Deterioration of glucose homeostasis in type 2 diabetic patients one year after beginning of statins therapy. Effects of 90-day hypolipidemic treatment on insulin resistance, adipokines and proinflammatory cytokines in patients with mixed hyperlipidemia and impaired fasting glucose. Atorvastatin does not affect insulin sensitivity and the adiponectin or leptin levels in hyperlipidemic Type 2 diabetes Lifestyle Intervention and Adipokine Levels in Subjects at High Risk for Type 2 Diabetes Blood glucose lowering by means of lifestyle intervention has different effects on adipokines as compared with insulin treatment in subjects with type 2 diabetes Circulating cytokines as determinants of weight loss-induced improvements in insulin sensitivity The Effect of HMG-CoA Reductase Inhibitor on Insulin Resistance in Patients Undergoing Peritoneal Dialysis Statin therapy worsens insulin sensitivity in women with polycystic ovary syndrome (PCOS): a prospective, randomized, double-blind, placebo-controlled study. [Impact of weight loss on adipocytokines, C-reactive protein and insulin sensitivity in hypertensive women with central obesity]. 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 Adipocytokines, obesity, and insulin resistance during combined androgen blockade for prostate cancer. Comparison of the effects of simvastatin vs. rosuvastatin vs. simvastatin/ezetimibe on parameters of insulin resistance. Effects of long-term exercise and diet intervention on plasma adipokine concentrations. Coenzyme Q10 does not improve peripheral insulin sensitivity in statin-treated men and women: the LIFESTAT study. Effects of GH treatment in GH-deficient adults on adiponectin, leptin and pregnancy-associated plasma protein-A. Effect of exercise training combined with phytoestrogens on adipokines and C-reactive protein in postmenopausal women: a randomized trial. Pravastatin does not affect insulin sensitivity and adipocytokines levels in healthy nondiabetic patients.
OBJECTIVE We evaluated the long-term effects of rosuvastatin and simvastatin on insulin sensitivity and secretion in patients with well-controlled type 2 diabetes . METHODS After a 3 weeks run-in , 27 eligible patients were r and omly assigned to receive either rosuvastatin 20 mg daily ( Group 1 ) or simvastatin 20 mg daily ( Group 2 ) for 6 months ; thereafter they were switched to the other treatment for additional 6 months . Patients were recruited among individuals attending the outpatient service of the Diabetology Unit of the " Policlinico Tor Vergata " University Hospital , Rome , Italy . Serum lipids , glucose and insulin , glycated hemoglobin , C-reactive protein , TNF-α , leptin , adiponectin , insulin sensitivity by euglycemic-hyperinsulinemic clamp , β-cells function by HOMA-β were assessed at months 0 , 6 and 12 . Additionally , endothelial function was assessed by use of the brachial artery reactivity technique . RESULTS Besides marked reduction in lipid levels , glycated hemoglobin significantly increased from baseline after 12 months in both Group 1 ( + 0.8 ± 0.2 % , p < 0.001 ) and Group 2 ( + 0.9 ± 0.3 % ; p < 0.001 ) . Similar trends were observed for fasting glucose in both groups . No changes in insulin sensitivity were detected throughout the study , whereas HOMA-β significantly decreased from baseline after 12 months in both Group 1 ( -21.9 % , p < 0.01 ) and Group 2 ( -38.9 % ; p < 0.001 ) . In addition , both treatments similarly decreased C-reactive protein and leptin , as well as improved endothelial function . No changes in anthropometric measures were observed . CONCLUSIONS In well-controlled type 2 diabetic patients  both rosuvastatin and simvastatin significantly impaired glycemic control and insulin secretion , without affecting insulin sensitivity 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 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 OBJECTIVE —We investigated whether circulating adipokine concentrations can be altered by lifestyle intervention according to general recommendations in subjects at risk for diabetes as well as the potential of leptin , adiponectin , and resistin as biomarkers for lifestyle-induced improvements in glucose metabolism and insulin resistance . RESEARCH DESIGN AND METHODS —In the Study on Lifestyle intervention and Impaired glucose tolerance Maastricht , 147 men and