title: Oral L-Arginine Administration Improves Anthropometric and Biochemical Indices Associated With Cardiovascular Diseases in Obese Patients: A Randomized, Single Blind Placebo Controlled Clinical Trial Arginine supplementation modulates pig plasma lipids, but not hepatic fatty acids, depending on dietary protein level with or without leucine L-arginine but not D-arginine stimulates insulin-mediated glucose uptake. Changes in mineral status are associated with improvements in insulin sensitivity in obese patients following l-arginine supplementation The combination of arginine and leucine supplementation of reduced crude protein diets for boars increases eating quality of pork. Oral L-arginine improves endothelium-dependent dilation in hypercholesterolemic young adults. Effect of oral supplementation of free amino acids in type 2 diabetic patients-- a pilot clinical trial. L-Arginine enhances the triglyceride-lowering effect of simvastatin in patients with elevated plasma triglycerides. Effects of low‐dose l‐arginine on insulin‐mediated vasodilatation and insulin sensitivity Endocrine and lipid effects of oral L-arginine treatment in healthy postmenopausal women. Effect of 3-month L-arginine supplementation on insulin resistance and tumor necrosis factor activity in patients with visceral obesity. Canadian Cardiovascular Society position statement--recommendations for the diagnosis and treatment of dyslipidemia and prevention of cardiovascular disease. Dyslipidemia and Hyperglycemia Predict Coronary Heart Disease Events in Middle-Aged Patients With NIDDM L-arginine supplementation and risk factors of cardiovascular diseases in healthy men: a double-blind randomized clinical trial. Oral L-arginine supplementation improves endothelial function and ameliorates insulin sensitivity and inflammation in cardiopathic nondiabetic patients after an aortocoronary bypass.
abstract: Background : Recently , the potential of L-arginine supplementation as a novel and effective strategy for weight loss and improving biochemical parameters in obese patients has been under consideration . Objectives : To evaluate the influence of 8-week oral L-arginine supplementation on body mass index ( BMI ) , waist circumference ( WC ) , triceps skinfold ( TS ) , subscapular skinfold ( SS ) , systolic blood pressure ( SBP ) , diastolic blood pressure ( DBP ) , plasma fasting blood sugar ( FBS ) , glycated hemoglobin ( HbA1c ) , triglyceride ( TG ) , total cholesterol ( TC ) , low-density lipoprotein ( LDL ) , high-density lipoprotein ( HDL ) , and malondialdehyde ( MDA ) in patients with BMI values > 29.9 or visceral obesity ( WC > 102 cm in men or > 88 cm in women ) . Patients and Methods : Ninety obese patients were included in a single-blind r and omized controlled trial . Patients were r and omized to receive either L-arginine ( 3 or 6 g thrice daily ) or placebo for 8 weeks . Anthropometric and biochemical indices , dietary intake , and blood pressure values were measured at the baseline and after the 8-week intervention . Results : Significant decreases in anthropometric parameters , blood pressure ( SBP , DBP ) , FBS , HbA1c , LDL , MDA ( P < 0.001 ) , TG ( P = 0.02 ) , and TC ( P = 0.002 ) and a significant increase in HDL ( P < 0.001 ) were observed in the intervention group , compared to the control group . In the control group , no significant differences were found between the baseline and end-of-intervention measurements . Conclusions : In conclusion , oral L-Arginine supplementation appears to improve anthropometric parameters , blood pressure values , and some blood biochemical indices associated with cardiovascular disease prevention Background In the present study , the effect of arginine and leucine supplementation , and dietary protein level , were investigated in commercial crossbred pigs to clarify their individual or combined impact on plasma metabolites , hepatic fatty acid composition and mRNA levels of lipid sensitive factors . The experiment was conducted on fifty-four entire male pigs ( Duroc × Pietrain × Large White × L and race crossbred ) from 59 to 92 kg of live weight . Each pig was r and omly assigned to one of six experimental treatments ( n = 9 ) . The treatments followed a 2 × 3 factorial arrangement , providing two levels of arginine supplementation ( 0 vs. 1 % ) and three levels of basal diet ( normal protein diet , NPD ; reduced protein diet , RPD ; reduced protein diet with 2 % of leucine , RPDL ) . Results Significant interactions between arginine supplementation and protein level were observed across plasma lipids . While dietary arginine  increased total lipids , total cholesterol , HDL-cholesterol , LDL-cholesterol , VLDL-cholesterol and triacylglycerols in NPD , the inverse effect was observed in RPD . Overall , dietary treatments had a minor impact on hepatic fatty acid composition . RPD increased 18:1c9 fatty acid while the combination of leucine and RPD reduced 18:0 fatty acid . Arginine supplementation increased the gene expression of FABP1 , which contributes for triacylglycerols synthesis without affecting hepatic fatty acids content . RPD , with or without leucine addition , upregulated the lipogenic gene CEBPA but downregulated the fat oxidation gene LPIN1 . Conclusions Arginine supplementation was responsible for a modulated effect on plasma lipids , which is dependent on dietary protein level . It consistently increased lipaemia in NPD , while reducing the correspondent metabolites in RPD . In contrast , arginine had no major impact , neither on hepatic fatty acids content nor on fatty acid composition . Likewise , leucine supplementation of RPD , regardless the presence of arginine , promoted no changes on total fatty acids in the liver . Ultimately , arginine , leucine and dietary protein reduction seem to be unrelated with fatty liver development Our study aims at investigating a possible role for L-arginine and D-arginine in insulin-mediated glucose uptake .  Twelve lean healthy subjects volunteered for the study and were su bmi tted to three euglycemic-hyperinsulinemic glucose clamps to investigate the effect of L-arginine ( 0.5 g/min in the last 60 minutes of the clamp ) , D-arginine ( 0.5 g/min in the last 60 minutes of the clamp ) , and saline 0.9 % NaCl on insulin-mediated glucose uptake . All tests were made in r and om order . In study 1 , L-arginine versus saline infusion was associated with a significant increase in blood flow ( 131 % + /- 7 % v 87 % + /- 5 % , P < .001 ) and whole-body glucose disposal ( [ WBGD ] 61.4 + /- 4.4 v 41.3 + /- 3.5 mumol/kg fat-free mss [FFM].min , P < .001 ) . Analysis of substrate oxidation demonstrated that both oxidative and nonoxidative glucose metabolism was improved by L-arginine delivery . After adjustment for the change in blood flow , WBGD was still greater after L-arginine than after saline infusion . Along with L-arginine infusion and independently of the change in blood flow , the percent change in WBGD correlated with the percent change in plasma cGMP ( r = .55 , P < .05 ) . D-Arginine infusion did not affect insulin-mediated glucose uptake . In particular , WBGD ( 42.1 + /- 3.4 v 41.3 + /- 3.5 mumol/kg FFM.min , P = NS ) was similar in both experimental conditions . Basal levels ( 2.8 + /- 0.2 v 2.7 + /- 0.3 nmol/L , P = NS ) and the insulin-mediated increase ( 43 % + /- 5 % v 39 % + /- 4 % , P = NS ) in plasma cGMP were also superimposable along with insulin plus D-arginine and insulin alone , respectively . Finally , blood flow ( 224 + /- 29 v 230 + /- 35 mL/min , P = NS ) was not different at baseline and was similarly stimulated ( 84 % + /- 4 % v 87 % + /- 5 % , P = NS ) by insulin infusion . In conclusion , L-arginine but not D-arginine stimulates insulin-mediated glucose uptake . Nitric oxide ( NO ) , the metabolic mediator for L-arginine , potentiates insulin-mediated glucose uptake through the increase in blood flow . Nevertheless , an independent effect of intracellular cGMP on WBGD can not be ruled out Purpose The aim of this study is to evaluate the long-term influence of l-arginine intake on mineral concentration in patients with obesity and to assess the changes in lipid serum levels , fat content , and insulin resistance that result . Methods A r and omized double-blind placebo-controlled study was conducted . 88 obese patients were r and omly assigned to receive either 9 g of l-arginine or placebo daily , for 6 months . At baseline and after 6 months , selected anthropometrical measurements and blood biochemical analyses were performed and mineral levels were assessed . To assess insulin sensitivity , the gold-st and ard euglycemic clamp methodology was used . Results We found that 6 months of l-arginine supplementation result ed in significant increases in insulin sensitivity ( Δ1.1 mg/kg/min , P < 0.01 ) and zinc levels ( Δ1.5 μmol/L , P < 0.001 ) . Moreover , a positive correlation between the change in zinc concentration in serum and the change in insulin sensitivity was observed ( R = 0.80 , P < 0.01 ) . In the group of patients treated with l-arginine , a negative correlation between the change in zinc concentration in serum and the change in body fat content was noted ( R = −0.38 , P < 0.05 ) . Conclusions l-Arginine supplementation affects zinc status in obese patients . One beneficial influence is related to the improvements in insulin sensitivity Fifty-four entire