title: Effect of simvastatin and/or pioglitazone on insulin resistance, insulin secretion, adiponectin, and proinsulin levels in nondiabetic patients at cardiovascular risk--the PIOSTAT Study. Additive Beneficial Effects of Losartan Combined With Simvastatin in the Treatment of Hypercholesterolemic, Hypertensive Patients Treatment with pravastatin and fenofibrate improves atherogenic lipid profiles but not inflammatory markers in ACTG 5087. Atorvastatin causes insulin resistance and increases ambient glycemia in hypercholesterolemic patients. Aerobic training increases the expression of adiponectin receptor genes in the peripheral blood mononuclear cells of young men Reduction of serum ubiquinol-10 and ubiquinone-10 levels by atorvastatin in hypercholesterolemic patients. Effects of pravastatin on serum adiponectin levels in female patients with type 2 diabetes mellitus. Additive beneficial effects of atorvastatin combined with amlodipine in patients with mild-to-moderate hypertension. Effects of pravastatin and rosuvastatin on the generation of adiponectin in the visceral adipose tissue in patients with coronary artery disease. Pravastatin does not affect insulin sensitivity and adipocytokines levels in healthy nondiabetic patients. Effect of Atorvastatin on Inflammation and Modification of Vascular Risk Factors in Rheumatoid Arthritis Secondary prevention of cardiovascular events with long-term pravastatin in patients with diabetes or impaired fasting glucose: results from the LIPID trial. Effects of 90-day hypolipidemic treatment on insulin resistance, adipokines and proinflammatory cytokines in patients with mixed hyperlipidemia and impaired fasting glucose. Effect of high-dose pitavastatin on glucose homeostasis in patients at elevated risk of new-onset diabetes: insights from the CAPITAIN and PREVAIL-US studies Effects of lipid-lowering therapy with rosuvastatin on atherosclerotic burden in patients with chronic kidney disease.
abstract: We investigated the effect of pioglitazone in comparison with and in combination with simvastatin on insulin resistance , plasma adiponectin , postpr and ial plasma glucose , insulin , and intact proinsulin levels in a nondiabetic population at cardiovascular risk . One hundred twenty-five nondiabetic patients at cardiovascular risk were r and omized to pioglitazone ( PIO ) , pioglitazone and simvastatin ( PIO/SIM ) , or simvastatin ( SIM ) treatments . Blood sample s were taken for the measurement of adiponectin and lipid levels . In addition , an oral glucose load with the measurements of glucose , insulin , and intact proinsulin levels was performed . Adiponectin levels increased from 14.0+/-8.2 to 27.6+/-14.5 microg/mL ( P<.0001 ) during PIO treatment and from 11.7+/-10.0 to 26.7+/-15.7 microg/mL ( P<.0001 ) during PIO/SIM treatment . A decrease in adiponectin levels from 15.5+/-12.7 to 11.6+/-7.0 microg/mL ( P<.05 ) was observed during SIM treatment . Although fasting intact proinsulin levels remained unchanged , the increase in postpr and ial intact proinsulin levels could be reduced from 29.5+/-21.4 to 22.1+/-17.5 pmol/L ( P<.01 ) during PIO treatment and from 24.3+/-27.4 to 21.1+/-16.5 mmol/L ( P<.05 ) during PIO/SIM treatment . Lipid parameters improved during SIM treatment but not during PIO treatment . Combined treatment with PIO/SIM was superior in improving overall cardiovascular risk profile than every single drug Background —Biological mechanisms underlying statin and angiotensin II type 1 receptor blocker therapies differ . Therefore , we compared vascular and metabolic responses to these therapies either alone or in combination in hypercholesterolemic , hypertensive patients . Methods and Results —This was a r and omized , double-blind , placebo-controlled crossover trial with 3 treatment arms ( each 2 months ) and 2 washout periods ( each 2 months ) . Forty-seven hypertensive , hypercholesterolemic patients were given simvastatin 20 mg and placebo , simvastatin 20 mg and losartan 100 mg , or losartan 100 mg and placebo daily during each 2-month treatment period . Losartan alone or combined therapy significantly reduced blood pressure compared with simvastatin alone . Compared with losartan alone , simvastatin alone or