women with impaired glucose tolerance ( IGT ) were r and omized to either a combined diet- and -exercise intervention or a control program . At baseline and after 1 year , an oral glucose tolerance test , an exercise test , and anthropometric measurements were performed . After 1 year , complete data of 103 subjects ( 50 intervention and 53 control subjects ) were obtained . RESULTS —Lifestyle intervention reduced plasma leptin concentrations ( −14.2 % ) in IGT subjects but did not alter plasma adiponectin ( −0.3 % ) or resistin ( −6.5 % ) concentrations despite marked improvements in glucose tolerance and insulin resistance . CONCLUSIONS —Changes in leptin concentration were related to improvements in insulin sensitivity independent of changes in body composition Aims /hypothesisAdipokines may be important in mediating signals from adipocytes to insulin-sensitive tissue and vasculature . We studied the effect of different glucose-lowering therapies on serum levels of plasminogen activator inhibitor-1 ( PAI-1 ) , high-sensitivity C-reactive protein ( hs-CRP ) , TNF-α , leptin , adiponectin and ghrelin in patients with type 2 diabetes . Subjects and methods Twenty-eight patients with poorly controlled type 2 diabetes who were receiving oral hypoglycaemic agents  were allocated to one of the following groups , and treated for 1 year : ( 1 ) lifestyle intervention ( L ) ; ( 2 ) insulin treatment ( I ) ; and ( 3 ) combined treatment ( L+I ) . Results Similar improvements in glycaemic control occurred in all three groups . There was a reduction in body weight of 3.0 kg ( median ) ( 95 % CI −5.9 to −2.0 ) in group L , whereas in groups L+I and I body weight increased by 3.5 kg ( 95 % CI 1.5–4.9 ) and 4.9 kg ( 95 % CI −3.1 to 8.2 ) , respectively . By trend analyses , group L had reduced levels of PAI-1 ( p=0.002 ) , hs-CRP ( p<0.0001 ) and TNF-α ( p=0.006 ) , while no significant changes were observed in the levels of leptin or adiponectin . In group I , the median levels of PAI-1 ( p=0.008 ) , TNF-α ( p=0.058 ) and leptin ( p=0.004 ) increased . In the L+I group there was a reduction in PAI-1 levels ( p=0.014 ) and an increase in levels of leptin ( p<0.001 ) . The differences in changes in the levels of PAI-1 , hs-CRP , TNF-α and leptin between groups were also significant ( all p<0.01 ) . Conclusions /interpretationImprovement of glycaemic control through lifestyle intervention in type 2 diabetes had more beneficial effects on adipokine levels than when the same lowering of HbA1c was achieved with insulin treatment Dietary calorie restriction and exercise promote weight loss and may have additive effects for improving insulin sensitivity , independent of weight loss . It is not known if these effects are attributable to changes in circulating cytokines . We evaluated the hypothesis that modest , matched weight loss induced by calorie restriction and exercise have additive effects on circulating cytokines and these changes correlate with improvements in insulin sensitivity . Overweight and sedentary women and men ( n = 52 , 45–65 years ) were r and omized to undergo 7 % weight loss by using 3–6 months of calorie restriction , exercise , or a combination of both calorie restriction and exercise . Concentrations of cytokines and hormones were measured in fasting and oral glucose tolerance test blood sample s. Insulin sensitivity was estimated based on oral glucose tolerance test for glucose and insulin . With all groups combined , fasting leptin ( p < 0.0001 ) and high molecular weight adiponectin ( p = 0.04 ) decreased and pentraxin-3 increased ( p < 0.0001 ) , in a manner that correlated with improvements in insulin sensitivity ( all p ≤ 0.0002 ) . These changes , combined with decreases in glucose-dependent insulinotropic polypeptide from the oral glucose tolerance test , explained 63 % of the variance ( p < 0.0001 ) in insulin sensitivity improvements . Exercise and calorie restriction had additive effects on leptin , with a similar trend for high molecular weight adiponectin . Monocyte chemoattractant protein-1 and C-reactive protein concentrations did not change . Calorie restriction and exercise had opposite effects on soluble tumor necrosis factor receptor-1 .  