male pigs ( Duroc × Pietrain × Large White × L and race ) from a commercial crossbred operation were used to investigate the effect of dietary Arg supplementation , protein reduction ( PR ) , and Leu supplementation on performance , carcass traits , and meat quality . Pigs weighing 58.9 ± 1.6 kg BW were r and omly assigned to 1 of 6 treatments ( n = 9 ) . The 6 dietary treatments were normal CP diet ( 16 % CP , NPD ) , reduced CP diet ( 13 % CP , RPD ) , reduced CP diet with Leu addition to 2.0 % ( RPDL ) , normal CP diet supplemented with 1 % Arg ( 16 % CP , Arg-NPD ) , reduced CP diet supplemented with 1 % Arg ( 13 % CP , Arg-RPD ) , and reduced CP diet with Leu addition to 2.0 % and supplemented with 1 % Arg ( 13 % CP , Arg-RPDL ) . Pigs were slaughtered at 91.7 ± 1.6 kg BW . Dietary Arg supplementation had no effect on intramuscular fat ( IMF ) content but produced meat off-flavor and increased meat tenderness and overall acceptability . The PR increased ( P < 0.001 ) IMF content ( 45 % to 48 % ) but negatively affected the growth performance of pigs . In addition , PR increased ( P < 0.05 ) back fat thickness and decreased loin weight . Leucine addition did not affect IMF content , back fat thickness , or loin weight . There was an increase of juiciness with PR and Leu addition , which accompanied the increase of IMF content with the low-CP diet . The PR increased meat deposition of 18:1c9 , SFA , MUFA , and PUFA , which were not correlated with any pork sensory trait . The main combined effect of Arg was an increased tenderness and overall acceptability of pork . In conclusion , it was confirmed that dietary CP reduction enhances pork eating quality but negatively affects growth performance and carcass characteristics of pigs In hypercholesterolemic rabbits , oral L-arginine ( the substrate for endothelium derived nitric oxide ) attenuates endothelial dysfunction and atheroma formation , but the effect in hypercholesterolemic humans is unknown . Using high resolution external ultrasound , we studied arterial physiology in 27 hypercholesterolemic subjects aged 29+/-5 ( 19 - 40 ) years , with known endothelial dysfunction and LDL-cholesterol levels of 238+/-43 mg/dl . Each subject was studied before and after 4 wk of L-arginine ( 7 grams x 3/day ) or placebo powder , with 4 wk washout , in a r and omized double-blind crossover study . Brachial artery diameter was measured at rest , during increased flow ( causing endothelium-dependent dilation , EDD ) and after sublingual glyceryl trinitrate ( causing endothelium-independent dilation ) . After oral L-arginine , plasma L-arginine levels rose from 115+/-103 to 231+/-125 micromol/liter ( P<0.001 ) , and EDD improved from 1.7+/-1.3 to 5.6+/-3.0 % ( P<0.001 ) . In contrast there was no significant change in response to glyceryl trinitrate . After placebo there were no changes in endothelium-dependent or independent vascular responses . Lipid levels were unchanged after L-arginine and placebo . Dietary supplementation with L-arginine significantly improves EDD in hypercholesterolemic young adults , and this may impact favorably on the atherogenic process BACKGROUND Oral amino acid intake reduces plasma glucose in Streptozotocin-induced diabetic rats . This study examined the effect of oral amino acid supplementation in patients with type 2 diabetes mellitus ( DM ) . MATERIAL / METHODS A double blind pilot clinical trial was conducted for a period of 2 months on 77 subjects with type 2 DM . Subjects of both sexes , ages 30 - 60 , were included in the trial . All were receiving oral antidiabetic tablets . They were divided into groups on the basis of oral supplementation : ( A ) lysine , ( B ) essential amino acids , ( C ) amino acids and vitamins ( fat and water-soluble ) , and ( D ) calcium phosphate ( control ) . The subjects were periodically examined for fasting and post-pr and ial plasma glucose , fasting and post-pr and ial immunoreactive insulin , plasma amino acids , glycosylated haemoglobin ( HbA1c ) , proteins and albumin in serum , urea and creatinine in plasma and sugar , and proteins and ketones in urine . RESULTS The results revealed a significant decrease in PP plasma glucose ( P<0.05 ) in group B when compared to groups C and D after 45 days . Plasma Arginine was increased in group C from 3.84 to 9.24 mg/dl . There were no statistically significant changes seen in other parameters between groups and visits . CONCLUSIONS Oral supplementation with amino acids for patients with type 2 DM appears to decrease PP plasma glucose without any change in plasma insulin levels , perhaps due to improved insulin sensitivity . However , the long term effects of amino acids need further study We recently noticed a possible triglyceride-lowering effect during dietary supplementation with L-arginine . The major limitation of prior studies on L-arginine , however , was that triglyceride levels were not the primary end point , and patients were not necessarily hypertriglyceridemic . Therefore , we conducted a 2-arm , r and omized , double-blind study in 33 hypertriglyceridemic patients to investigate the hypothesis that oral L-arginine may lower serum triglyceride levels in hypertriglyceridemic patients on and off statins .  