The relationship between reduced choroidal thickness due to high plasma asymmetrical dimethylarginine level and increased severity of diabetic retinopathy / Altos níveis de dimetil-arginina assimétrica no plasma podem aumentar a gravidade da retinopatia diabética através da redução da espessura da coroide

ABSTRACT Purpose: To evaluate the relationship between subfoveal choroidal thickness and plasma asymmetrical dimethylarginine level and the severity of diabetic retinopathy in patients with type 2 diabetes mellitus. Methods: A total of 68 cases, including 15 patients without diabetic retinopathy, 17 patients with nonproliferative diabetic retinopathy, 16 patients with type 2 diabetes mellitus and proliferative diabetic retinopathy, and 20 healthy patients (control group), were enrolled in this study. Subfoveal choroidal thickness was measured manually using the enhanced depth imaging optical coherence tomography scanning program, and plasma asymmetrical dimethylarginine level was measured using a commercial micro enzyme-linked immunosorbent assay kit. Results: The subfoveal choroidal thickness values and plasma asymmetrical dimethylarginine levels were significantly different between the four groups (p<0.001 and p<0.001). The subfoveal choroidal thickness values were significantly lower in the proliferative diabetic retinopathy group than in the other three groups (no diabetic retinopathy, nonproliferative diabetic retinopathy, and control groups; p<0.001, p=0.045, and p<0.001, respectively). The plasma asymmetrical dimethylarginine levels were significantly higher in the proliferative diabetic retinopathy group than in the other three groups (p<0.001, p<0.04, and p<0.001, respectively). In addition, a significant negative correlation was also found between plasma asymmetrical dimethylarginine level and subfoveal choroidal thickness (p<0.001, r=-0.479). Conclusion: Asymmetrical dimethylarginine is an important marker of endothelial dysfunction and endogenous endothelial nitric oxide synthase inhibitor. The severity of diabetic retinopathy was related to increased plasma asymmetrical dimethylarginine level and reduced subfoveal choroidal thickness in type 2 diabetic patients with diabetic retinopathy.

RESUMO Objetivo: Avaliar a relação da espessura subfoveal da coroide e dos níveis plasmáticos de dimetil-arginina assimétrica com a gravidade da retinopatia diabética em pacientes com diabetes mellitus tipo 2. Métodos: Foram incluídos 68 casos, compreendendo 15 pacientes sem retinopatia diabética, 17 pacientes com retinopatia diabética não proliferativa, 16 pacientes com retinopatia diabética proliferativa, e 20 casos saudáveis (grupo de controle). A espessura subfoveal da coroide foi medida manualmente, usando o programa de varredura com tomografia computadorizada óptica com imagem profunda aprimorada, e os níveis plasmáticos de dimetil-arginina assimétrica foram medidos usando um kit microELISA comercial. Resultados: Os valores da espessura subfoveal da coroide e os níveis plasmáticos de dimetil-arginina assimétrica foram significativamente diferentes nos quatro grupos (p<0,001 para ambos os parâmetros). Os valores da espessura subfoveal da coroide foram significativamente menores no grupo com retinopatia diabética proliferativa do que nos outros três grupos (sem retinopatia diabética, retinopatia diabética não proliferativa e grupo de controle, com p<0,001, p=0,045 e p<0,001, respectivamente). Já os níveis plasmáticos de dimetil-arginina assimétrica foram significativamente maiores no grupo com retinopatia diabética proliferativa do que nos outros três grupos (p<0,001, p=0,04 e p<0,001, respectivamente). Além disso, também foi encontrada uma correlação negativa significativa entre os níveis plasmáticos de dimetil-arginina assimétrica e a espessura subfoveal da coroide (p<0,001, r=-0,479). Conclusão: A dimetil-arginina assimétrica é um importante marcador de disfunção endotelial e um inibidor endógeno da óxido nítrico sintase. Foi encontrada uma relação da gravidade da retinopatia diabética e de níveis elevados de dimetil-arginina assimétrica no plasma com a redução da espessura subfoveal da coroide em pacientes diabéticos tipo 2 com retinopatia diabética.