Modest weight loss in overweight adults  decreases serum leptin and high molecular weight adiponectin , and increases pentraxin-3 concentrations in a manner that correlates with increased insulin sensitivity . Exercise has additive effects to those induced by calorie restriction for reductions in leptin and possibly adiponectin . These changes may contribute to the additive effects of calorie restriction and exercise for improving insulin sensitivity Background Insulin resistance is associated with the progression of atherosclerosis and is reported to predict cardiovascular mortality in patients with end-stage renal disease ( ESRD ) . Although statins exert pleiotropic effects , it is uncertain whether statin therapy improves insulin resistance in these patients . In this prospect i ve r and omized controlled trial , we aim ed to evaluate the effects of statin on insulin resistance among 70 patients undergoing peritoneal dialysis ( PD ) . Methods Patients were r and omized into a statin group ( n = 35 ) or a control group ( n = 35 ) . The statin group received 10 mg per day of rosuvastatin for 6 months . We determined insulin resistance by homeostatic model assessment of insulin resistance ( HOMA-IR ) index . Serum concentrations of adipokines such as adiponectin , leptin , and resistin were measured using enzyme-linked immunosorbent ( ELISA ) assay . As inflammatory markers , high sensitive C-reactive protein ( hsCRP ) and interleukin-6 were also measured . Results There were no significant differences in baseline characteristics between the two groups . Compared to baseline value , statin treatment significantly decreased HOMA-IR index from 2.37 ± 1.08 to 2.05 ± 0.82 ( P = 0.014 ) . There was a concordant decrease in hsCRP levels in the statin group ( 2.05 ± 1.57 to 1.21 ± 0.84 mg/L , P < 0.001 ) , but such improvements were not observed in the control group . When between-group differences in these parameters were compared , hsCRP levels were more decreased in the statin group than in the control group ( P = 0.021 for between-group difference ) , whereas HOMA-IR index was not ( P = 0.189 for between-group difference ) . During this period , statin treatment did not result in the improved adipokine profiles . Conclusion This study showed that statin therapy failed to improve insulin resistance in PD patients despite a significant decline in hsCRP levels after statin treatment . Our finding suggests that reducing inflammation by statin is of limited help to fully attenuate insulin resistance in these patients 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 mg/d , n = 15 ) or placebo  ( n = 13 ) for 6 months . INTERVENTIONS Fasting serum sample s were collected at baseline and at 3 and 6 months . Oral and iv glucose tolerance tests were performed at 0 and 6 months . MAIN OUTCOME MEASURES And rogen secretion and glucose metabolism were measured . RESULTS Fasting levels and area under the curve of insulin increased significantly and insulin sensitivity ( insulinogenic and Matsuda indexes ) decreased during 6 months of atorvastatin therapy . Serum levels of dehydroepi and rosterone sulfate decreased in the atorvastatin group , whereas no change was observed in serum testosterone levels . Levels of C-reactive protein , total and low-density lipoprotein-cholesterol , and triglycerides decreased significantly during statin therapy . CONCLUSIONS Atorvastatin therapy improves chronic inflammation and lipid profile , but it impairs insulin sensitivity in women with PCOS . Because women with PCOS have an increased risk of developing type 2 diabetes mellitus , the results suggest that statin therapy should be initiated on the basis of generally accepted criteria and individual risk assessment of cardiovascular disease , and not only because of PCOS OBJECTIVE To assess the impact of weight reduction on serum adipocytokines , C-reactive protein ( CRP ) , and insulin sensitivity in hypertensive female patients with central obesity . METHODS This study was performed using the data base and stored serum sample s of female patients who had participated in an intervention study focused on weight loss . Thirty hypertensive women aged 18 to 65 , body mass index ( BMI ) > 27 kg/m2 , and central obesity were selected . They were r and omly assigned to receive either a low-calorie diet plus orlistat 120 mg three times daily or a low-calorie diet alone for 16 weeks . Patients who experienced weight loss greater than 5 % ( n = 24 ) were