***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    ***EXAMPLES*** 
    Input: Background : In addition to lipid lowering , further pleotropic effects of statins have been postulated . We aim ed to study if the various pleotropic effects are due indirectly to the modulation of adipocytokines . Material s and methods : We studied the effect of atorvastatin on insulin sensitivity and the plasma adiponectin and leptin concentrations . Our r and omized open labeled study had 29 hyperlipidemic Type 2 diabetic patients ( 14 females , 15 males , mean age 60.0±2.2 yr ) . They were r and omized into three 12-week atorvastatin intervention types . Each day patients were given either 10 mg ( no.=10 ) , 20 mg ( no.=10 ) or 40 mg ( no.=9 ) . Evaluations were performed before and after intervention . Results : All baseline characteristics were statistically identical in the 3 groups . Drop in total cholesterol , LDL-cholesterol , and triglyceride levels were measured at the end . With 10 mg the drop was 30 % , 37 % , and 30 % . The 20 mg group was 43 % , 54 % , and 34 % . The 40 mg group was 42 % , 51 % , and 27 % . Groups had no significant change of body mass index , HDL-cholesterol , and glycated hemoglobin levels . Also , levels of insulin , adiponectin , leptin , homeostasis model assessment index ( HOMA ) and Quantitative Insulin Sensitivity Check Index ( QUICKI ) stayed the same . Pooled parameters of all 29 patients showed no difference in levels of insulin , adiponectin , leptin , HOMA , and QUICKI before and after treatment . Conclusions : Atorvstatin does not affect insulin sensitivity and the adiponectin or leptin levels in hyperlipidemic Type 2 diabetes INTRODUCTION Diabetes is a prothrombotic state involving a more thrombogenic fibrin network . In the present study we investigated the effects of lipid-lowering therapy with atorvastatin on fibrin network structure and platelet-derived microparticles in patients with type 1 diabetes and dyslipidemia . MATERIAL S AND METHODS Twenty patients were treated with atorvastatin ( 80 mg daily ) or placebo during 2 months in a r and omized , double-blind , cross-over study . Fibrin network permeability , expression of glycoprotein IIIa , P-selectin and tissue factor on platelet-derived microparticles , plasma endogenous thrombin potential , plasminogen activator inhibitor-1 and tissue plasminogen activator antigen levels were assessed . Additionally , levels of plasma fibrinogen , high-sensitivity C-reactive protein and glycated haemoglobin were measured . RESULTS During treatment with atorvastatin , fibrin network permeability increased ( p=0.01 ) , while endogenous thrombin potential and expression of glycoprotein IIIa , P-selectin and tissue factor decreased ( p<0.01 ) . In vitro experiments indicated that platelet-derived microparticles influence the fibrin network formation as fibrin network permeability decreased significantly when platelet-derived microparticles were added to normal plasma . Baseline levels of plasminogen activator inhibitor-1 and tissue plasminogen activator antigen as well as plasma fibrinogen and high-sensitivity C-reactive protein were within reference values and not significantly changed during atorvastatin treatment , while glycated haemoglobin increased 0.3 % ( p<0.001 ) . CONCLUSIONS Novel treatment effects were found in patients with type 1 diabetes and dyslipidemia during atorvastatin therapy , i.e. a more porous fibrin network , to which reduced expression of glycoprotein IIIa , P-selectin and tissue factor on platelet-derived microparticles may contribute . The observed impairment of glycemic control during long-term statin treatment deserves attention Summary Background The lowering of cholesterol concentrations in individuals at high risk of cardiovascular disease improves outcome . No study , however , has assessed benefits of cholesterol lowering in the primary prevention of coronary heart disease ( CHD ) in hypertensive patients who are not conventionally deemed dyslipidaemic . Methods Of 19 342 hypertensive patients ( aged 40–79 years with at least three other cardiovascular risk factors ) r and omised to one of two antihypertensive regimens in the Anglo-Sc and inavian Cardiac Outcomes Trial , 10 305 with nonfasting total cholesterol concentrations 6.5 mmol/L or less were r and omly assigned additional atorvastatin 10 mg or placebo .  