***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 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background The US Federal and Drug Administration ( FDA ) recently revised statin drug labels to include the information that increases in fasting serum glucose and glycated haemoglobin levels have been reported with the use of statins . Yet in a survey , 87 % of the doctors stated that they had never or infrequently observed increases in glucose or HbA1c levels in patients on statin .  In this study we would like to determine the association between the use of statins and glycaemic control in a retrospective cohort of patients with hypertension . Methods A retrospective review of 1060 medical records of patients with hypertension at a primary care clinic was conducted . These records were selected using systematic r and om sampling ( 1:4 ) . Data on patient socio-demographic factors ; clinical profile ; investigation results and prescribed medications were collected . Independent t-test was used for continuous variables while Pearson ’s χ 2 test was used for categorical variables . Logistic regression was done to adjust for confounders . Results 810 ( 76.4 % ) patients with hypertension were on statins  , out of which 792 ( 97.8 % ) were taking simvastatin 10 mg or 20 mg daily . Analysis of the whole group regardless of diabetes status showed that the statin user group had higher HbA1c and fasting blood glucose values . The difference in HbA1c levels remained significant ( adjusted OR = 1.290 , p = 0.044 , 95 % CI 1.006 , 1.654 ) after adjustment for diabetes , diabetic medication and fasting blood glucose . In the study population who had diabetes , statin users again had significantly higher HbA1c level compared to statin non-users . This difference remained significant ( adjusted OR 1.208 , p = 0.037 , 95 % CI 1.012 , 1.441 ) after adjustment for age and diabetic medications . Conclusions Statins use is associated with increased HbA1c levels among hypertensive patients and hypertensive patients with diabetes . Clinicians managing hypertensive patients on statins  should consider monitoring the HbA1c level and ensure that those with diabetes have their hyperglycaemia kept under control 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 ) OBJECTIVE This study evaluated the effect of a atorvastatin-fenofibrate combination on lipid profile , in comparison to each drug alone , in patients with type 2 diabetes and combined hyperlipidemia ( CHL ) . RESEARCH DESIGN AND METHODS A total of 120 consecutive patients , who were free of coronary artery disease ( CAD ) at entry , were studied for a period of 24 weeks . These patients were r and omly assigned to atorvastatin ( 20 mg/day , n = 40 ) , micronized fenofibrate ( 200 mg/day , n = 40 ) , or a combination of both ( atorvastatin 20 mg/day plus fenofibrate 200 mg/day , n = 40 ) . The effect of treatment on LDL cholesterol , triglycerides ( TGs ) , HDL cholesterol , apolipoprotein A-I and B , lipoprotein(a ) , and plasma fibrinogen ( PF ) was recorded . Moreover , the percentage of patients that reached the American Diabetes Association treatment goals and the estimated CAD risk status were calculated . RESULTS No patient was withdrawn from the study because of side effects . The atorvastatin-fenofibrate combination reduced total cholesterol by 37 % , LDL cholesterol by 46 % , TGs by 50 % , and PF by 20 % , whereas it increased HDL cholesterol by 22 % ( P < 0.0001 for all ) . These changes were significantly better than those of both monotherapies . Of the patients on drug combination , 97.5 % reached the LDL cholesterol treatment goal of < 100 mg/dl , 100 % reached the desirable TG levels of < 200 mg/dl , and 60 % reached the optimal HDL cholesterol levels of > 45 mg/dl . These rates were significantly higher than those of both monotherapies . Combined treatment reduced the 10-year probability for myocardial infa rct ion from 21.6 to 4.2 % . CONCLUSIONS The atorvastatin-fenofibrate combination has a highly beneficial effect on all lipid parameters and PF in patients with type 2 diabetes and CHL . It improved patients ' CAD risk status significantly more than each drug alone Objective . To investigate the effect of simvastatin on glucose homeostasis in streptozotocin induced type 2 diabetic rats . Methods . Forty male Wistar rats were r and omly divided into four groups . Normal control rats were fed with st and ard diet , others were fed with high-fat diet . Diabetic rats were induced by a single intraperitoneal injection of STZ . The simvastatin intervention rats were fed with simvastatin during the experiment process , and the simvastatin treatment rats were fed with simvastatin after diabetes rats were induced . We measured body weight , fasting plasma glucose , cholesterol , high-density lipoprotein cholesterol , and triglyceride after an overnight fast . Results . The FPG was higher in diabetic rats when compared to normal control ones ; the simvastatin intervention rats had a higher FPG compared to the diabetic rats and were more easily be induced to diabetes at the end of 4 weeks , FPG level of simvastatin treatment rats was