assessed for blood pressure , anthropometric parameters , visceral fat , insulin resistance ( HOMA-R - homeostasis model assessment of insulin resistance ) and sensitivity ( ISI - Insulin Sensitivity Index ) indices , plus serum lipids , adipocytokines ( adiponectin , leptin , IL-6 , and TNF-alpha ) and CRP levels . RESULTS After BMI had been reduced by approximately 5 % in both groups , visceral fat , fasting glucose , triglycerides , and TNF-alpha decreased . Only the orlistat group , which was more insulin resistant at baseline , showed a significant reduction in blood glucose after oral glucose load , in addition to increased insulin sensitivity . CONCLUSION This study 's findings indicate that a weight loss greater than 5 % is associated with improved inflammatory status and decreased insulin resistance , regardless of changes in adiponectin and TNF-a levels . The greatest improvements in insulin sensitivity experienced by the orlistat-treated patients could not be attributed to the use of this drug because of the higher number of insulin-resistant subjects in this group 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 OBJECTIVES Gonadotropin-releasing hormone agonists increase fat mass , decrease insulin sensitivity , and increase serum triglycerides . To better characterize the metabolic effects of gonadotropin-releasing hormone agonist treatment , we prospect ively evaluated the changes in body composition , insulin sensitivity , and levels of adiponectin , resistin , C-reactive protein ( CRP ) , and plasminogen activator inhibitor type 1 ( PAI-1 ) . We also assessed the relationships among changes in adipocytokines , body composition , and insulin sensitivity . METHODS In this prospect i ve , 12-week study , 25 nondiabetic men with locally advanced or recurrent prostate cancer and no radiographic evidence of metastases were treated with leuprolide depot and bicalutamide . The outcomes studied included changes from baseline to week 12 in body composition , insulin sensitivity , and levels of adiponectin , resistin , CRP , and PAI-1 . RESULTS The mean + /- st and ard error percentage of fat body mass increased by 4.3 % + /- 1.3 % from baseline to week 12 ( P = 0.002 ) . The insulin sensitivity index decreased by 12.9 % + /- 7.6 % ( P = 0.02 ) . The serum adiponectin levels increased by 37.4 % + /- 7.2 % from baseline to week 12 ( P < 0.001 ) . In contrast , the resistin , CRP , and PAI-1 levels did not change significantly . Changes in body composition tended to be associated with changes in adiponectin , but not insulin sensitivity . CONCLUSIONS Combined and rogen blockade with leuprolide and bicalutamide significantly increased fat mass and adiponectin levels and decreased insulin sensitivity but did not alter the resistin , CRP , or PAI-1 levels . This pattern of metabolic changes appears distinct from the classic metabolic syndrome BACKGROUND Statin treatment may be associated with adverse effects on glucose metabolism . Whether this is a class effect is not known . In contrast , ezetimibe monotherapy may beneficially affect insulin sensitivity . OBJECTIVE The aim of this study was to compare the effects of three different regimens of equivalent low-density lipoprotein cholesterol ( LDL-C ) lowering capacity on glucose metabolism . METHODS A total of 153 patients ( 56 men ) , who had not achieved the LDL-C goal recommended by the National Cholesterol Education Program Adult Treatment Panel III ( NCEP-ATP III ) despite a 3-month dietary and lifestyle intervention , were r and omly allocated to receive open-label simvastatin 40 mg or rosuvastatin 10 mg or simvastatin/ezetimibe 10/10 mg for 12 weeks . The primary end point was changes in homeostasis model assessment of insulin resistance ( HOMA-IR ) . Secondary endpoints consisted of changes in fasting insulin levels , fasting plasma glucose ( FPG ) , glycosylated haemoglobin ( HbA(1c ) ) , the HOMA of β-cell function ( HOMA-B ) ( a marker of basal insulin secretion by pancreatic β-cells ) , LDL-C and high sensitivity C reactive protein ( hsCRP ) . RESULTS At week 12 , all three treatment regimens were associated with significant increases in HOMA-IR and fasting insulin levels ( p < 0.05 compared with baseline ) . No significant difference was observed between groups . No change in FPG , HbA(1c ) and HOMA-B levels compared with