These patients formed the lipid-lowering arm of the study . We planned follow-up for an average of 5 years , the primary endpoint being non-fatal myocardial infa rct ion and fatal CHD . Data were analysed by intention to treat . Findings Treatment was stopped after a median follow-up of 3.3 years . By that time , 100 primary events had occurred in the atorvastatin group compared with 154 events in the placebo group ( hazard ratio 0.64 [ 95 % CI 0.50–0.83 ] , p = 0.0005 ) . This benefit emerged in the first year of follow-up . There was no significant heterogeneity among prespecified subgroups . Fatal and non-fatal stroke ( 89 atorvastatin vs 121 placebo , 0.73 [ 0.56–0.96 ] , p = 0.024 ) , total cardiovascular events ( 389 vs 486 , 0.79 [ 0.69–0.90 ] , p = 0.0005 ) , and total coronary events ( 178 vs 247 , 0.71 [ 0.59–0.86 ] , p = 0.0005 ) were also significantly lowered . There were 185 deaths in the atorvastatin group and 212 in the placebo group ( 0.87 [ 0.71–1.06 ] , p = 0.16 ) . Atorvastatin  lowered total serum cholesterol by about 1.3 mmol/L compared with placebo at 12 months , and by 1.1 mmol/L after 3 years of follow-up . Interpretation The reductions in major cardiovascular events with atorvastatin are large , given the short follow-up time . These findings may have implication s for future lipid-lowering guidelines 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 ) BACKGROUND Despite established effects of atorvastatin on level of serum lipid profile in patients with different underlying clinical conditions , the effects of this drug on other serum biomarkers remain uncertain . We examined the effects of atorvastatin therapy on lipid profile , glycemic control , and liver enzymes in patients with ischemic cerebrovascular accident without any history or clinical evidence s of diabetes , heart failure , renal failure , or hepatic disease . METHODS In a r and omized double-blinded controlled trial , 140 hospitalized patients with an ischemic cerebrovascular accident were included and r and omly assigned to receive either atorvastatin 40 mg ( n = 70 ) or atorvastatin 20 mg daily ( n = 70 ) for 3 months . The levels of biomarkers were measured at the time of administrating drugs as well as at the time of completing the treatment . RESULTS A significant reduction was revealed in serum triglyceride , total cholesterol , low-density lipoprotein , non-high-density lipoprotein ( HDL ) cholesterol , and also aspartate aminotransferase levels as well as a significant increase in serum HDL level following administration of atorvastatin in both case and control groups who received the atorvastatin 40 mg/day and 20 mg/day , respectively ( all P < 0.050 ) . Although a significant increase in fasting blood sugar and hemoglobin A1c was observed in the case group received atorvastatin 40 mg/day ( both P < 0.001 ) , but this elevation was not occurred in another group treated with lower dose of the drug ( both P > 0.050 ) . CONCLUSION Daily administration of 20 mg and 40 mg doses of atorvastatin for 3 months provides improvement in serum lipid profiles ; however , because of interfering effect of high-dose atorvastatin on glycemic control status , the use of the former dose may be preferred . This is very important in these patients because the positive effects of high-dose atorvastatin in stroke patients are not confirmed In this prospect i ve study , we examined the effect of atorvastatin treatment on baroreflex sensitivity ( BRS ) in subjects with type 2 diabetes . A total of 79 patients with type 2 diabetes with dyslipidaemia were recruited . A total of 46 subjects were enrolled to atorvastatin 10 mg daily and low-fat diet and 33 patients to low-fat diet only . BRS was assessed non-invasively using the sequence method at baseline , 3 , 6 and 12 months . Treatment with atorvastatin  increased BRS after 12 months ( from 6.46 ± 2.79 ms/mmHg to 8.05 ± 4.28 ms/mmHg , p = 0.03 ) , while no effect was seen with low-fat diet . Further sub- analysis according to obesity status showed that BRS increased significantly only in the non-obese group ( p = 0.036 ) . A low dose of atorvastatin increased BRS in non-obese subjects with type 2 diabetes and dyslipidaemia after 1-year treatment . This finding emphasizes the beneficial effect of atorvastatin on cardiovascular system , beyond the lipid-lowering effects CONTEXT Statins have been shown to improve hyper and rogenism in women with polycystic ovary syndrome ( PCOS ) . However , their use has also been associated with impairment of glucose metabolism and an increased risk of type 2 diabetes mellitus . Because women with PCOS are prone to disturbances in glucose metabolism , statin therapy could also have negative effects . OBJECTIVE Our objective was to explore the effects of atorvastatin therapy on hormonal and metabolic parameters in women with PCOS . DESIGN AND SETTING We conducted a r and omized , double-blind , placebo-controlled 6-month follow-up study conducted at Oulu University Hospital , Finl and . PATIENTS Women with PCOS ( Rotterdam criteria ) were treated with atorvastatin ( 20 m 
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Other studies showed that fasting plasma glucose and HbA1c levels were increased by atorvastatin .
The majority of these articles showed that patients who used atorvastatin  had a higher dose-dependent risk of developing NOD .
Conclusion This systematic review suggests that there is an association between atorvastatin treatment and NOD .
Moreover , it showed that atorvastatin in high dose causes worsening of the glycemic control in patients with DM