1·43 ± 0·06 mmol/l, P < 0·05), and low-density lipoprotein cholesterol (LDL-C) (2·70 ± 0·15 vs 3·37 ± 0·17 mmol/l, P < 0·05) without changes in triglyceride concentration, TC/HDL-C and LDL-C/HDL-C ratio. Although the acute insulin response (AIR) to intravenous glucose and disposition index (measured as the ability of pancreatic ,-cell compensation in the presence of insulin resistance) remained unchanged, the insulin sensitivity (SI) and glucose effectiveness (SG) were remarkably elevated (0·38 ± 0·06 vs 0·54 ± 0·09 × 10,5 min,1/pmol, P < 0·05; 0·017 ± 0·002 vs 0·021 ± 0·001 min,1, P < 0·05, respectively) in the ROS group. The glucose, insulin, and c-peptide areas under curve (AUC) in response to OGTT and the glucose and insulin AUC during meal were significantly ameliorated in the ROS group. Five out of 15 (33%) and two out of 15 (13%) subjects treated with ROS and placebo, respectively, reversed to normal response during OGTT (P < 0·05). Conclusion, Rosiglitazone treatment significantly improved insulin resistance and reduced postchallenge glucose and insulin concentrations in patients with impaired glucose tolerance without remarkable effects on ,-cell secretory function. [source]

Effect of ABCA1 variant on atherogenic dyslipidaemia in patients with Type 2 diabetes treated with rosiglitazone

DIABETIC MEDICINE, Issue 6 2009
S. E. Park
Abstract Aims, To investigate the effect of two common ATP-binding cassette transporter 1 (ABCA1) polymorphisms (rs4149263 and rs2020927) on atherogenic dyslipidaemia in Korean Type 2 diabetic patients who were treated with rosiglitazone. Patients and methods, Two hundred and fifty-six patients with Type 2 diabetes who had never previously received peroxisome proliferator-activated receptor gamma (PPAR-,) agonists or lipid-lowering treatment were treated with 4 mg of rosiglitazone daily for 12 weeks without any adjustment to their glucose-lowering regimen. The primary outcome was the change in atherogenic index of plasma (AIP), calculated as log [triglyceride (mmol/l)/high-density lipoprotein cholesterol (mmol/l)], before and after rosiglitazone treatment. The effect of rosiglitazone on the change in AIP was compared across the ABCA1 single nucleotide polymorphisms (SNPs) rs41429263 and rs2020927. Results, Before adjustment, the change in AIP at 12 weeks was significantly different across the rs4149263 genotypes [median (interquartile range): ,0.05 (,0.21, 0.09) for TT; 0.02 (,0.09, 0.17) for TC; and 0.11 (0.03, 0.25) for CC; P = 0.003], but not across the rs2020927 [,0.04 (,0.18, 0.10) for TT; 0.03 (,0.17, 0.15) for TC; and ,0.03 (,0.13, 0.10) for CC; P = 0.401]. After controlling for age, gender and duration of diabetes, the presence of the C-allele was significantly associated with an increase in AIP by 0.13 [95% confidence interval (CI), 0.04,0.21; P = 0.003]. This association did not change significantly when body mass index and pretreatment metabolic parameters were additionally controlled for (the change in AIP: 0.14; 95% CI, 0.04,0.24; P = 0.007). Conclusions, The ABCA1 SNP rs4149263 may be associated with the change in atherogenic lipid profile in Type 2 diabetes treated with rosiglitazone. [source]

Avandamet: combined metformin,rosiglitazone treatment for insulin resistance in type 2 diabetes

INTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 9 2004
C.J. Bailey
Summary Insulin resistance is a major endocrinopathy underlying the development of hyperglycaemia and cardiovascular disease in type 2 diabetes. Metformin (a biguanide) and rosiglitazone (a thiazolidinedione) counter insulin resistance, acting by different cellular mechanisms. The two agents can be used in combination to achieve additive glucose-lowering efficacy in the treatment of type 2 diabetes, without stimulating insulin secretion and without causing hypoglycaemia. Both agents also reduce a range of atherothrombotic factors and markers, indicating a lower cardiovascular risk. Early intervention with metformin is already known to reduce myocardial infarction and increase survival in overweight type 2 patients. Recently, a single-tablet combination of metformin and rosiglitazone, Avandamet, has become available. Avandamet is suitable for type 2 diabetic patients who are inadequately controlled by monotherapy with metformin or rosiglitazone. Patients already receiving separate tablets of metformin and rosiglitazone may switch to the single-tablet combination for convenience. Also, early introduction of the combination before maximal titration of one agent can reduce side effects. Use of Avandamet requires attention to the precautions for both metformin and rosiglitazone, especially renal, cardiac and hepatic competence. In summary, Avandamet is a single-tablet metformin,rosiglitazone combination that doubly targets insulin resistance as therapy for hyperglycaemia and vascular risk in type 2 diabetes. [source]

Rosiglitazone treatment attenuates renal tissue inflammation generated by urinary tract obstruction

Rosiglitazone Inhibits Cell Proliferation by Inducing G1 Cell Cycle Arrest and Apoptosis in ADPKD Cyst-Lining Epithelia Cells

BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 6 2010
Yawei Liu
Many drugs inhibiting cell proliferation have been proved to be effective in slowing the disease progression in ADPKD. Recent evidence has suggested that peroxisome proliferator-activated receptor , (PPAR,) ligands have anti-neoplasm effects through inhibiting cell growth and inducing cell apoptosis in various cancer cells. In the present study, we examined the expression of PPAR, in human ADPKD kidney tissues and cyst-lining epithelial cell line, and found that the expression of PPAR, was greater in ADPKD kidney tissues and cyst-lining epithelial cell line than in normal kidney tissues and human kidney cortex (HKC) cell line. Rosiglitazone inhibited significantly proliferation of cyst-lining epithelial cells in a concentration- and time-dependent manner. These effects were diminished by GW9662, a specific PPAR, antagonist. Cell cycle analysis showed a G0/G1 arrest in human ADPKD cyst-lining epithelial cells with rosiglitazone treatment. Analysis of cell cycle regulatory proteins revealed that rosiglitazone decreased the protein levels of proliferating cell nuclear antigen, pRb, cyclin D1, cyclin D2 and Cdk4 but increased the levels of p21 and p27 in a dose-dependent manner. Rosiglitazone also induced apoptosis in cyst-lining epithelial cells, which was correlated with increased bax expression and decreased bcl-2 expression. These results suggest PPAR, agonist might serve as a promising drug for the treatment of ADPKD. [source]