increased compared with diabetic model rats after 12 weeks . Conclusion . These data indicate that simvastatin intervention rats may cause hyperglycemia by impairing the function of islet β cells and have an adverse effect on glucose homeostasis , especially on FPG level While a large numbers of clinical trials using various kinds of statins has been reported , a possible preventive effect on new onset of type 2 diabetes mellitus was shown only by the sub analysis of The West of Scotl and Coronary Prevention Study ( WOSCOPS ) using pravastatin . The aim of this study was to investigate whether pravastatin has a preferable effect on glucose tolerance among statins . An open-label prospect i ve cross-over trial was performed to compare the effect of pravastatin ( 10 mg/day ) or atorvastatin ( 10 mg/day ) in Japanese early-state type 2 diabetes mellitus with hypercholesterolemia . The analyzed study subjects were treated with pravastatin ( 10 mg/day , n = 12 ) or atorvastatin ( 10 mg/day , n = 12 ) for 12 weeks . After a 4-week-washout period , the drugs were switched and treatment was continued for another 12 weeks . Oral glucose tolerance test ( OGTT ) was performed to evaluate several parameters including the appropriateness of beta cell function for the individual insulin sensitivity ( disposition index : product of a vali date d secretion parameter and sensitivity ) at the end of each therapy . HbA(1c ) and 2 h-glucose levels during OGTT in the pravastatin treatment were significantly lower than atorvastatin treatment . Disposition index after pravastatin treatment was significantly higher than after atorvastatin treatment . In conclusion , our study suggests that pravastatin has a favorable effect on pancreatic beta cell function compared with atorvastatin AIM To compare the long-term efficacy and safety of pitavastatin with atorvastatin in patients with type 2 diabetes and combined ( mixed ) dyslipidaemia . METHODS R and omised , double-blind , active-controlled , multinational non-inferiority study . Patients were r and omised 2 : 1 to pitavastatin 4 mg ( n = 279 ) or atorvastatin 20 mg ( n = 139 ) daily for 12 weeks . Patients completing the core study could continue on pitavastatin 4 mg ( n = 141 ) or atorvastatin 20 mg ( n = 64 ) [ 40 mg ( n = 7 ) if lipid targets not reached by week 8 ] for a further 44 weeks ( extension study ) . The primary efficacy variable was the change in low-density lipoprotein cholesterol ( LDL-C ) . RESULTS Reductions in LDL-C were not significantly different at week 12 between the pitavastatin ( -41 % ) and atorvastatin ( -43 % ) groups . Attainment of National Cholesterol Education Program and European Atherosclerosis Society targets for LDL-C and non-high-density lipoprotein cholesterol ( non-HDL-C ) was similarly high for both treatment groups . Changes in secondary lipid variables ( e.g. HDL-C , apolipoprotein B and triglycerides ) were similar between treatments . Post hoc analysis showed that adjusted mean treatment differences for pitavastatin vs. atorvastatin were within the non-inferiority margin at weeks 16 ( + 0.11 % ; 95 % confidence interval ( CI ) , -5.23 to 5.44 ) and 44 ( -0.02 % ; 95 % CI , -5.46 to 5.41 ) of the extension study . Both treatments were well tolerated ; atorvastatin increased fasting blood glucose from baseline ( + 7.2 % ; p < 0.05 ) , whereas pitavastatin had no significant effect ( + 2.1 % ) . CONCLUSIONS Reductions in LDL-C and changes in other lipids were not significantly different in patients treated with pitavastatin 4 mg or atorvastatin 20 or 40 mg . Pitavastatin may , however , have a more favourable effect on the glycaemic status To clarify whether 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors ( statin ) increases lipoprotein lipase mass in preheparin plasma ( preheparin LPL mass ) , we observed the change in preheparin LPL mass during administration of atorvastatin and pravastatin to type 2 diabetes mellitus patients with hypercholesterolemia . The subjects were r and omly divided into two groups . One group was 24 patients given atorvastatin  ( 10 mg/day ) , and the other was 23 patients given pravastatin ( 20 mg/day ) for 4 months . After 4 months of administration , no significant change of HbA1c was observed . TC significantly decreased in the atorvastatin group compared to the pravastatin group . TG significantly decreased in the atorvastatin group . Low density lipoprotein cholesterol level significantly decreased in both groups ( - 36.3 % , p < 0.01 in atorvastatin , - 24.3 % , p < 0.01 in pravastatin ) . Preheparin LPL mass slightly increased in both groups after  
    Output:
    
Statins were found to affect glucose control through several ways , namely , by affecting insulin production and secretion by & bgr;‐pancreatic cells , insulin resistance , insulin uptake by the muscles and adipocytes and production of adipokines .
Current evidence available shows that most of the statins give unfavorable side effects with regards to glucose control among diabetic patients .
A dose‐dependent and time‐dependent effect was also observed in some statins which may be present among other statins as well