combined therapy significantly changed lipoproteins . All 3 treatment arms significantly improved flow-mediated dilator response to hyperemia and decreased plasma malondialdehyde and monocyte chemoattractant protein-1 levels relative to baseline measurements . However , these parameters were changed to a greater extent with combined therapy compared with simvastatin or losartan alone ( both P<0.001 and P=0.030 for monocyte chemoattractant protein-1 by ANOVA ) . Combined therapy or losartan alone significantly increased plasma adiponectin levels and insulin sensitivity ( determined by QUICKI ) relative to baseline measurements . These changes were significantly greater than in the group treated with simvastatin alone ( P<0.001 for adiponectin , P=0.029 for QUICKI by ANOVA ) . Conclusions —Simvastatin combined with losartan improves endothelial function and reduces inflammatory markers to a greater extent than monotherapy with either drug in hypercholesterolemic , hypertensive patients OBJECTIVES Statins and fibrates alter lipids , apolipoproteins and inflammatory markers in persons without HIV . The objective of this study was to evaluate changes in lipoproteins , apolipoproteins and other markers of inflammation with the use of pravastatin and fenofibrate . DESIGN Evaluation of participants in ACTG A5087 , a r and omized trial of pravastatin 40 mg/day or fenofibrate 200 mg/day for the treatment of dyslipidemia . Participants that failed single-agent therapy at week 12 were given the combination . METHODS Participants with available specimens were tested for apolipoproteins A1 and B , adiponectin , plasminogen-activator inhibitor type 1 ( PAI-1 ) , P-selectin , and high-sensitivity C-reactive protein ( hs-CRP ) . RESULTS 74 participants ( 37 per r and omized arm ) received either pravastatin or fenofibrate for 12 weeks with 60 receiving combination treatment from weeks 12 - 48 . There were no significant changes in hs-CRP , PAI-1 , and P-selectin . From baseline to week 12 , the median Apo B levels (-8 mg/dL , P=0.01 for fenofibrate and -27 mg/dL , P<0.01 for pravastatin ) and ApoB/A1 ratios ( -0.16 , P<0.01 for both arms ) significantly decreased . From baseline to week 48 , median adiponectin ( -1 ng/dL , P<0.01 ) , Apo B ( -22 mg/dL , P<0.01 ) and Apo B/A1 ratios ( -0.2 , P<0.01 ) all decreased in those who went on combination therapy , whereas Apo A1 ( 9.5 mg/dL , P=0.01 ) levels increased . CONCLUSION Treatment with pravastatin or fenofibrate improves the atherogenic lipid profile within the first 12 weeks and is sustained through 48 weeks with combination therapy . Adiponectin levels decrease with lipid-lowering therapy . However , markers of inflammation and platelet activation were not appreciably changed suggesting that the biologic properties of these agents differ in persons with HIV infection OBJECTIVES We investigated whether atorvastatin might decrease insulin sensitivity and increase ambient glycemia in hypercholesterolemic patients . BACKGROUND Clinical trials suggest that some statin treatments might increase the incidence of diabetes despite reductions in low-density lipoprotein ( LDL ) cholesterol and improvement in endothelial dysfunction . METHODS A r and omized , single-blind , placebo-controlled parallel study was conducted in 44 patients taking placebo and in 42 , 44 , 43 , and 40 patients given daily atorvastatin 10 , 20 , 40 , and 80 mg , respectively , during a 2-month treatment period . RESULTS Atorvastatin 10 , 20 , 40 , and 80 mg significantly reduced LDL cholesterol ( 39 % , 47 % , 52 % , and 56 % , respectively ) and apolipoprotein B levels ( 33 % , 37 % , 42 % , and 46 % , respectively ) after 2 months of therapy when compared with either baseline ( all p < 0.001 by paired t test ) or placebo ( p < 0.001 by analysis of variance [ ANOVA ] ) . Atorvastatin 10 , 20 , 40 , and 80 mg significantly increased fasting plasma insulin ( mean changes : 25 % , 42 % , 31 % , and 45 % , respectively ) and glycated hemoglobin levels ( 2 % , 5 % , 5 % , and 5 % , respectively ) when compared with either baseline ( all p < 0.05 by paired t test ) or placebo ( p = 0.009 for insulin and p = 0.008 for glycated hemoglobin by ANOVA ) . Atorvastatin 10 , 20 , 40 , and 