Pleiotropic effects of rosuvastatin on microvascular function in type 2 diabetes

Parson,

doi:10.2147/dmsott.s8376

Cited by 6 publications

(3 citation statements)

References 28 publications

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“…According to the studies done previously [12][13][14] atorvastatin and rosuvastatin are two potent statins which can effi ciently lower hs-CRP levels. So, in the present study effects of atorvastatin and rosuvastatin were evaluated and compared on the basis of the effects on hs-CRP levels and lipid profi le in obese T2DM patients.…”

Section: Introductionmentioning

confidence: 99%

Effects of atorvastatin and rosuvastatin on high-sensitivity C-reactive protein and lipid profile in obese type 2 diabetes mellitus patients

Sindhu¹,

Singh²,

Salman³

et al. 2011

Journal of Pharmacology and Pharmacotherapeutics

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Objective:To evaluate and compare the effects on high-sensitivity C-reactive protein (hs-CRP) levels and lipid profile of atorvastatin and rosuvastatin in obese type 2 diabetes mellitus (T2DM) patients.Materials and Methods:A total of 40 subjects with 20 in each group were randomly allocated to two groups. Group 1 patients received atorvastatin and that of Group 2 rosuvastatin treatment for 6 months. The patients were administered atorvastatin (40-80 mg) and rosuvastatin(10-40 mg) in accordance to their LDL-C status as per NCEP-ATP III guidelines. The parameters studied were, hs-CRP and lipid profile comprising LDL-C, HDL-C, TG and TC.Results:Results obtained from the study, clearly indicate that atorvastatin (A) as well as rosuvastatin(R) have significant effect on lowering of hs-CRP levels (for A P=0.001; for R P=0.002), reducing LDL-C levels (for A P=0.008; for R P=0.001), elevating HDL-C levels (for A P=0.02; for R P=0.001) along with reducing TC (for A P=0.003; for R P=0.002) and TG (for A P=0.000; for R P=0.000) levels in obese T2DM patients. It is also seen that there is no significant (P>0.05) difference in effect of atorvastatin and rosuvastatin in lowering of hs-CRP levels, elevating HDL-C levels and reducing TG levels in obese T2DM patients. However, percentage lowering of LDL-C (P=0.000) and TC (P=0.001) by rosuvastatin is to a greater extent than that caused by atorvastatin in these patients.Conclusions:Thus this study throws light on the fact that rosuvastatin should be preferred over atorvastatin in obese T2DM patients in whom LDL-C and TC levels are deviated from normal reference values. In rest of obese T2DM either of atorvastatin or rosuvastatin can be employed to lower hs-CRP levels, to elevate HDL-C levels or to reduce TG levels.

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Section: Introductionmentioning

confidence: 99%

Effects of atorvastatin and rosuvastatin on high-sensitivity C-reactive protein and lipid profile in obese type 2 diabetes mellitus patients

Sindhu¹,

Singh²,

Salman³

et al. 2011

Journal of Pharmacology and Pharmacotherapeutics

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“…Statins also reduce reactive oxygen species via vascular nicotinamide adenine dinucleotide phosphate oxidase and antagonize the pro-oxidant effects of angiotensin II and endothelin-1 18. Further, rosuvastatin reduces oxidation of low-density lipoprotein 19,20. Therefore, we evaluated the effects of rosuvastatin in patients with DPN.…”

Section: Introductionmentioning

confidence: 99%

Effect of rosuvastatin on diabetic polyneuropathy: a randomized, double-blind, placebo-controlled Phase IIa study