Visceral adiposity index and triglyceride/high-density lipoprotein cholesterol ratio in hypogonadism

ABSTRACT Background Cardiometabolic risk is high in patients with hypogonadism. Visceral adiposity index (VAI) and triglyceride/high-density lipoprotein cholesterol (TG/HDL-C) ratio are the practical markers of atherosclerosis and insulin resistance and independent predictors of cardiaovascular risk. To date, no study has evaluated VAI levels and TG/HDL-C ratio in hypogonadism. Subjects and methods A total of 112 patients with congenital hypogonadotrophic hypogonadism (CHH) (mean age, 21.7 ± 2.06 years) and 124 healthy subjects (mean age, 21.5 ± 1.27 years) were enrolled. The demographic parameters, VAI, TG/HDL-C ratio, asymmetric dimethylarginine (ADMA), high-sensitivity C-reactive protein (hs-CRP), and homeostatic model assessment of insulin resistance (HOMA-IR) levels were measured for all participants. Results The patients had higher total cholesterol (p = 0.04), waist circumference, triglycerides, insulin, and HOMA-IR levels (p = 0.001 for all) than the healthy subjects. VAI and ADMA and TG/HDL-C levels were also higher in patients than in healthy subjects (p < 0.001 for all). VAI was weakly correlated with ADMA (r = 0.27, p = 0.015), HOMA-IR (r = 0.22, p = 0.006), hs-CRP (r = 0.19, p = 0.04), and total testosterone (r = −0.21, p = 0.009) levels, whereas TG/HDL-C ratio was weakly correlated weakly with ADMA (r = 0.30, p = 0.003), HOMA-IR (r = 0.22, p = 0.006), and total testosterone (r = −0.16, p = 0.03) levels. Neither VAI nor TG/HDL-C ratio determined ADMA, HOMA-IR, and hs-CRP levels. Conclusions The results of this study demonstrate that patients with hypogonadism have elevated VAI and TG/HDL-C ratio. These values are significantly correlated with the surrogate markers of endothelial dysfunction, inflammation, and insulin resistance. However, the predictive roles of VAI and TG/HDL-C ratio are not significant. Prospective follow-up studies are warranted to clarify the role of VAI and TG/HDL-C ratio in predicting cardiometabolic risk in patients with hypogonadism.

Nitric oxide and asymmetric dimethyl arginine (ADMA) levels in an experimental hydronephrotic kidney caused by unilateral partial ureteral obstruction

ABSTRACT Aim Our aim is to measure asymmetric dimethyl arginine and nitric oxide levels in rats with induced unilateral acute ureteral obstruction to research the effects on the kidney. Material and Methods The study included 21 adolescent (average age 6 weeks) Sprague-Dawley male rats weighing between 240-290g divided at random into 3 groups. Group-1: Control group (n=6): underwent no procedures. Group-2: Sham group (n=6): underwent the same procedures as the experimental group without ureter and psoas muscle dissection. Group-3: Group with induced partial unilateral ureteral obstruction (n=9). All rats were sacrificed after 12 weeks. Superoxide dismutase enzyme activity and nitrite and nitrate salt levels were measured in renal tissue. Plasma nitrite-nitrate and ADMA levels were examined. Results In the experimental group histopathological changes observed included renal pelvis dilatation, flattened papillae, sclerotic glomerulus and fibrosis. In the experimental group tissue SOD and blood ADMA levels were higher than the control and sham groups (p<0.05) while tissue NO and plasma NO values were lower than in the sham and control groups (p<0.05). Conclusion Oxidative stress and disruption of NO synthesis play an important role in renal function and histopathological changes after obstructive renal disease. To prevent renal complications developing after obstructive nephropathy we believe that a new strategy may be research on reducing ADMA.

High plasma concentrations of asymmetric dimethylarginine inhibit ischemic cardioprotection in hypercholesterolemic rats

A low concentration of nitric oxide associated with a high concentration of asymmetric dimethylarginine (ADMA) can explain the lack of ischemic cardioprotection observed in the presence of hypercholesterolemia. The objective of the present study was to evaluate the effect of hypercholesterolemia on ischemic pre- and postconditioning and its correlation with plasma concentrations of ADMA. Male Wistar rats (6-8 weeks old) fed a 2% cholesterol diet (n = 21) for 8 weeks were compared to controls (n = 25) and were subjected to experimental myocardial infarction and reperfusion, with ischemic pre- and postconditioning. Total cholesterol and ADMA were measured in plasma before the experimental infarct and the infarct area was quantified. Weight, total cholesterol and plasma ADMA (means ± SE; 1.20 ± 0.06, 1.27 ± 0.08 and 1.20 ± 0.08 vs 0.97 ± 0.04, 0.93 ± 0.05 and 0.97 ± 0.04 µM) were higher in animals on the hypercholesterolemic diet than in controls, respectively. Cardioprotection did not reduce infarct size in the hypercholesterolemic animals (pre: 13.55% and post: 8% compared to 7.95% observed in the group subjected only to ischemia and reperfusion), whereas infarct size was reduced in the animals on a normocholesterolemic diet (pre: 8.25% and post: 6.10% compared to 12.31%). Hypercholesterolemia elevated ADMA and eliminated the cardioprotective effects of ischemic pre- and postconditioning in rats.

