Rates of whole body amino nitrogen flux were measured in 16 obese adolescents undergoing weight reduction with a high protein low energy diet. The subjects received approximately 2.5 g of animal protein per day per kilogram ideal body weight and maintained nitrogen balance throughout the 18 days on the diet. Flux rates were calculated separately from the cumulative excretion of 15N in urinary ammonia and urea following the administration of a single dose of [15N]glycine. The pattern of 15N label appearance in urinary ammonia and urea nitrogen was followed for 72 h after the administration of [15N]glycine. Significant amounts of label continued to be excreted in both urinary ammonia and nitrogen for 36-48 h after label administration. The weight-reducing diet accelerated 15N cumulative excretion in urinary urea, but not in ammonia nitrogen compared with the control diet. Whole body nitrogen flux rates increased rapidly and significantly on the diet. Using the urea end product, this increase was evident on the 4th diet day, but not by the 7th or subsequent days. On the other hand, using the ammonia end product, flux rate increased markedly (p less than 0.0001) and remained elevated throughout the whole study. Our results demonstrate adaptive changes in whole body amino-nitrogen metabolism in response to the reducing diet. Different patterns of change are seen depending upon whether an ammonia or a urea end product is used. Our data thus add to the evidence for compartmentation of the body's amino-nitrogen pools.
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Am J Kidney Dis
January 2025
Division of Nephrology and Hypertension, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Renal tubular acidoses (RTAs) are a subset of non-anion gap metabolic acidoses that result from complex disturbances in renal acid excretion. Net acid excretion is primarily accomplished through the reclamation of sodium bicarbonate and the buffering of secreted protons with ammonia or dibasic phosphate, all of which require a series of highly complex and coordinated processes along the renal tubule. Flaws in any of these components lead to the development of metabolic acidosis and/or a failure to compensate fully for other systemic acidoses.
View Article and Find Full Text PDFCureus
December 2024
Emergency and Critical Care Medicine, Iizuka City Hospital, Iizuka, JPN.
Urinary tract infections (UTIs) caused by urease-producing bacteria are known to cause hyperammonemia; however, non-urease-producing bacteria can also cause it. This report describes a case of an 87-year-old woman who developed hyperammonemia and impaired consciousness resulting from a UTI caused by the non-urease-producing bacterium, (). On admission, the patient presented with urinary retention, hyperammonemia (281 μg/dL), and alkaline urine (pH 8.
View Article and Find Full Text PDFJ Anim Sci
December 2024
College of Animal Science and Technology, Northwest A&F University, Yangling Shaanxi 712100, China.
The differences between the high-starch diet commonly used in rabbit farming and the natural feeding habits of rabbits may pose certain health risks. In our study, we replaced part of the starch in the feed with soybean oil and conducted a four-week feeding trial with weaned Rex rabbits. The results indicated that rabbits fed the oil-supplemented diet had a lower incidence of diarrhea, improved growth performance, and higher feed conversion efficiency, along with increased absorptive capacity of small intestine.
View Article and Find Full Text PDFNeurol Genet
December 2024
From the Department of Pediatrics (C.Z., J. Shan, J. Su, G.W., R.X., M.D.), Qilu Hospital of Shandong University; Department of Respiratory Disease (J. Su), Children's Hospital affiliated to Shandong University, Jinan; and Department of General Practice (Q.H.), Fourth People's Hospital of Jinan, China.
Background And Objectives: Cases and studies of neurologic symptoms in children caused by genetic metabolic diseases have been widely reported. Ornithine transcarbamylase deficiency (OTCD) is the most common urea cycle disorder, which is due to mutations in the OTC gene located on chromosome Xp21.1.
View Article and Find Full Text PDFFEMS Microbes
September 2024
University of Minnesota Medical School, Minneapolis, MN 55455, United States.
is a commensal bacterium in the gastrointestinal (GI) tract of humans and other organisms. also causes infections in root canals, wounds, the urinary tract, and on heart valves. metabolizes arginine through the arginine deiminase pathway, which converts arginine to ornithine and releases ATP, ammonia, and CO.
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