80 mg decreased insulin sensitivity ( 1 % , 3 % , 3 % , and 4 % , respectively ) when compared with either baseline ( p = 0.312 , p = 0.008 , p < 0.001 , and p = 0.008 , respectively , by paired t test ) or placebo ( p = 0.033 by ANOVA ) . CONCLUSIONS Despite beneficial reductions in LDL cholesterol and apolipoprotein B , atorvastatin treatment result ed in significant increases in fasting insulin and glycated hemoglobin levels consistent with insulin resistance and increased ambient glycemia in hypercholesterolemic patients . ( Effects of Atorvastatin on Adiponectin Levels and Insulin Sensitivity In Hypercholesterolemic Patients ; NCT00745836 ) Little is known about the effect of exercise training on the expression of adiponectin receptor genes in peripheral blood mononuclear cells ( P BMC s ) . In this study , we investigated the effects of aerobic training on the expression of AdipoR1 and AidpoR2 mRNAs in P BMC s , whole body insulin sensitivity , and circulating adiponectins in men . Thirty young men were r and omly assigned to either a control ( n=15 ) or an exercise ( n=15 ) group . Subjects assigned to the exercise group underwent a 12-week jogging and /or running programme on a motor-driven treadmill at an intensity of 60%-75 % of the age-based maximum heart rate with duration of 40 minutes per session and a frequency of 5 days per week . Two-way mixed ANOVA with repeated measures was used to test any significant time-by-group interaction effects for the measured variables at p=0.05 . We found significant time-by-group interaction effects for waist circumference ( p=0.001 ) , VO2max ( p<0.001 ) , fasting insulin ( p=0.016 ) , homeostasis model assessment for insulin resistance ( HOMA-IR ) ( p=0.010 ) , area under the curve ( AUC ) for insulin response during the 75-g oral glucose tolerance test ( p=0.002 ) , high-molecular weight ( HMW ) adiponectin ( p=0.016 ) , and the P BMC mRNA levels of AdipoR1 ( p<0.001 ) and AdipoR2 ( p=0.001 ) . The exercise group had significantly increased mRNA levels of AdipoR1 and AdipoR2 in P BMC s , along with increased whole body insulin sensitivity and HMW adiponectin , decreased waist circumference , and increased VO2max compared with the control group . In summary , the current findings suggest that exercise training modulates the expression of AdipoR1 and AdipoR2 mRNAs in P BMC s , implying that manipulation of the expression of these genes could be a potential surrogate for lifestyle intervention-mediated improvements of whole body insulin sensitivity and glucose homeostasis Reduction of serum cholesterol levels with statin therapy decreases the risk of coronary heart disease . Inhibition of HMG-CoA reductase by statin results in decreased synthesis of cholesterol and other products downstream of mevalonate , which may produce adverse effects in statin therapy . We studied the reductions of serum ubiquinol-10 and ubiquinone-10 levels in hypercholesterolemic patients treated with atorvastatin . Fourteen patients were treated with 10 mg/day of atorvastatin  , and serum lipid , ubiquinol-10 and ubiquinone-10 levels were measured before and after 8 weeks of treatment . Serum total cholesterol and LDL-cholesterol levels decreased significantly . All patients showed definite reductions of serum ubiquinol-10 and ubiquinone-10 levels , and mean levels of serum ubiquinol-10 and ubiquinone-10 levels decreased significantly from 0.81 + /- 0.21 to 0.46 + /- 0.10 microg/ml ( p < 0.0001 ) , and from 0.10 + /- 0.06 to 0.06 + /- 0.02 microg/ml ( p = 0.0008 ) , respectively . Percent reductions of ubiquinol-10 and those of total cholesterol showed a positive correlation ( r = 0.627 , p = 0.0165 ) . As atorvastatin reduces serum ubiquinol-10 as well as serum cholesterol levels in all patients , it is imperative that physicians are forewarned about the risks associated with ubiquinol-10 depletion OBJECTIVE Pravastatin has been reported to elevate circulating adiponectin levels in patients with various insulin resistant state , hypertension , coronary artery disease , and hypercholesterolemia . This study aim ed to evaluate whether pravastatin increase serum total and high molecular weight adiponectin levels and improve insulin sensitivity in female