Mecanismos moleculares e celulares envolvidos na modulação da via L-arginina-óxido nítrico em hipertensão e insuficiência renal crônica / Molecular and cellular mechanisms involved in modulation of L-arginine-nitric oxide in hypertension and chronic renal failure

A Insuficiência renal crônica (IRC) e a hipertensão arterial sistêmica (HAS) são patologias com alta morbidade e mortalidade, consumindo grandes verbas de saúde pública. A disfunção endotelial presente tanto na IRC, como na hipertensão, contribui para a manutenção de elevada resistência periférica, favorecendo complicações como a aterosclerose. Esta disfunção endotelial é parte de um estado pró-trombótico, levando à ocorrência de eventos cardiovasculares, principal causa de morte nestas patologias. O óxido nítrico (NO) tem um papel importante na modulação da atividade plaquetária. Anormalidades na síntese e/ou inativação do NO são descritas tanto na insuficiência renal crônica como na hipertensão. Estudos prévios demonstraram uma redução do influxo de L-arginina em eritrócitos e plaquetas de pacientes hipertensos e em um modelo animal de hipertensão. Além disso, em IRC, nosso grupo mostrou uma ativação da via L-arginina-NO em plaquetas. O objetivo dessa tese é avaliar a via L-arginina-NO na HAS e em diferentes estágios de IRC, bem como investigar o ciclo da uréia, e a presença de marcadores de estresse nesses pacientes. De acordo com o presente estudo pôde-se verificar que não houve alteração na síntese de NO em eritrócitos na hipertensão, todavia ocorre uma ativação do ciclo da uréia, que pode ser dada pelo aumento do influxo de L-arginina eritrocitário previamente demonstrado. Não foi demonstrada diferença significativa na peroxidação lipídica sistêmica, em plaquetas ou eritrócitos na HAS. Em plaquetas, no entanto, houve uma redução da atividade da NO sintase (NOS), que não foi acompanhada por alteração da expressão das isoformas da NOS, da arginase, da fosfodiesterase 5 (PDE5) ou da guanilato ciclase (GC) solúvel. Essa redução na síntese de NO em plaquetas pode ser explicada por um menor influxo de L-arginina que está presente na hipertensão. Os eritrócitos de pacientes renais crônicos em hemodiálise mostraram um maior influxo de L-arginina...

Chronic renal failure (CRF) and essential hypertension (EH) are diseases associated with high rates of morbidity and mortality, consuming huge amounts of money from the public health system. The endothelial dysfunction existent in both diseases, CRF and EH, contributes to the maintenance of the high peripheral resistance, and contribute to circulatory complications such as atherosclerosis. This endothelial dysfunction is part of a pro-thrombotic state, leading to cardiovascular events, which are the major cause of death in these disorders. Nitric oxide (NO) plays an important role in the modulation of platelet function. Abnormalities of NO synthesis or inactivation are described in CRF and EH. It was previously reported an inhibition of L-arginine transport in erythrocytes of hypertensive patients and in an animal model of hypertension. Moreover, we have also demonstrated an activation of L-arginine-NO pathway in platelets taken from uraemic patients. The aim of the present thesis is to investigate L-arginine-NO pathway in arterial hypertension and in different stages of chronic renal failure. It will also be evaluated urea cycle and the presence of oxidative stress markers in these patients. According to the present study it was not detected any alteration in erythrocytes NO synthesis in hypertension, however, there was an activation of urea cycle, which could be explained by an increase in L-arginine influx. The present study has not demonstrated significative difference in markers of lipid peroxidation in the serum, platelets or erythrocytes in hypertension. In platelets however, there was an inhibition of NO synthase (NOS) activity without any alterations of NOS isoforms, arginase, phosphodiesterase 5 (PDE5) or soluble guanylyl cyclase (sGC) expression. This reduction of NO synthesis may be explained by a lower influx of L-arginine that is present on hypertension. Erythrocytes from chronic renal failure patients under haemodyalysis...

