Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162275 (ketonuria)
 553 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Urine ketone levels were measured in patients receiving peripheral amino acid solutions, and the results were correlated with changes in nitrogen balance. Thirty well-nourished patients who were to undergo cystectomy were placed on liquid, noncarbohydrate diets 3 days before operation, and no oral intake was allowed until 7 days after operation. Crystalline amino acid (1.3 to 1.5 gm/kg/day) solutions were infused continuously from 3 days before to 7 days after operation. Blood was obtained 3 days before and 3, 7, and 10 days after operation; 24-hour urine outputs were determined daily. Qualitative urine acetone levels were determined four times daily. During the infusion period, 14 (47%) patients developed ketonuria (group I); 16 patients did not (group II). The mean serum glucose levels ranged from 99 to 107 mg/dl in group I and from 108 to 113 mg/dl in group II (P less than 0.05). The mean serum transferrin level decreased after operation to 117 mg/dl in group I and 97 mg/dl in group II. The mean cumulative adjusted nitrogen balance was -24 +/- 8 gm in group I and -47 +/- 9 gm in group II (P less than 0.05). No patient developed sepsis. Qualitative testing of urinary ketones correlated with significant alterations in blood urea nitrogen, serum glucose, transferrin, and cumulative adjusted nitrogen balance. The bedside determination of urinary ketones may be useful in assessing a patient's adaptation to peripheral amino acid infusions.
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PMID:Adaptation to amino acid infusion in patients undergoing operation. 683 5

The metabolic adaptation in man to starvation, semistarvation, and carbohydrate restriction is complex and involves a number of hormones, substrates, and tissues. In particular, however, the need for the ketoacids beta-hydroxybutyric acid and acetoacetic acid to replace glucose as the primary fuel for the brain of fasting man appears to be the key to maximum protein conservation. That is, ketogenesis is necessary to provide the brain with a fat-derived, water-soluble, insulin-independent, glucose-equivalent fuel. This adaptation is associated with a small loss of the ketoacids into the urine (100-150 mM/day or 40-60 calories/day). The ketonuria, in turn, necessitates increased renal utilization of muscle-derived glutamine. Synthesis of glutamine by muscle requires muscle proteolysis. Administration of glucose in amounts needed to meet the requirements of the brain results in suppression of ketogenesis in fasting man and a significant diminution in nitrogen mobilization and utilization as well.
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PMID:Metabolic adaptations to starvation, semistarvation, and carbohydrate restriction. 702 58

The purpose of these experiments was to determine if augmented renal ammoniagenesis in chronic metabolic acidosis could increase the negative nitrogen balance during prolonged fasting. To explore this question, rats and rabbits were fasted for up to 10 days because acidosis would markedly augment ammonium excretion in the rat but not in the rabbit. Since the ketoacidosis of fasting was mild in both species (less than 2 mM) and ketonuria virtually absent, a hydrochloric acid load was given to stimulate renal ammoniagenesis. Under these conditions, nitrogen balance was significantly more negative during acidosis in the rat but not in the rabbit. This increment in nitrogen excretion appeared as ammonium with no detectable difference in urea nitrogen excretion. Therefore, it appears that if more nitrogen is excreted as ammonium, net protein breakdown increases to furnish the substrate for ammoniagenesis rather than reducing the excretion of the other nitrogenous waste component urea. The implications of these findings will be discussed.
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PMID:Role of acidosis in the protein wasting of fasting in the rat and the rabbit. 707 21

Effects of feeding a dry glycerin product (minimal 65% of food grade glycerol, dry powder) to 39 multiparous Holstein dairy cows (19 control and 20 glycerin-supplemented; lactation number = 2.2 +/- 1.3 SD) on feed intake, milk yield and composition, and blood metabolic profiles were investigated. Dry glycerin was fed at 250 g/d as a top dressing (corresponding to 162.5 g of glycerol/d) to the common lactating total mixed ration from parturition to 21 d postpartum. Individual milk was sampled from 2 consecutive milkings weekly and analyzed for components. Blood was sampled from the coccygeal vein at 4, 7, 14, and 21 (+/-0.92, pooled SD) d in milk and analyzed for urea nitrogen, glucose, insulin, nonesterified fatty acids, and beta-hydroxybutyrate. Urine was tested for the acetoacetate level weekly by using Ketostix. Average feed intake, milk yield and components, blood metabolites, and serum insulin concentrations were not affected by dry glycerin supplementation. Glycerin-supplemented cows experienced a more positive energy status (higher concentrations of plasma glucose, lower concentrations of plasma beta-hydroxybutyrate, and lower concentrations of urine ketones), which was observed during the second week of lactation, suggesting that energy availability may have been improved. This glucogenic effect of dry glycerin did not result in an increase in feed intake or milk yield during the first 3 wk of lactation, likely because of the relatively less negative energy status of cows transitioning into lactation. The tendency toward higher milk yield for glycerin-supplemented cows during wk 6 of lactation (52 vs. 46 kg/d) after the supplementation period (dry glycerin was terminated at wk 3 of lactation) suggested a potential benefit of dry glycerin on subsequent milk production, perhaps through changes in metabolism, which requires further investigation.
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PMID:Effects of feeding dry glycerin to early postpartum Holstein dairy cows on lactational performance and metabolic profiles. 1802 60


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