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Biomedical subjects

J A Milner

Publications and source records attributed to J A Milner.

At least 127 records · Page 7Linked to original sources
PubMed1979

Assessment of the essentiality of methionine, threonine, tryptophan, histidine and isoleucine in immature dogs.

A completely purified L-amino acid diet was used to evaluate the indispensability of methionine, threonine, tryptophan, histidine and isoleucine in the immature dog. Immature dogs fed diets devoid of methionine, threonine, tryptophan, histidine or isoleucine had severely depressed food intakes, accompanying weight loss, and a distinctly negative nitrogen balance. Partial or total removal of these amino acids resulted in a marked increase in blood and urinary urea. Estimates are made for the dietary requirements for these amino acids in the immature dog.

Alanine Transaminase↗
PubMed1978

Liver lipid alterations in rats fed arginine deficient diets.

Arginine deficiency is associated with a marked increase in liver lipids in the rat. Triglyceride accumulation accounts for most of the fatty infiltration. Cholesterol concentration per gram of liver increased approximately 280% above control rats receiving dietary arginine. The percentage of phospholipids was significantly decreased in the arginine-deficient rat liver compared to controls. The fatty acid composition revealed a significant reduction in the reduction in the percentage of palmitic, palmitoleic, oleic, and linoleic acids. However, both stearic and arachidonic acids were increased approximately 250 and 160%, respectively, in arginine-deficient livers compared to controls. Arginine deficiency in the rat causes a marked alteration in lipid metabolism similar to that observed with orotic acid feeding. The similarities or arginine deficiency and orotic acid feeding are discussed.

Animals↗
PubMed1978

Factors affecting amino acid induced orotic aciduria in rats.

Administration of individual amino acids is known to induce an orotic aciduria. The present studies show that the induction of orotic aciduria by glycine is highly influenced by stage of digestion of the test animal and the nitrogen content of the test diet. Short term fasting for 24 hours prevented glycine induced orotic aciduria. However, longer term fasting for 1, 3, 5, or 7 days resulted in a return in the ability of glycine to stimulate pyrimidine biosynthesis. The maximum induced orotic aciduria occurred after 3 days of fasting. The ability of glycine to induce orotic aciduria in the fed rat was also dependent on the dietary protein content. Glycine injections were unable to elicit an orotic aciduria in rats fed a protein-free diet. Addition of increasing quantities of nitrogen to the basal diet resulted in a proportional increase in glycine induced orotic aciduria.

Ammonia↗
PubMed1978

Arginine requirements in immature dogs.

Labrador Retriever puppies (3 kg) were fed L-amino acid (L-AA) diets, containing the equivalent of 14% protein, to determine dietary argnine requirements for optimal growth and maintenance of normal intermediary metabolism. Growth and food consumption were depressed by decreasing the dietary arginine concentration. Urinary citrate and orotate increased with decreasing dietary arginine. Elevated blood orotate, urea and NH4+-N were detected in arginine deficient dogs. More than 0.56% arginine was required to support optimum growth and prevent abnormal loss of urinary metabolites. The effect of dietary nitrogen concentration (14, 21, or 28% L-AA) on arginine requirements was examined in immature Beagles. All arginine deficient dogs and dogs fed the 28% L-AA with arginine showed signs of emesis, excessive salivation and muscle tremors. Hyperammonemia and hyperglycemia were observed 2 hours after force feeding an L-AA diet devoid of arginine. Only hyperammonemia was observed in the Labrador Retrievers fed the same diet but incorporated into a 2% agar gel. Dietary nitrogen concentration or dietary arginine content dit not significantly influence glucose tolerance response to oral glucose loading. These data show that dietary arginine is required in the immature dog and that the requirement is influenced by dietary nitrogen concentration.

Amino Acids↗
PubMed1978

Dietary protein intake and arginine requirements in the rat.

Experiments were conducted with immature rats fed L-amino acid purified diets varying in total N and arginine. The experiments demonstrated that total N intake was the factor responsible for increased orotic acid excretion during arginine deficiency. Increased orotic acid excretion was accompanied by increased liver transaminase activities and increased liver concentrations of NH4-N and glutamine. Arginine requirements for growth and normal metabolite excretion increased as dietary N was increased. Accompanying elevated urinary citrate during N deprivation and arginine deficiency was a depression of liver isocitrate dehydrogenase activity. Citrate excretion was lower if arginine was fed as the HCl compared to the free base. During a partial or total arginine deficiency citrate excretion was elevated at varying dietary N concentrations. Urinary pH was not significantly changed by level of dietary N or arginine.