Asymmetric dimethylarginine [ADMA]: an emerging contributor to endothelial dysfunction in hyperthyroidism

Cardiovascular manifestations are frequent findings in patients with hyperthyroidism. Nitric oxide [NO], a key regulator of endothelial function, is synthesized from L-arginine by nitric oxide synthase [NOS]. Evidence has accumulated that asymmetric dimethylarginine [ADMA] is an endogenous competitive inhibitor of NOS. To measure plasma L-arginine and dimethylarginines [ADMA and SDMA] in patients with hyperthyroidism in order to assess their contribution to endothelial dysfunction and their relationship to plasma NO. The study was conducted on 50 newly diagnosed patients with overt hyperthyroidism as well as 30 age and sex matcned healthy controls. Plasma L-arginine, ADMA and SDMA were analyzed by HPLC. Plasma NO was measured by a colorimetric method based on Griess reagent. L-arginine, ADMA and SDMA were significantly increased, while NO and L-arginine/ADMA ratio were significantly decreased in hyperthyroid patients compared to controls. Serum freeT4 and free T3 were negatively correlated with plasma NO and L-arginine/ADMA ratio and positively correlated with L-arginine, ADMA and SDMA. Moreover, NO was significantly negatively correlated with each of the L-arginine and ADMA and significantly positively correlated with T.arginine/ADMA ratio. Results provide evidence of the presence of endothelial dysfunction in hyperthyroidism. The decrease in NO, and the increase in ADMA emphasizes that ADMA is an emerging contributor of endothelial dysfunction in hyperthyroidism

Endothelial nitric oxide synthase gene polymorphisms [G894T] in diabetes mellitus in Egypt

Diabetic nephropathy [DN] is one of the major microvascular complications of diabetes. Genetic predisposition has been implicated in DN. The eNOS protein synthesizes nitric oxide constitutively via a reaction including the conversion of L-arginine to L-citrulline, which involves the transfer of five electrons provided by nicotinamide adenine dinucleotide phosphate The aim of this study is to evaluate the association of G894T polymorphisms of endothelial nitric oxide synthase [eNOS] gene with the development of diabetic nephropathy [DN] among Egyptian patients with type 1,2 diabetes mellitus in Egypt. Study subjects comprised 86 patients of type 2 diabetes with nephropathy,23 patients of type 1 diabetes with nephropathy and 46 patients of type 2 diabetes without nephropathy. G894T genotypes was determined by SSP- PCR analysis. Mutant T allele, GT and TT genotypes of G894TSNP had no significant frequencies in type 1.2 diabetic patients with nephropathy compared to those without nephropathy. These findings indicate that G894T polymorphism of eNOS gene may be not considered as genetic risk factors for DN among Egyptian type 1, 2 diabetic patients. T2DM: type 2 diabetes mellitus-DN: diabetic nephropathy eNOS: Endothelial nitric oxide synthase:- SNP: single nucleotide polymorphism- SSP-PCR: sequence specific primer- polymerase chain reaction

Asymmetric dimethylarginine (ADMA) and endothelial dysfunction: implications for atherogenesis: [review]

Atherosclerotic coronary heart disease is the leading cause of morbidity and mortality in industrialized countries, and endothelial dysfunction is considered a precursor phenomenon. The nitric oxide produced by the endothelium under the action of endothelial nitric oxide synthase has important antiatherogenic functions. Its reduced bioavailabilty is the beginning of the atherosclerotic process. The addition of two methyl radicals to arginine, through the action of methyltransferase nuclear proteins, produces asymmetric dimethylarginine, which competes with L-arginine and promotes a reduction in nitric oxide formation in the vascular wall. The asymmetric dimethylarginine, which is itself considered a mediator of the vascular effects of the several risk factors for atherosclerosis, can be eliminated by renal excretion or by the enzymatic action of the dimethylarginine dimethylaminohydrolases. Several basic science and clinical research studies suggest that the increase in asymmetric dimethylarginine occurs in the context of chronic renal insufficiency, dyslipidemia, high blood pressure, diabetes mellitus, and hyperhomocysteinemy, as well as with other conditions. Therapeutic measures to combat atherosclerosis may reverse these asymmetric dimethylarginine effects or at least reduce the concentration of this chemical in the blood. Such an effect can be achieved with competitor molecules or by increasing the expression or activity of its degradation enzyme. Studies are in development to establish the true role of asymmetric dimethylarginine as a marker and mediator of atherosclerosis, with possible therapeutic applications. The main aspects of the formation and degradation of asymmetric dimethylarginine and its implication in the atherogenic process will be addressed in this article.