Hernández-Ojeda¹,

Román-Pintos²,

Rodríguez-Carrizález³

et al. 2014

DMSO

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BackgroundDiabetic neuropathy affects 50%–66% of patients with diabetes mellitus. Oxidative stress generates nerve dysfunction by causing segmental demyelinization and axonal degeneration. Antioxidants are considered to be the only etiologic management for diabetic polyneuropathy, and statins such as rosuvastatin increase nitric oxide bioavailability and reduce lipid peroxidation. The aim of this study was to evaluate the antioxidant effect of rosuvastatin in diabetic polyneuropathy.MethodsWe conducted a randomized, double-blind, placebo-controlled Phase IIa clinical trial in patients with type 2 diabetes and diabetic polyneuropathy (DPN) stage ≥1b. We allocated subjects to two parallel groups (1:1) that received rosuvastatin 20 mg or placebo for 12 weeks. Primary outcomes were neuropathic symptom score, disability score, and nerve conduction studies, and secondary outcomes were glycemic control, lipid and hepatic profile, lipid peroxidation, and nerve growth factor beta (NGF-β) levels.ResultsBoth groups were of similar age and duration since diagnosis of diabetes and DPN. We observed improvement of DPN in the rosuvastatin group from stage 2a (88.2%) to stage 1b (41.2%), improvement of neuropathic symptom score from 4.5±2 to 2.4±1.8, and significant (P=0.001) reductions of peroneal nerve conduction velocity (from 40.8±2.2 to 42.1±1.6 seconds) and lipid peroxidation (from 25.4±2 to 12.2±4.0 nmol/mL), with no significant change in glycemic control or β-NGF.ConclusionThe severity, symptoms, and nerve conduction parameters of DPN improved after 12 weeks of treatment with rosuvastatin. These beneficial effects appear to be attributable to reductions in lipid peroxidation and oxidative stress.

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“…Moreover, rosuvastatin has been found to be a highly effective hypolipidemic agent in patients with metabolic syndrome [8]. In addition, rosuvastatin reduces the risk of cardiovascular disease, decrease vascular reactive oxygen species generation independently of cholesterol reduction [9] and exerts several “pleiotropic”, but also achieve significant improvement in endothelial function [10] effects that may result in a further clinical benefit [11,12]. …”

Section: Introductionmentioning

confidence: 99%

Pleiotropic effects of rosuvastatin on the glucose metabolism and the subcutaneous and visceral adipose tissue behavior in C57Bl/6 mice

Neto-Ferreira

Rocha

Souza-Mello

et al. 2013

Diabetol Metab Syndr

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The aim of this study was to evaluate whether rosuvastatin (HMG-CoA reductase inhibitor) modulates the carbohydrate and lipid metabolism, the development of non-alcoholic fatty liver disease (NAFLD), and the increase in body mass in a model of diet-induced obesity. Male C57Bl/6 mice (3-months-old) were fed a high-fat diet (HF, 60% lipids) or the standard chow (SC, 10% lipids) for 15 weeks. The animals were then treated with 10 mg/kg/day (HF-R10 group), 20 mg/kg/day (HF-R20), or 40 mg/kg/day (HF-R40) of rosuvastatin for five weeks. The HF diet led to glucose intolerance, insulin resistance, weight gain, increased visceral adiposity with adipocyte hypertrophy, and hepatic steatosis (micro and macrovesicular). The rosuvastatin treatment decreased the adiposity and the adipocyte size in the HF-R10 and HF-R20 groups. In addition, rosuvastatin changed the pattern of fat distribution in the HF-R40 group because more fat was stored subcutaneously than in visceral depots. This redistribution improved the fasting glucose and the glucose intolerance. Rosuvastatin also improved the liver morphology and ultrastructure in a dose-dependent manner. In conclusion, rosuvastatin exerts pleiotropic effects through a dose-dependent improvement of glucose intolerance, insulin sensitivity and NAFLD and changes the fat distribution from visceral to subcutaneous fat depots in a mouse model of diet-induced obesity.

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Pleiotropic effects of rosuvastatin on microvascular function in type 2 diabetes

Cited by 6 publications

References 28 publications

Effects of atorvastatin and rosuvastatin on high-sensitivity C-reactive protein and lipid profile in obese type 2 diabetes mellitus patients

Effects of atorvastatin and rosuvastatin on high-sensitivity C-reactive protein and lipid profile in obese type 2 diabetes mellitus patients

Effect of rosuvastatin on diabetic polyneuropathy: a randomized, double-blind, placebo-controlled Phase IIa study

Pleiotropic effects of rosuvastatin on the glucose metabolism and the subcutaneous and visceral adipose tissue behavior in C57Bl/6 mice

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