The study consisted of a 6-week run-in phase , 6 weeks of treatment with L-arginine ( n = 22 , 1.5 g bid ) or placebo ( n = 11 ) , and a 6-week extension period where simvastatin ( 20 mg qd ) was added . All patients received dietary advice during each study visit . Routine and lipid laboratory parameters were determined in the local routine clinical laboratory . Treatment with L-arginine alone had no effects on serum lipids compared to placebo . The combination of L-arginine with simvastatin led to a significantly stronger reduction in triglycerides compared to placebo plus simvastatin ( -140.5 + /- 149.2 mg/dL vs -56.1 + /- 85.0 mg/dL ; P = .048 ) . In addition , we found simvastatin-induced  increases in aspartate transaminase and fibrinogen to be attenuated by L-arginine as compared to placebo . We conclude from our data that L-arginine enhances the effects of simvastatin on lipid metabolism , but it has no triglyceride-lowering effects when given alone The present study was carried out to evaluate the effect of a low‐dose intravenous supplementation of l‐arginine on insulin‐mediated vasodilatation and insulin sensitivity . The study was performed in healthy subjects ( n = 7 ) and patients with obesity ( n = 9 ) and non‐insulin‐dependent diabetes mellitus ( NIDDM ) ( n = 9 ) . Insulin‐mediated vasodilatation was measured by venous occlusion plethysmography during the insulin suppression test , evaluating insulin sensitivity . Experiments were performed twice in each subject in the presence or absence of a concomitant infusion of l‐arginine ( 0.52 mg kg−1 min−1 ) . l‐Arginine restored the impaired insulin‐mediated vasodilatation observed in obesity ( 22.4 ± 4.1 % , P < 0.01 vs. without l‐arginine ) and NIDDM ( 20.3 ± 3.2 % , P < 0.01 vs. without l‐arginine ) . In healthy subjects , no effect on insulin mediated‐vasodilatation was observed ( 24.8 ± 3.1 % vs. 21.4 ± 3.1 % ) . Insulin sensitivity was improved significantly ( P < 0.001 ) in all three groups by infusion of l‐arginine . No effect of l‐arginine  was observed on insulin , insulin‐like growth factor I ( IGF‐I ) , free fatty acids ( FFAs ) or C‐peptide levels during the insulin suppression test . Our data indicate that defective insulin‐mediated vasodilatation in obesity and NIDDM can be normalized by intravenous l‐arginine . Furthermore , l‐arginine  improves insulin sensitivity in obese patients and NIDDM patients as well as in healthy subjects , indicating a possible mechanism that is different from the restoration of insulin‐mediated vasodilatation As a substrate for nitric oxide synthesis , L-arginine may give the same protection as estrogen , but its other biologic effects may adversely affect atherogenesis . Therefore , possible endocrine and lipid effects of L-arginine were investigated in a double-blind , placebo-controlled , single crossover study . After r and omization , oral L-arginine ( 9 g ) or placebo was given daily for 1 month , with crossover to the alternate therapy after a 1-month washout period , to 10 postmenopausal women receiving no estrogen .  Compared with placebo , L-arginine increased growth hormone ( 1.5+/-1.8 mg/L vs. 0.6+/-0.6 mg/L , P = .04 ) but had no effect on insulin and catecholamines . Total cholesterol , triglyceride , apolipoprotein E , and low- , very-low- , and high-density lipoprotein cholesterol levels were also unaffected . Lipoprotein(a ) measured by an immunoturbidimetric method was increased by L-arginine in 9 of 10 women relative to placebo ( 0.46+/-0.35 g/L vs. 0.38+/-0.30 g/L , P = .053 ) , and the changes in lipoprotein(a ) levels significantly correlated with the relative increase in growth hormone ( r = 0.85 , P = .03 ) . However , lipoprotein(a ) measured by an enzyme-linked immunosorbent assay failed to demonstrate significant changes . Lack of an increase by  L-arginine in lipoprotein(a ) with a verifiable apolipoprotein(a ) isoform-independent method , despite an increase in growth hormone , questions the validity of previous observations for growth hormone-induced increases in lipoprotein(a ) . The observed lack of effect on major endocrine hormones and lipid profile support the safety of