We hypothesized that subcutaneous (s.c.) adipose tissue would differ in monounsaturated (MUFA) and saturated fatty acid (SFA) composition among different depots throughout a beef carcass. To test this, 50 carcasses from a variety of breed types and backgrounds were sampled. External fat samples were collected from eight different carcass locations: round, sirloin, loin, rib, chuck, brisket, plate and flank. Samples were used to provide information on slip points, fatty acid composition and MUFA:SFA ratios. Lipids were extracted from s.c. adipose tissue by a modified chloroform:methanol procedure, and fatty acid composition and slip points were measured. The brisket was significantly lower in palmitic (16:0) and stearic (18:0) acid than the other seven sampling sites (P = 0.001). The brisket demonstrated the highest values of MUFA (P = 0.001) with the exception of possessing the lowest value of transvaccenic (18:1t11) acid (P = 0.002). There were also significant differences in the amounts of PUFA among the eight sampling sites. The lowest values were from the brisket with a mean of 25.1. The flank had the highest slip point with a mean of 39.0 (P ≤ 0.001). There was a high negative correlation shown between palmitoleic and stearic acid (R2 = 0.827). The brisket displayed the highest values for MUFA:SFA ratios (P = 0.001), whereas the flank was the lowest. Due to the significant differences amongst fat depots within bovine carcasses in their fatty acid composition we conclude that substantial differences exist across fat depots.

The primary functions of the cardiovascular system are to transport the required nutrients to sustain the metabolic activity of tissues and to remove the metabolic waste products from tissue. Therefore, a steady supply of oxygen for the cells is crucial. Vascular endothelium synthesizes both relaxing and contracting factors to regulate the local tissue blood flow. Nitric oxide (NO) is one of the major endothelium-derived relaxing factor. It is synthesized by endothelial nitric oxide synthase (eNOS), which interacts with soluble guanylyl cyclase in smooth muscle to produce cyclic guanosine monophosphate (cGMP) resulting in vascular relaxation. Nitroglycerin (GTN) is an organic nitrate used for the management of angina pectoris, hypertension and congestive heart failure, it is converted to NO or closely related moleculesin the vasculature resulting in vasodilatation. It has been demonstrated that chronic administration of GTN leads to nitrate tolerance, which is associated with increased arginase activity and reactive oxidative species (ROS)production. Supplement of L-arginine appears to reduce nitrate tolerance, however, the bioavailability of L-arginine is limited. It has been reported that L-citrulline supplement in human results in elevated plasma level of L-arginine. This study was designed to investigate the effect of long-term GTN treatment on the expressions and activities of arginase I, arginase II and eNOS, and on the production of cGMP inhuman umbilical vein endothelial cells (HUVECs).Moreover, the effect of L-citrulline on nitrate tolerance due to GTN treatment was examined. HUVECs were treated with GTN (10 µM), thrombin, L-arginine, L-citrulline and L-norvaline, alone or in combinations, for 1 hour (short-term treatment) or 24 hours(long-term treatment) followed by 30 minutes stimulation by GTN (100 µM).Western immunoblotting was used to measure the protein expression levelsof eNOS, arginase I and arginase II. Enzyme immunoassay and colorimetric assay were performed to determine the cGMP level and the arginase activities, respectively. Our results suggested that the amount of cGMP release in response to acute (30 minutes) GTN stimulation (100 µM)was reduced in HUVECs that were pre-treated with24 hour GTN(10 µM), and this is associated with an increased arginase activity. L-arginine,L-citrullineor L-norvaline alone was not able to prevent this reduction in cGMP release (nitrate tolerance), although L-arginine and L-norvaline, but not L-citrulline, prevented the increase in arginase activity. The combination of L-arginine or L-citrulline with L-norvaline is effective to protect HUVECs against nitrate tolerance. On the other hand, thrombin (a stimulator of eNOS, 1 U/ml) pre-treatment for 24 hours also reduced cGMP production toacute GTN stimulation. Similar to long-term GTN-induced nitrate tolerance, long-term thrombin-induced nitrate tolerance was not prevented by concomitant presence of L-arginine, L-citrulline or L-norvaline. Long-term thrombinpre-treatment also increased arginase activity and this effect was inhibited by L-arginine, L-citrulline and L-norvaline. The increased arginase activity by long-term GTN or thrombin pre-treatment was not associated with increased arginase protein expression. In conclusion, the present data suggested that prolonged pre-exposure to exogenous GTN or endogenous increase NO by thrombin induced nitrate tolerance in HUVECs, and this is unlikely the consequence of the increased arginase activity. In addition, neither L-arginine nor L-citrulline were effective in protecting HUVECs against nitrate tolerance, and only the combination of L-citrulline and L-norvaline or L-arginine and L-norvaline were effective. / published_or_final_version / Pharmacology and Pharmacy / Master / Master of Medical Sciences