baseline were noted in any of the three treatment groups . Changes in serum lipids and hsCRP were similar across groups . CONCLUSION To the extent that simvastatin 40 mg , rosuvastatin 10 mg and simvastatin/ezetimibe 10/10 mg are associated with adverse effects on insulin resistance , they appear to be of the same magnitude BACKGROUND In a r and omized , controlled , 2 x 2 factorial trial on the effect of long-term changes in diet and exercise , a significant reduction in body weight and fat mass was observed . Alterations in leptin and plasminogen activator inhibitor-1 concentrations were previously reported from this study . OBJECTIVE We examined the separate and combined effects of a 1-y exercise and diet intervention on several adipokines ; adiponectin , interleukin-6 and -8 , tumor necrosis factor-alpha , monocyte chemoattractant protein-1 , hepatocyte growth factor , nerve growth factor , C-reactive protein , and resistin . DESIGN One hundred eighty-eight men with several risk factors for diabetes and cardiovascular disease were r and omly allocated to 4 groups : diet , exercise , combined diet and exercise , and control . RESULTS Plasma adiponectin concentrations remained unchanged , whereas body mass index and fat mass decreased after dietary changes and an increase in physical activity . In the control group , adiponectin concentrations were reduced . Analyzed according to the factorial design , only diet intervention had a significant ( P = 0.03 ) positive effect on plasma adiponectin relative to control , and this effect was largely explained by changes in fat mass . After adjustment for change in percentage body fat , there were significant positive effects on tumor necrosis factor-alpha in all 3 intervention groups ( P = 0.01 for the diet group , 0.03 for the exercise group , and 0.05 for the combined diet and exercise group ) . Minor changes were observed for the other adipokines . Neither baseline concentrations of nor changes in adiponectin and plasminogen activator inhibitor-1 were significantly correlated to the other adipokines , whereas concentrations of and changes in the other adipokines were significantly correlated . CONCLUSION Diet intervention had a significant positive effect on adiponectin concentrations , which is largely explained by a reduction in fat mass Simvastatin is a cholesterol-lowering drug that is prescribed to lower the risk of cardiovascular disease following high levels of blood cholesterol . There is a possible risk of new-onset diabetes mellitus with statin treatment but the mechanisms behind are unknown . Coenzyme Q10 ( CoQ10 ) supplementation has been found to improve glucose homeostasis in various patient population s and may increase muscle glucose transporter type 4 content . Our aim was to investigate if 8 weeks of CoQ10 supplementation can improve glucose homeostasis in simvastatin-treated subjects . Thirty-five men and women in treatment with a minimum of 40 mg of simvastatin daily were r and omized to receive either 2 × 200 mg/day of CoQ10 supplementation or placebo for 8 weeks . Glucose homeostasis was investigated with fasting blood sample s , oral glucose tolerance test ( OGTT ) and intravenous glucose tolerance test . Insulin sensitivity was assessed with the hyperinsulinemic-euglycemic clamp . Different indices were calculated from fasting sample s and OGTT as secondary measures of insulin sensitivity . A muscle biopsy was obtained from the vastus lateralis muscle for muscle protein analyzes . There were no changes in body composition , fasting plasma insulin , fasting plasma glucose , or 3-h glucose with intervention , but glycated hemoglobin decreased with time . Glucose homeostasis measured as the area under the curve for glucose , insulin , and C-peptide during OGTT was unchanged after intervention . Insulin secretory capacity was also unaltered after CoQ10 supplementation . Insulin sensitivity was unchanged but hepatic insulin sensitivity increased . No changes in muscle GLUT4 content was observed after intervention . CoQ10 supplementation does not change muscle GLUT4 content , insulin sensitivity , or secretory capacity , but hepatic insulin sensitivity may improve OBJECTIVE  GH deficiency ( GHD ) in adults is associated with adverse effects on metabolism and increased cardiovascular risk . Pregnancy-associated plasma protein-A ( PAPP-A ) is a protease that promotes IGF-I availability in vascular tissues . PAPP-A levels appear to correlate with carotid intima-media thickness and have been proposed as an early predictor of cardiac events . The aim of our study was to evaluate PAPP-A levels in GHD adults at baseline and after GH replacement and correlate them with changes in body composition , lipid profile , glucose homeostasis , inflammatory markers and in leptin and adiponectin . PATIENTS AND METHODS Fourteen GHD adults were evaluated at baseline and after 1 year of GH therapy .  