patients with type 2 diabetes mellitus and hypercholesterolemia . PATIENTS AND DESIGN This study was design ed as a multicenter , double-blind , placebo-controlled , factorial r and omized trial ( placebo and pravastatin at 20 or 40 mg per day ) . A total of 73 female patients with type 2 diabetes and hypercholesterolemia were enrolled . Changes in total and high molecular weight ( HMW ) serum adiponectin levels , the ratio of HMW adiponectin to total adiponectin , insulin sensitivity measured by homeostasis model assessment of insulin resistance ( HOMA-IR ) and lipid profiles were evaluated after 16 weeks in each group . RESULTS Total cholesterol and low-density lipoprotein ( LDL ) cholesterol levels were significantly reduced after 16 weeks in the pravastatin 20 mg and 40 mg treatment groups compared with the placebo group ( P = 0.008 and P = 0.004 , respectively ) . However , there were no significant differences between the 20 mg and 40 mg pravastatin treatment groups in terms of total adiponectin and HMW adiponectin serum levels , as well as insulin sensitivity ( P = 0.348 and P = 0.991 ) . CONCLUSIONS In female patients with type 2 diabetes and hypercholesterolemia , 16 weeks pravastatin therapy did not affect on serum total adiponectin or HMW adiponectin levels BACKGROUND We hypothesized that atorvastatin combined with amlodipine has additive beneficial vascular and metabolic effects that are superior to monotherapy in patients with hypertension . METHODS Forty-two patients were given atorvastatin 20mg/day and placebo , atorvastatin 20mg/day and amlodipine 10mg/day , or amlodipine 10mg/day and placebo during each 2-month treatment period of a r and omized , single-blind , placebo-controlled cross-over trial with two 2-month washout periods . RESULTS Atorvastatin combined with amlodipine or amlodipine alone significantly reduced blood pressure to a greater extent than atorvastatin alone ( all P < 0.001 by ANOVA ) . Atorvastatin combined with amlodipine significantly reduced plasma malondialdehyde and improved flow-mediated dilation to a greater extent than atorvastatin or amlodipine alone ( all P < 0.001 by ANOVA ) . Atorvastatin therapy significantly increased insulin levels ( P = 0.004 ) and decreased plasma adiponectin levels ( P = 0.016 ) and insulin sensitivity ( determined by QUICKI ; P = 0.026 ) relative to baseline measurements . Amlodipine therapy significantly decreased insulin levels ( P = 0.001 ) and increased adiponectin levels ( P < 0.001 ) and insulin sensitivity ( P = 0.003 ) relative to baseline measurements . Atorvastatin combined with amlodipine therapy significantly increased adiponectin levels ( P < 0.001 ) and insulin sensitivity ( P = 0.034 ) relative to baseline measurements . Effects of all three therapeutic arms on adiponectin levels and insulin sensitivity were statistically significant ( P < 0.001 by ANOVA ) . CONCLUSIONS Atorvastatin combined with amlodipine therapy improves endothelial function and increases adiponectin levels and insulin sensitivity to a greater extent than monotherapy with either drug in hypertensive patients Pravastatin increases the plasma adiponectin level . We examined whether this is a statins ' class effect or specific to pravastatin . Of 50 patients undergoing cardiac surgery for coronary artery disease ( CAD , n = 36 ) and valvular heart disease ( VHD , n = 14 ) , 23 with CAD and serum LDL-cholesterol level > 100 mg/dL were r and omized  to pravastatin at 10 mg/day ( PRAVA , n = 12 ) or rosuvastatin at 2.5 mg/day ( ROSUVA , n = 11 ) for 2 months , and the other 13 with CAD and LDL-cholesterol ≤100 mg/dL were not treated with statin ( Non-statin , n = 13 ) . Patients with VHD did not have CAD and were not treated with statin . Blood was sample d at baseline and surgery . Visceral ( VIS ) and subcutaneous ( SC ) adipose tissues were harvested during surgery . At baseline , the plasma adiponectin level was low in patients with CAD compared with that of patients with VHD . At surgery , adiponectin level in PRAVA was increased to the level in VHD , whereas those in ROSUVA and Non-statin were unchanged . VIS contents and gene expressions of adiponectin in PRAVA and VHD were similar to each other and were both higher than