Diabetic rats exhibit decrease in plasma arginine, NO synthesis and tetrahydrobiopterin in endothelial cells (EC). Treatment with L-arginine may be beneficial for enhancing NO synthesis in diseases associated with endothelial dysfunction. However, little is known about the mechanism responsible for the stimulatory effect of arginine on endothelial NO synthesis. We hypothesized that dietary arginine supplementation increases BH4 for NO synthesis in EC of diabetic rats, thereby preventing endothelial dysfunction. In experiment I, streptozotocin (STZ) induced-diabetic male Sprague Dawley (SD) rats (a model of type-I diabetes) were individually pair-fed a casein-based diet on the basis of feed intake (per kg body weight) of non-diabetic SD rats. Addition of arginine-HCl or alanine to drinking water for the rats were adjusted daily to ensure isonitrogenous provision per kg body weight. In non-diabetic rats, arginine supplementation increased plasma arginine (144%), plasma insulin (44%), EC arginine (88%), EC BH4 (106%) and EC NO synthesis (80%), compared with alanine treatment. In diabetic rats, arginine supplementation reduced body weight loss (36%), and plasma glucose (54%), and increased plasma arginine (110%), plasma insulin (209%), EC arginine (173%), EC BH4 (128%) and EC NO synthesis (125%), compared with alanine treatment. In experiment II, male Zucker diabetic fatty (ZDF) rats (a model of type-II diabetes) were individually pair-fed a Purina 5008 diet on the basis of feed intake by alanine-treated diabetic rats (per kg body wt). Addition of arginine-HCl or alanine to drinking water for the rats was adjusted daily to ensure isonitrogenous provision per kg body weight. Arginine supplementation to ZDF rats did not affect plasma glucose and insulin, reduced epidididmal fat (30%), abdominal fat (43%) and body weight gain (18%), and increased plasma arginine (273%), EC arginine (197%), EC BH4 (120%) and EC NO synthesis (122%), compared with alanine-treated ZDF rats. These results show that dietary L-arginine supplementation increases BH4 and NO synthesis in EC of both STZ-diabetic and ZDF rats. Strikingly, arginine treatment prevented hyperglycemia in STZ-diabetic SD rats and reduced obesity in ZDF rats. Collectively, results demonstrate that oral administration of arginine is beneficial for both type-I and type-II diabetic rats.

No description available.