Efetividade das dietas enriquecidas com imunonutrientes na redução de complicações e mortalidade em pacientes críticos: abordagem pela utilização de metanálise / Effectiveness of diets enriched with imunonutrients in reducing complications and mortality in critical patients: metanalysis usage approach

Nutrientes específicos, denominados farmaconutrientes, demonstraram possuir a capacidade de modular a resposta imunológica e inflamatória de animais e seres humanos, em estudos clínicos e laboratoriais. Dentre os substratos conhecidos, os que têm maior relevância e açãoimunomoduladora são a arginina, glutamina, ácido graxo n-3 e nucleotídeos. No entanto, revisõessistemáticas e meta-análises buscam consenso em relação aos vários e controversos resultados publicados sobre os possíveis benefícios da imunonutrição em pacientes críticos. Objetiva avaliar a efetividade das dietas enriquecidas com Imunonutrientes na redução de complicações e mortalidade nos diferentes tipos de pacientes críticos. O presente estudo é umarevisão sistemática com metanálise onde foram inseridos ensaios clínicos randomizados avaliando o uso de nutrientes imunomoduladores em doente adulto de ambos os sexos, definido como crítico traumatizado, séptico, queimado ou cirúrgico; as dietas utilizadas deveriam conter um ou mais dosimunonutrientes, em qualquer dose, administradas por via enteral comparadas à dieta padrão pelamesma via em pelo menos um dos grupos de comparação. As bases de dados consultadas foram Pubmed e Cinhal, utilizando os termos: Immunonutrition, arginine, glutamine, n-3, nucleotides e criticall illness...

Comparative effect of antioxidants and l-arginine treatment on nerve conduction velocity and regeneration in streptozotocin-induced diabetic rats

Diabetic polyneuropathy [DPN] is the most common chronic complication of diabetes. In the last two decades it has become increasingly evident that underlying vascular and metabolic mechanisms emerged as a prominent pathogenetic factors for DPN. Oxidative stress is increased in both human and experimental diabetes and has been related to the development of diabetic neuropathy. Vascular factors include increased peripheral resistance also have been implicated in the pathogenesis of experimental diabetic neuropathy [EDN]. It seems still controversial, whether EDN is primarily of vascular or metabolic origin and the aim of the present study was to evaluate the possible contribution of two pathways to the development of such neural complications in type II diabetic animals. Ninety male albino rats were included. The animals groups were as follows: Group I: Control rats which were injected by intraperitoneal [i.p.] by vehicle solution alone, Group II: Diabetic rats not receiving any form of treatment [with fasting blood glucose level above 300mg/kg], Group III: Diabetic rats received daily subcutaneous insulin injection in a dose IIU/day, Group IV: Diabetic rats received intramuscular injection of Vitamin E in a dose 300mg/kg BW, three times/week, Group V: Diabetic rats received intramuscular injection of Vitamin E in a dose 600mg/kg BW, three times/week, Group VI: Diabetic rats received subcutaneous insulin [IIU/day], and intramuscular injection of Vitamin E [300mg/kg BW, three times/week], Group VII: Diabetic rats received subcutaneous insulin [IIU/day], and intramuscular injection of Vitamin E [600mg/kg BW, three times/week], Group VIII: Diabetic rats received daily intragastric L-arginine in a dose of 50mg/kg BW, Group IX: Diabetic rats received daily intragastric L-arginine in a dose of 50mg/kg BW, and subcutaneous insulin [IIU/day]. After 4 weeks, nerve conduction velocity studies were performed, serum glucose was measured, and sciatic nerves malondialdehyde [MDA], glutathione peroxidase [GTPx], endothelial nitric oxide synthase [eNOS] were measured. Diabetic rats had significant higher serum glucose levels, oxidative stress markers, lower eNOS, with delayed nerve conduction velocity [NCV] and lower amplitude of muscle contraction [AMC] as compared with the control group. Treating rats with insulin corrected serum glucose to control values. Treating rats with vitamin E significantly reduced oxidative stress markers, and corrected NCV and improved AC. L-arginine treatment had no effect on serum glucose, oxidative stress markers, but significantly improved NCV and AMC. It can be concluded that EDN is a multifactorial disease, caused by hyperglycemia, oxidative stress and vascular impairment. Conjugate treatment with vitamin E especially in higher doses [600mg/kg B. W.] with insulin could be of great value. Moreover correction of impaired nerve blood flow by drugs that induce NO has proved to be efficient in the protection against, and correction of EDN