those in Non-statin and ROSUVA . SC content and gene expression of adiponectin were similar among 4 groups . Protein carbonyl ( PC ) level , an indicator of oxidative stress , in VIS was lower in PRAVA and VHD than in ROSUVA and Non-statin . There was a negative correlation between the plasma adiponectin and VIS PC levels ( r = -0.41 , P < 0.05 ) . Thus , pravastatin  increases adiponectin generation , whereas rosuvastatin does not BACKGROUND The effect of statins on insulin resistance is controversial and poorly studied in nondiabetic subjects . In addition , the effect of statins on leptin and adiponectin has never been studied . METHODS Forty healthy nondiabetic volunteers ( 22 men and 18 women ) aged 28 to 72 were r and omized either to placebo or pravastatin 40 mg daily for a 12-week period . Insulin resistance , assessed using the Quantitative Insulin Sensitivity Check Index ( QUICKI ) , as well as serum leptin and adiponectin levels , was measured at baseline and at the end of therapy . RESULTS Pravastatin treatment decreased total cholesterol , low-density lipoprotein cholesterol , and triglycerides levels by 24 % , 32 % , and 14 % , respectively ( P < .05 for all ) , but did not affect glucose and insulin levels , the ( QUICKI ) index , and adiponectin and leptin levels . When stratification was performed according to QUICKI index or sex , no significant differences were observed in the prevalues and postvalues of leptin , adiponectin , or QUICKI index in the pravastatin group . Adiponectin , leptin , and QUICKI index were statistically higher in women than in men ( P < .001 for both variables ) . Adiponectin was negatively correlated with body mass index ( BMI ; r = -0.39 , P < .05 ) and positively correlated with the QUICKI index ( r = 0.54 , P < .001 ) and with high-density lipoprotein cholesterol ( r = 0.50 , P < .01 ) . The relation between adiponectin and QUICKI index remained significant after adjustment for sex and BMI ( P = .005 and P = .007 , respectively ) . Leptin was only related to BMI ( r = 0.57 , P < .001 ) and to sex ( P < .001 ) with no significant correlations with lipid parameters or QUICKI index . Both sex and BMI are independent predictors of leptin ( P < .001 and P < .001 ) . CONCLUSION A 12-week treatment with pravastatin 40 mg/d does not change the QUICKI index and leptin and adiponectin levels in healthy volunteers . In addition , our results emphasize the importance of sex and BMI in the determination of both adiponectin and leptin . Adiponectin was also related to QUICKI index , whereas this relation was not found with leptin Objective . To investigate the effect of atorvastatin therapy on inflammation , disease activity , endothelial dysfunction , and arterial stiffness in patients with rheumatoid arthritis ( RA ) . Methods . This study included 30 patients with early RA , r and omly divided into 2 groups . Group 1 ( n = 15 ) received methotrexate ( MTX ; 0.2 mg/kg/week ; mean ( 15.5 ± SD 1.3 ) plus prednisone ( 10 mg/day ) . Group 2 ( n = 15 ) received MTX and prednisone with the same previous doses plus atorvastatin therapy ( 40 mg/day ) . Ten healthy individuals of similar age and sex served as controls  . Disease activity , lipid profile , serum malondialdehyde ( MDA ) , tumor necrosis factor-α ( TNF-α ) , resistin , adiponectin , and brachial artery flow-mediated dilation ( FMD ) were measured before and after 6 months of treatment . Results . Atorvastatin combined with MTX therapy significantly reduced serum total cholesterol , low-density lipoprotein cholesterol , and triglycerides , and increased high-density lipoprotein cholesterol ( p < 0.001 ) . Disease activity variables , serum MDA , TNF-α , resistin , adiponectin , and FMD were significantly improved by the drug combinations ( p < 0.001 ) . Conclusion . Atorvastatin therapy in patients with RA  reduced disease activity and conventional and novel vascular risk factors that promote the atheromatous lesion . Therapy was also associated with concomitant improvement in endothelial function OBJECTIVE Diabetes , a major health problem worldwide , increases the risk of cardiovascular disease and its associated mortality : The Long-Term Intervention with Pravastatin in Ischemic Disease ( LIPID ) trial showed that cholesterol-lowering treatment with pravastatin reduced mortality and coronary heart disease ( CHD ) events in 9014 patients aged 31 - 75 years with CHD and total cholesterol 4.0 - 7.0 mmol/l . We measured the effects of pravastatin therapy , 40 mg/day over 6.0 years , on the risk of CHD death or nonfatal myocardial infa rct ion and other cardiovascular outcomes in 1,077 LIPID patients with diabetes and 940 patients with impaired fasting glucose ( IFG ) . RESULTS In patients allocated to placebo , the risk of a major CHD event was 61 % higher in patients with diabetes and 23 % higher in the IFG group than in patients with normal fasting glucose , and the risk of any cardiovascular event was 37 % higher in the diabetic group and 19 % higher in the IFG group . Pravastatin therapy reduced the risk of a major CHD event overall from 15.9 to 12.3 % ( relative risk reduction [ RRR ] 24 % , P < 0.001 ) and from 23.4 to 19.6 % in the diabetic group ( 19 % , P = 0.11 ) ; in the diabetic group , the reduction was not significantly different from the reductions in the other groups . Pravastatin reduced the risk of any cardiovascular event from 52.7 to 45.2 % ( 21 % , P < 0.008 ) in patients with diabetes and from 45.7 to 37.1 % ( 26 % , P = 0.003 ) in the IFG group . Pravastatin reduced the risk of stroke from 9.9 to 6.3 % in the diabetic group ( RRR 39 % , CI 7 - 61 % , P = 0.02 ) and from 5.4 to 3.4 % in the IFG group ( RRR 42 % , CI -9 to 69 % , P = 0.09 ) . Pravastatin did not reduce the incidence of diabetes . Over 6 years , pravastatin therapy prevented one major CHD event ( CHD death or nonfatal myocardial infa rct ion ) in 23 patients with IFG and 18 patients with diabetes . A meta- analysis of other major trials confirmed the high absolute risks of diabetes and IFG and the absolute benefits of statin therapy in these patients . CONCLUSIONS Cholesterol-lowering treatment with pravastatin therapy prevents cardiovascular events , including stroke , in patients with diabetes or IFG and established CHD OBJECTIVE Concerns regarding worsening insulin sensitivity associated with statin treatment have recently emerged . Therefore the aim of this study was to assess and compare the effects of 90-day monotherapies with fenofibrate and atorvastatin , as well as combined therapy , on fasting plasma glucose , insulin resistance index , adipokines ( leptin , resistin , adiponectin ) and levels of proinflammatory cytokines ( TNF-α , IL-6 ) in patients with impaired fasting glucose ( IFG ) and mixed hyperlipidemia . MATERIAL S AND METHODS 67 patients were r and omly assigned to four treatment arms : monotherapy with atorvastatin , monotherapy with fenofibrate , combined therapy ( fenofibrate and torvastatin ) or therapeutic lifestyle change . The study lasted for 90 days . All participants received counseling regarding proper diet and physical activity . RESULTS Compared to the control subjects , prediabetic patients exhibited elevated plasma levels of leptin , resistin , TNF-α and IL-6 , and a lower plasma level of adiponectin . All therapeutic interventions result ed in significant alterations in the lipid profile . Insulin resistance index ( HOMA-IR ) was reduced after treatment with fenofibrate . The effect of atorvastatin on insulin resistance was comparable to therapeutic lifestyle change alone . Therapy with hypolipidemic drugs caused increases in adiponectin levels and decreases in leptin and resistin . An additive effect of the combined treatment on plasma IL-6 level was also observed . CONCLUSIONS Fenofibrate-based treatment was associated with improved insulin sensitivity . Atorvastatin did not cause a deterioration in insulin sensitivity . Hypolipidemic therapies result ed in significant changes in the proinflammatory cytokine network as well as in adipokine levels . At the end of the study the measured parameters nearly resembled those of the healthy subjects Abstract Aims : Statin treatment may impair glucose homeostasis and increase the risk of  new-onset diabetes mellitus  , although this may depend on the statin , dose and patient population . We evaluated the effects of pitavastatin 4 mg/day on glucose homeostasis in patients with metabolic syndrome in