The thesis discusses the design of potential inhibitors of Angiotensin Converting Enzyme (ACE). The synthesis of pep tide inhibitors containing arginine and histidine-type residues is described. Successful incorporation of these residues during peptide synthesis requires the use of protecting groups on the side-chains* and new developments in this area are described. Ch. 1 reviews the currently available protecting groups for histidine. A methodology for regiospecific introduction of protecting groups of type ROCH₂-, via their corresponding chloromethyl ethers, is described. A convenient synthesis of these reagents (specifically t-Butoxymethylchloride, Dum-Cl and 2,4,6-TrimethyIbenzyloxymethyl- chloride, Tom-Cl) is given. Ch. 2 demonstrates that a knowledge of the location of histidine protecting groups has become mandatory, both in peptide synthesis and elsewhere. Two methods) a), nuclear Overhauser enhancement measurements and b), a procedure involving methylation, deprotection and amino-acid analysis are presented, which have allowed the differentiation of ? and ? derivatised histidines. Ch. 3 reviews the currently available protecting groups for arginine. Using 2-phenylethyIguanidine as a model for arginine, a number of haloacylguanidines and 5,5-disubstituted pyrimidinones wBe synthesised, and this chapter describes their structures, and the potential use of the corresponding reagents in protecting arginine during peptide synthesis. Ch. 4 describes the synthesis of his tidyIphenylalanylarginine and several variants on this structure. Biological data showing the level of inhibition both of A.C-E- and of Renal ^ndopeptidase by these compounds is presented. The syntheses also provide a further demonstration of the efficacy of the recently introduced benzyloxymethyI, (Bom)protecting group.

Thirty-two Quarter horse mares (468 to 668 kg BW; 3 to 19 yr) were utilized in a randomized complete block design. Animals were blocked by expected foaling date and randomly assigned to treatments within block. Treatments began 110 d prior to expected foaling date and were arranged as a 2 x 2 factorial consisting of two planes of nutrition, moderate (Mod; 0.5% BW as fed grain/d) or high (High; 1% BW as fed grain/d) and two levels of L-arginine supplementation, 0.21 g/kg BW/d (Arg) or no supplemental Arg (Con; L-alanine to maintain isonitrogenous diets). Mares were housed by block, allowed ad libitum access to water and coastal bermudagrass (Cynodon dactylon) hay, and fed commercial grain twice daily in individual stalls. A modified frequent sampling i.v. glucose tolerance test (FSIGT) was performed on mares during the 11th month gestation and on foals at 5 and 30 d of age. Jugular catheters were placed 1 h before FSIGT, and horses were allowed ad libitum access to bermudagrass hay and water throughout. After a baseline plasma sample was collected, a glucose bolus of 0.3 g/kg BW was administered. Blood samples were collected at 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 14, 16, and 19 min. At minute 20, an insulin bolus of 30 mU/kg BW was administered. Blood samples continued to be collected at 22, 23, 24, 25, 27, 30, 35, 40, 50, 60, 70, 80, 90, 100, 120, 150, and 180 min. Samples were placed into tubes containing sodium heparin, immediately placed on ice, and centrifuged within 20 min. Plasma was then collected, placed in microtubes and frozen at -20 degrees C for later analysis. Glucose concentrations were analyzed using a colorimetric assay and insulin concentrations determined using a commercial RIA kit. There was no influence of dietary treatment on mare glucose area under the curve (AUCg) or peak glucose (PG) and insulin (PI) concentrations (P >= 0.55). Mare insulin area under the curve (AUCi) tended to be influenced by the interaction between nutritional plane and ARG supplementation (P <= 0.06) with HighCon mares having greater AUCi than ModCon (P <= 0.05), and HighCon mares having greater AUCi than mares fed HighArg (P <= 0.05). Foal AUCg, AUCi, and PI were not influenced by maternal diet. However, PG concentration in foals tended to be influenced by mare AA supplementation with foals from Con mares having higher concentrations compared to Arg (P <= 0.09) An influence of age was observed on foal AUCg and AUCi. Foal AUCg was greater at 5 d compared to 30 d (P <= 0.003). Foal AUCi tended to be greater at 30 d compared to 5 d (P <= 0.08). Data suggest maternal plane of nutrition and arginine supplementation can alter mare and foal glucose and insulin dynamics.

Proefschrift Universiteit van Amsterdam. / Omslagtitel: Implications of arginine deficiency for growth and organ development. Met bibliogr., lit. opg. - Met samenvatting in het Nederlands.

Thesis (M. Phil.)--University of Hong Kong, 1997. / Includes bibliographical references (leaf 150-164).

Thesis (M.S.)--University of Wisconsin--Madison, 1950. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1975. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.