Amino Acids↗
PubMed1978

Amino acid induced orotic aciduria.

Twenty amino acids were examined for their effects on urinary orotic acid excretion. Except for arginine and ornithine, all of the remaining amino acids tested induced a mild orotic aciduria in rats 2 hours post feeding. Two ammonium salts, and urease also acted, as inducers of orotic aciduria. The ammoneogenic properties of the amino acids tested could not solely explain the induced excretion of orotic acid. Only serine, glutamine, NH4Cl, (NH4)2CO3, and urease increased orotic acid excretion in the 24 hour fasted rat. Administration of 0.5 mmoles of arginine or ornithine ameliorated the mild orotic aciduria induced by either glycine or lysine. Arginine was shown to be more efficacious in preventing glycine induced orotic aciduria than was ornithine. Amino acid induced orotic aciduria is dependent upon the physiological state of the animal, varying with the state of digestion and the supply of arginine.

Amino Acids↗
PubMed1975

Urinary metabolites characteristic of urea-cycle amino acid deficiency.

Experiments with 45-75-g male rats gave conclusive evidence that the simultaneous absence from the diet of arginine, ornithine, or citrulline caused an immediate and persistent elevation of orotic and citric acids in the urine. The experiments also demonstrated that a deficiency of no other individual amino acid increased urinary citrate and orotate. Elevated urinary excretion of orotic and citric acid occurred independently of the form of nonessential nitrogen. Replacement of arginine isonitrogenously with ornithine or citrulline prevented the rise in urinary orotic acid, but had different effects on growth, urinary citrate, and urinary urea. These differences were probably due to differential uptake of arginine, ornithine, and citrulline by tissues; In the reported experiments employing L-amino acids as sources of dietary nitrogen, a deficiency of any amino acid indispensable for growth and nitrogen balance or a deficiency of arginine, ornithine, or citrulline retarded growth, increased urinary urea, and decreased urinary ammonia. It is concluded that the severe loss of orotic acid during urea-cycle amino acid deficiency arises from a decreased capacity of the urea cycle to detoxify ammonia, thereby causing increased shunting of intramitochondrial carbamyl phosphate into pyrimidine synthesis. The similarities in metabolism during arginine deficiency and ammonia intoxication are discussed. The evidence shows that urinary orotic acid may be a valuable measure of arginine nutrition in mammals.

Amino Acids↗
PubMed1975

Urea, citrate and orotate excretion in growing rats fed amino acid-deficient diets.

Male, weanling rats were fed a control purified amino acid diet or the same diet with lysine, phenylalanine, tryptophan, valine, or arginine omitted singly, or both arginine and lysine omitted. Blood urea reached three to four times that of control levels with all deficient diets. Urea excretion increased almost linearly with time during the first 3 days of amino acid deficiency. Rates of urea excretion on day 3 in decreasing order for various deficiencies were as follows: lysine and arginine combined are more than lysine is more than tryptophan equals valine is more that phenylalanine equals arginine. Urinary citrate was 26 and 21.8 times that of control values without arginine and 11.4 and 6.2 times that of control values without lysine on days 2 and 3, respectively. By day 8 citrate excretion had returned to control levels without lysine but not without arginine. Citrate excretion was unchanged with other deficiencies. Orotic acid excretion increased markedly only without arginine and slightly without tryptopahn. A deficiency of arginine and lysine increased urea and citrate excretions to a greater extent than either deficiency alone. Two injections of arginine or homoarginine (0.50 mmole/injection) given at 12-hour intervals to rats fed no lysine and arginine for 3 days decreased citrate excretion immediatedly and on the following day. Urea excretion decreased with injected homoarginine, but not with arginine. Orotic acid excretion increased more than four times on the day of homoarginine injection compared with that of the preceding day. Arginine injection returned orotic acid excretion to nearly control levels within 24 hours. Urea degradation in the gastrointestinal tract was increased in animals fed amino acid-deficient diets.

Amino Acids, Essential↗
PubMed1975

Arginine deficiency and orotic aciduria in mammals.

Dietary arginine deficiency in rats causes significant increases in urinary excretion of urea, citric acid and orotic acid independently of feed intake. Urea excretion during arginine deficiency depends upon the diet, sex, age, and species. Thus urea excretion has limitations as an indicator of arginine availability. Although elevated urinary citric acid during arginine deficiency is more consistently observed, it may be influenced by citric acid in natural dietary ingredients. Orotic acid excretion, however, appears to be a reliable indicator of available dietary arginine based upon studies in rats, mice, hamsters, guinea pigs, rabbits, and dogs.

Animals↗