Role of nitric oxide in the pathophysiology of lead- induced cardiovascular diseases in rats

Exposure to lead is an environmental and occupational sitting continues to be a serious public health problem. Lead affects many organs and systems in human, where the cardiovascular system is one of the important targets. The mechanism of lead induced hypertension and cardiac diseases remain unclear. This study is designed to investigate the role of nitric oxide [NO] in the pathophysiologic mechanisms of lead- induced cardiovascular diseases in rats. 40 rats were used and divided into 4 equal groups. The first group was left without treatment served as a control group. The rest of groups were treated with lead acetate [0.48 mmol/L in distilled water] orally daily for 8 weeks, the third group concomitantly administered L arginine intraperitoneal injection while, the last group co administered L- N-Nitro-L arginine methyl ester intraperitoneal injection [L-NAME]. Blood samples were collected at the 4[th] and 8[th] week of the study for biochemical analysis of mean blood lead level and serum nitric oxide, lipid peroxide, total antioxidants, HDL and LDL. Measurements of systolic blood pressure were done. The mean blood lead levels, lipid peroxidation levels and LDL- cholesterol of lead treated rats were significantly higher in all groups than control. While the serum totals antioxidant levels and HDL- cholesterol significantly decreased below control levels. There was a positive correlation between mean blood lead and each of serum LDL, serum lipid peroxide and systolic blood pressure. Moreover, a significant negative correlation was observed between serum nitric oxide and each of mean blood lead, serum LDL and systolic blood pressure. These findings point to the role of nitric oxide [NO] in the pathophysiologic mechanisms of lead induced cardiovascular diseases and hypertension

Effect of tamoxifen on plasma arginine vasopressen levels

Ovariectomy of the mature female rat results in a fall in the plasma vasopressin concentration, although the ovarian content of the hormone is low. To investigate this further, functional ovariectomy was done in the rats by administration of an anti-oestrogen acting drug [Tamoxifen]. Studies performed on female rats indicated significant reductions in uterine weight and plasma vasopressin levels. The uterine weights decreased from 206.9 mg /100 gm body weight in control group to 142.2 mg /100 gm body weight in experimental group. Plasma vasopressin levels decreased from 1.15 microunits / ml in the control group to 0.38 microunits /ml in the experimental group. The study confirms that like surgically ovariectomized rats, functional ovariectomy also causes decreases in uterine weights and plasma vasopressin levels

Diagnóstico tardío de argininemia en un niño en estado de coma / Late diagnosis of argininemia in a boy with coma

Se presenta el caso clínico de un niño de once años de edad, valorado en una Unidad de Cuidados Intensivos Pedíatricos, en estado de coma, con signos de hipertensión intracraneana, con historia de deterioro neurológico progresivo, espasticidad, convulsiones y diferentes diagnósticos previos. Se detectó hiperamonemia (360 mcg/dL), elevación de arginina en plasma y de ácido orótico en orina, sin acidosis. Se concluyó clínica y bioquímicamente el diagnóstico de argininemia; fue tratado con restricción de proteínas y benzoato de sodio, con lo que se normalizaron los valores de arginina en plasma. Por lo tardío del diagnóstico las funciones neurológicas, el electroencefalograma y los potenciales evocados mostraron solo mejoría parcial. Este es el primer caso publicado en américa Latina. Argininemia

Effect of addition of arginine and lysine to casein diets on serum lipids metabolism in rats

The effect of feeding casein diets supplemented by amino acids on serum lipids was studied on rats. Three groups of rats were fed casein diets supplemented by lysine or arginine, while the third was fed unsupplemented diet for 8 weeks. The results indicated that rats fed lysine added diets exhibited decrease in body weight comparable with casein only, whereas those fed the arginine showed significant increase for body weight. A significant decrease for serum total lipids, total cholesterol, triglycerides as well as phospholipids were also shown for the group fed the arginine diet, HDL-cholesterol showed no change in supplemented casein by lysine; however, largely increased triglycerides, while total lipids, total cholesterol were fairly increased