oral L-arginine administration BACKGROUND The role of tumor necrosis factor alpha ( TNF-alpha ) , one of the adipose tissue products , in the pathogenesis of insulin resistance is well-documented . Many recent studies have shown beneficial influence of L-arginine supplementation on cardiovascular system . However , molecular mechanisms of its positive actions are not fully eluci date d. AIM The aim of the study was to evaluate the influence of L-arginine supplementation on tumor necrosis factor alpha , insulin resistance and selected anthropometric and biochemical parameters in patients with visceral obesity . PATIENTS AND METHODS 60 patients with visceral obesity were r and omly assigned to either receive 9 g of L-arginine or placebo for 3 months . 20 healthy lean subjects were used as control . Selected anthropometrical measurements and blood biochemical analyses were performed at baseline and after 3-months . TNF-alpha and its soluble receptor 2 ( sTNFR2 ) were assessed in both treated groups . Insulin resistance in the participants was evaluated according to the homeostasis model assessment -insulin resistance ( HOMA-IR ) protocol . RESULTS The concentration of insulin , TNF-a and sTNFR2 and HOMA-IR level in both obese groups significantly exceeded these observed in the control . Basal TNF-alpha and sTNFR2 concentrations were positively correlated with basal body mass index ( BMI ) , waist circumference , percent of body fat and HOMA-IR . We found that 3-month L-arginine supplementation result ed in significant decrease of HOMA-IR and insulin concentration . Only insignificant tendency to decrease of TNF-alpha and sTNFR2 was observed . CONCLUSIONS Our results confirm TNF-alpha role in the complex pathogenesis of insulin resistance in patients with visceral obesity . 3-months L-arginine supplementation in a dose of 9 g improves insulin sensitivity in patients with visceral obesity with no impact on tumor necrosis factor alpha concentration Since the last publication of the recommendations for the management and treatment of dyslipidemia , new clinical trial data have emerged that support a more vigorous approach to lipid lowering in specific patient groups . The decision was made to up date the lipid guidelines in collaboration with the Canadian Cardiovascular Society . A systematic electronic search of medical literature for original research consisting of blinded , r and omized controlled trials was performed . Meta-analyses of studies of the efficacy and safety of lipid-lowering therapies , and of the predictive value of established and emerging risk factors were also review ed . All recommendations are evidence -based , and have been review ed in detail by primary and secondary review panels . Major changes include a lower low-density lipoprotein cholesterol ( LDL-C ) treatment target ( lower than 2.0 mmol/L ) for high-risk patients , a slightly higher intervention point for the initiation of drug therapy in most low-risk individuals ( LDL-C of 5.0 mmol/L or a total cholesterol to high-density lipoprotein cholesterol ratio of 6.0 ) and recommendations regarding additional investigations of potential use in the further evaluation of coronary artery disease risk in subjects in the moderate-risk category Patients with NIDDM are at increased risk for coronary heart disease ( CHD ) . However , information on the predictive value of cardiovascular risk factors and the degree of hyperglycemia with respect to the risk for CHD in diabetic patients is still limited . Therefore , we carried out a prospect i ve study on risk factors for CHD , including a large number of NIDDM patients . At baseline , risk factor levels of CHD were determined in 1,059 NIDDM patients ( 581 men and 478 women ) , aged from 45 to 64 years . These patients were followed up to 7 years with respect to CHD events . Altogether , 158 NIDDM patients ( 97 men [ 16.7 % ] and 61 women [ 12.8 % ] ) died of CHD and 256 NIDDM patients ( 156 men [ 26.8 % ] and 100 women [ 20.9 % ] ) had a serious CHD event ( death from CHD or nonfatal myocardial infa rct ion ) . A previous history of myocardial infa rct ion , low HDL cholesterol level ( < 1.0 mmol/l ) , high non-HDL cholesterol ( > 5.2 mmol/l ) , high total triglyceride level ( > 2.3 mmol/l ) , and high fasting plasma glucose ( > 13.4 mmol/l ) were associated with a twofold increase in the risk of CHD mortality or morbidity , independently of other cardiovascular risk factors . High calculated LDL cholesterol level ( ≥4.1 mmol/l ) was significantly associated with all CHD events . The simultaneous presence of high fasting glucose ( > 13.4 mmol/l ) with low HDL cholesterol , low HDL – to – total cholesterol ratio , or high total