the CAPITAIN trial . Findings were vali date d in a subset of patients enrolled in PREVAIL-US . Methods : Participants with a well defined metabolic syndrome phenotype were recruited to CAPITAIN to reduce the influence of confounding factors . Validation and comparison data sets were selected comprising phenotypically similar subsets of individuals enrolled in PREVAIL-US and treated with pitavastatin or pravastatin , respectively . Mean change from baseline in parameters of glucose homeostasis ( fasting plasma glucose [ FPG ] , glycated hemoglobin [ HbA1c ] , insulin , quantitative insulin-sensitivity check index [ QUICKI ] and homeostasis model of assessment –insulin resistance [ HOMA-IR ] ) and plasma lipid profile were assessed at 6 months ( CAPITAIN ) and 3 months ( PREVAIL-US ) after initiating treatment . Results : In CAPITAIN ( n = 12 ) , no significant differences from baseline in HbA1c , insulin , HOMA-IR and QUICKI were observed at day 180 in patients treated with pitavastatin . A small ( 4 % ) increase in FPG from baseline to day 180 ( P < 0.05 ) , was observed . In the validation data set ( n = 9 ) , no significant differences from baseline in glycemic parameters were observed at day 84 ( all comparisons P > 0.05 ) . Similar results were observed for pravastatin in the comparison data set ( n = 14 ) . Conclusions : Other than a small change in FPG in the CAPITAIN study , neutral effects of pitavastatin on glucose homeostasis were observed in two cohorts of patients with metabolic syndrome , independent of its efficacy in reducing levels of atherogenic lipoproteins . The small number of patients and relatively short follow-up period represent limitations of the study . Nevertheless , these data suggest that statin-induced diabetogenesis may not represent a class effect OBJECTIVE Although previous studies suggest that treatment of dyslipidemia with statins reduces mortality and morbidity that are associated with cardiovascular disease , only a few studies have examined the efficacy of statins on atherosclerotic status in patients with chronic kidney disease ( CKD ) . MATERIAL S AND METHODS A 12-month , prospect i ve , r and omized study was design ed to assess the efficacy of rosuvastatin in reducing circulating atherosclerotic parameters and renal function in patients with CKD . Thirty-eight patients with CKD and LDL cholesterol levels > or = 100 mg/dL were r and omly assigned to receive 2.5 mg/dL rosuvastatin ( group A , n=22 ) or nonrosuavastatin therapy ( group B , n=16 ) . Lipid profile , estimated glomerular filtration rate ( eGFR ) , high sensitivity C-reactive protein ( hs-CRP ) , and intima-media thickness ( IMT ) were measured before and 12 months after rosuvastatin was added to the treatment . RESULTS Total cholesterol , low-density lipoprotein cholesterol , remnant-like particle-cholesterol and triglycerides were significantly reduced only in patients who received rosuvastatin . These parameters remained unchanged in patients who were not treated with rosuvastatin .  eGFR was significantly increased from 50.7+/-18.7 mL/min/1.73 m(2 ) to 53.3+/-20.1 mL/min/1.73 m(2 ) and a significant reduction of U-P was detected in group A patients ( 0.17+/-0.29 vs. 0.13+/-0.3 g/day ; p<0.01 ) . In addition to the hypolipidemic effect , rosuvastatin treatment significantly reduced hs-CRP ( p=0.0054 ) . Moreover , maximal IMT at the baseline ( 1.89+/-0.98 mm ) decreased significantly to 1.75+/-0.87 mm at 12 months ( p=0.0231 ) . CONCLUSION Rosuvastatin treatment , in addition to its beneficial effect on cholesterol levels , reduced maximal IMT and modified the inflammatory state of these patients
target: The meta- analysis showed a significant increase in plasma adiponectin levels following statin therapy .
  Although statins are known to increase the risk for new onset diabetes mellitus , our data might suggest that the mechanism for this is unlikely to be due to a reduction in adiponectin expression
background: BACKGROUND AND AIMS The effect of statin therapy on plasma adiponectin levels has not been conclusively studied .
  Therefore , we aim ed to evaluate this effect through a systematic review and meta- analysis of available r and omized controlled trials ( RCTs ) .