All patients were compared at baseline with 28 age- , sex- and body mass index ( BMI ) -matched control subjects . RESULTS At baseline , GHD adults showed higher PAPP-A levels ( P=0.03 ) and higher leptin ( P=0.04 ) , fibrinogen ( P=0.002 ) and highly sensitive C-reactive protein ( P=0.01 ) values than controls . Therapy with GH  reduced PAPP-A ( P=0.03 ) and fibrinogen levels ( P=0.002 ) while increased BMI ( P=0.01 ) and reduced waist-hip ratio ( WHR ; P=0.05 ) were observed . Insulin and homeostasis model assessment of insulin resistance index increased after treatment ( P<0.004/P=0.007 ) , without changes in leptin or adiponectin levels . PAPP-A values correlated positively with BMI and WHR and negatively with adiponectin before and after treatment , with no correlation with glucose homeostasis parameters , lipid profile or leptin . CONCLUSIONS Our study suggests that PAPP-A expression is increased in GHD adults , and that 1 year of GH replacement therapy is able to reduce PAPP-A levels in this population . However , further studies are required to determine whether this decrease correlates with an improvement in atherosclerosis Phytoestrogens and training could be effective to reduce cardiovascular and type 2 diabetes mellitus risk factors in postmenopausal women . Nevertheless , the impact of their combination on adipokines and systemic inflammation was never investigated . The objective was to verify if 6 months of mixed training combined with phytoestrogens could have an additional effect on adipokine levels and systemic inflammation in obese postmenopausal women . Fifty-two obese women aged between 50 and 70 years were r and omly assigned to ( 1 ) exercise with placebo ( EX + PL ; n = 25 ) or ( 2 ) exercise with phytoestrogens ( EX + PHY ; n = 27 ) . Body weight , waist circumference , fat mass , and lean body mass ( dual-energy x-ray absorptiometry ) were assessed . Fasting plasma glucose and insulin , adiponectin , leptin , and C-reactive protein ( CRP ) levels were obtained after a 12-hour overnight fast . Total energy intake was measured with a 3-day dietary record . All measurements were performed before and after the 6-month intervention . Although energy intake remained unchanged , body composition was improved in all women ( all Ps < .02 ) . Plasma CRP and leptin levels decreased in both groups similarly ( all Ps < .03 ) , whereas plasma adiponectin and insulin did not change with exercise combined with placebo or phytoestrogens . Correlation analyses showed that homeostasis model assessment of insulin resistance ( r = -0.58 , P = .02 ) and fasting insulin levels ( r = -0.42 , P = .02 ) at baseline were both correlated with changes in leptin levels . Baseline fasting glucose ( r = -0.36 , P = .03 ) and adiponectin ( r = 0.45 , P = .005 ) levels were associated with changes in CRP concentrations . Although mixed exercise program combined with phytoestrogens does not seem to provide any additional effect , mixed training improves systemic inflammation and leptin concentrations in obese postmenopausal women 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
There was no association between the duration of statin therapy and changes in plasma leptin levels .
Furthermore , there was no differential effect of hydrophilic and lipophilic statins on plasma leptin concentrations .
OBJECTIVES The effects of statins on insulin sensitivity , metabolic homeostasis and adipokines in humans are controversial .
Several studies have investigated the impact of statin therapy on plasma leptin concentrations but the results have been inconsistent .
The aim of the present study was to conduct a systematic review and meta- analysis of available evidence to calculate the effect size of statin therapy in changing serum leptin concentrations .