triglycerides further increased the risk for CHD events up to threefold . Our 7-year follow-up study provides evidence that dyslipidemia and poor glycemic control predict CHD mortality and morbidity in patients with NIDDM Context : The effect of L-arginine on risk factors of cardiovascular diseases ( CVD ) has mostly focused on western countries . Since cardiovascular diseases is the second cause of death in Iran and , as far as we are aware , there have been no studies about the effect of L-arginine on CVD risk factors , the aim of this trial was to assess the effects of L-arginine supplementation on CVD risk factors in healthy men . Objective : The purpose of this study was to evaluate the effect of low-dose L-arginine supplementation on CVD risk factors ( lipid profile , blood sugar and blood pressure ) in Iranian healthy men . Design , setting , participants : We conducted a double-blind r and omized controlled trial in 56 patients selected from sport clubs at the Isfahan University of Medical Science between November 2013 and December 2013 . Interventions : Healthy men received L-arginine supplementation ( 2000 mg daily ) in the intervention group or placebo ( 2000 mg maltodextrin daily ) in the control group for 45 days . Main outcome measure : The primary outcome measures were we measured the levels of fasting blood sugar , blood pressure and lipid profile including triglyceride ( TG ) , cholesterol , LDL and HDL in healthy subjects . It was hypothesized that these measures would be significantly improved in those receiving L-arginine supplementation . at the beginning and end of the study . Results : In this trial , we had complete data for 52 healthy participants with mean age of 20.85±4.29 years . At the end of study , fasting blood sugar ( P=0.001 ) and lipid profile ( triglycerideTG ( P<0.001 ) , cholesterol ( P<0.001 ) , LDL ( P=0.04 ) , HDL ( P=0.015 ) ) decreased in the L-arginine group but we found no significant change in the placebo group . In addition , the reduction of fasting blood sugar and lipid profile in L-arginine was significant compared with placebo group . No significant changes were found about systolic ( P=0.81 ) and diastolic blood pressure either in L-arginine or placebo group . ( P=0.532 ) . Conclusion : The use of L-arginine significantly improved outcomes compared to placebo It is known that L-arginine treatment can ameliorate endothelial dysfunction and insulin sensitivity in type 2 diabetes mellitus patients , but little is known on L-arginine effects on these variables in nondiabetic patients with stable cardiovascular disease ( coronary artery disease ) . We evaluated the effects of long-term oral L-arginine treatment on endothelial dysfunction , inflammation , adipokine levels , glucose tolerance , and insulin sensitivity in these patients . Sixty-four patients with cardiovascular disease previously su bmi tted to an aortocoronary bypass and not known for type 2 diabetes mellitus had an oral glucose load to define their glucose tolerance . Thirty-two patients with nondiabetic response were eligible to receive , in a double-blind r and omized parallel order , L-arginine ( 6.4 g/d ) or placebo for 6 months . An evaluation of insulin sensitivity index during the oral glucose load , markers of systemic nitric oxide bioavailability and inflammation , and blood flow was performed before and at the end of the treatment in both groups . Compared with placebo , L-arginine decreased asymmetric dimethylarginine levels ( P < .01 ) , indices of endothelial dysfunction , and increased cyclic guanosine monophosphate ( P < .01 ) , L-arginine to asymmetric dimethylarginine ratio ( P < .0001 ) , and reactive hyperemia ( P < .05 ) . Finally , L-arginine increased insulin sensitivity index ( P < .05 ) and adiponectin ( P < .01 ) and decreased interleukin-6 and monocyte chemoattractant protein-1 levels . In conclusion , insulin resistance , endothelial dysfunction , and inflammation are important cardiovascular risk factors in coronary artery disease patients ; and L-arginine seems to have anti-inflammatory and metabolic advantages in these patients
target: This meta- analysis concludes that l-arginine supplementation can significantly reduce blood TAG levels ; however , there is insufficient evidence to support its hypocholesterolaemic effects .
background: A number of clinical trials have examined the effect of l-arginine on lipid profile in recent years ; however , the results remain equivocal .
  Therefore , the present study aims to summarise and quantitatively examine the available evidence on the effectiveness l-arginine supplementation on lipid parameters using a systematic review and meta-analytic approach .