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PubMed1995

Utilization and preferred metabolic pathway of ketone bodies for lipid synthesis by isolated rat hepatoma cells.

Morris hepatoma 7777 cells freshly isolated from highly malignant tumors grown in the hindlimb of buffalo rats actively convert ketone bodies to cholesterol and fatty acids. On the basis of results obtained with (-)-hydroxycitrate, an inhibitor of the ATP citrate lyase enzyme, the metabolic pathway for acetoacetate conversion to lipids is exclusively cytoplasmic, whereas that for 3-hydroxybutyrate involves both extra- and intramitochondrial compartments. Subcellular distribution studies indicated accumulation and compartmentation of 3-hydroxybutyryl CoA primarily in the cytoplasm of hepatoma cells incubated with either ketone body. In contrast, the compartmentation of acetoacetyl CoA is dependent on whether the substrate is acetoacetate or 3-hydroxybutyrate. With acetoacetate, the acetoacetyl CoA is entirely cytoplasmic, whereas with 3-hydroxybutyrate, it is equally divided between the intra- and extramitochondrial compartments. The results are discussed in terms of the known and proposed metabolic pathways for lipid synthesis from ketone bodies, particularly that from 3-hydroxybutyrate.

3-Hydroxybutyric Acid↗
PubMed1987

Study of ketone body kinetics in children by a combined perfusion of 13C and 2H3 tracers.

Ketone body kinetics were quantified in six children (3-5 yr old), who were fasted for 13-22 h, by a combined perfusion of [3-13C]acetoacetate ([13C]AcAc) and D-(-)-beta-[4,4,4-2H3]hydroxybutyrate (beta-[2H3]OHB) and gas chromatography-mass spectrometry analysis. Results were analyzed according to the "single-pool" (combined enrichments) or the "two-accessible pools" models. After 20-22 h of fasting, ketone body turnover rate was 30-50 mumol.kg-1.min-1, a rate achieved after several days of fasting in adults. At low ketosis, acetoacetate was the ketone body preferentially synthesized de novo and utilized irreversibly. When ketosis increased, acetoacetate irreversible disposal was not enhanced, since it was largely converted into beta-OHB, whereas beta-OHB irreversible disposal was very much increased. The single-pool and two-pool models gave similar ketone body turnover rates when [13C]AcAc was the tracer, whereas the use of beta-[2H3]OHB gave some more divergent results, especially at low ketosis. These studies demonstrate that ketogenesis is very active in short-term fasted children and that the use of a combined infusion of [13C]AcAc and beta-[2H3]OHB is a convenient way to give insight into individual ketone body kinetics.

3-Hydroxybutyric Acid↗
PubMed1990

Validation of two-pool model for in vivo ketone body kinetics.

Previous studies have indicated that simultaneous infusions of two ketone body tracers ([13C]acetoacetate and [14C]beta-hydroxybutyrate) provide accurate estimates of exogenous ketone body inflow when an open two-pool model is employed. In the present studies, net hepatic ketone body production was determined from surgically placed arterial, portal venous, and hepatic venous catheters in conscious diabetic (n = 6) and 4-day fasted (n = 7) dogs. [13C]acetoacetate and [14C]beta-hydroxybutyrate were infused simultaneously, and ketone body production was calculated from either acetoacetate (AcAc) single-isotope data, beta-hydroxybutyrate (beta-OHB) single-isotope data, the sum of individual fluxes, or the two-pool model. In fasted animals, both the AcAc single-isotope calculation and the sum of individual fluxes overestimated net hepatic production by approximately 50% (P less than 0.05), whereas the beta-OHB single-isotope calculation and the two-pool model gave accurate estimates. In the diabetic animals, the beta-OHB single-isotope calculation underestimated net hepatic production by approximately 30% (P less than 0.05). The sum of individual fluxes overestimated net hepatic production by approximately 46% (P less than 0.05), whereas both the AcAc single-isotope calculation and the two-pool model gave accurate estimates. In conclusion, single-isotope methods give erroneous estimates of net hepatic production of ketone bodies. In contrast, a two-pool model provided an accurate estimate of net hepatic production and thus appears to be suitable for determination of ketone body kinetics in humans.

3-Hydroxybutyric Acid↗
PubMed1976

Metabolism of ketone bodies by ovine brain in vivo.

Ketosis was produced by intravenous infusion (5 mmol/kg per h) of [3-14C]acetoacetate (sp act 0.5 muCi/mmol) into fed and 7-day-fasted sheep. Changes in arterial and sagittal sinus blood samples. During acetoacetate infusion, there was a significant increase in ketone body uptake (P less than 0.001) and conversion to 14CO2 in both fed and fasted sheep. Changes in arterial concentrations and cerebral removal of various metabolites were investigated by simultaneous collection of arterial and sagittal sinus blood samples. During acetoacetate infusion, there was a significant increase in ketone body uptake (P less than 0.001) and conversion to 14CO2 in both fed and fasted sheep when compared to control periods (saline infusion). The percent conversion of ketone bodies to 14CO2 was slightly higher in fasted sheep (22%) compared to fed sheep (18%). Blood glucose and free fatty acid concentrations were decreased, but there was a significant increase in blood lactic acid and lactic acid production by the brain. The plasma insulin concentration was increased significantly both in fed and fasted animals. These results indicate that ovine brain can utilize ketone bodies irrespective of nutritional state. In addition, ketone bodies stimulated the production of lactate by ovine brain.

Acetoacetates↗
PubMed1988

Metabolic mapping of functional activity in the olfactory system of normal and hypogonadal (hpg) mice.

The hypogonadal mouse, which lacks gonadotropin-releasing hormone, has been suggested as an animal model of Kallmann's syndrome, one symptom of which is hyposmia. We have determined the metabolic activity of the olfactory system, in normal and hypogonadal mice, using [14C]-2-deoxyglucose quantitative autoradiography. In the olfactory lobes, deoxyglucose uptake was greatest in the glomerular and granule cell layers and low in the olfactory nerve layer and bulb core. The pattern of uptake was similar in both hypogonadal and normal mice breathing filtered air. Exposure of normal mice to ethyl acetoacetate significantly increased deoxyglucose uptake in the olfactory nerve layer and glomerular layer, but not in the granule cell layer. Several foci of intense metabolic activity were produced, apparently corresponding to small groups of activated glomeruli. There were no changes in the secondary or tertiary projections of the olfactory system. In hypogonadal mice, ethyl acetoacetate failed to increase the number of foci and the density of labelling in the olfactory nerve layer and glomerular layer. These data show that the functional activity of the olfactory system in hypogonadal mice breathing air is apparently normal. However, the olfactory response to ethyl acetoacetate is significantly less in hypogonadal mice. Whether this is due to their lack of gonadotropin-releasing hormone requires further experimentation.

Acetoacetates↗
PubMed1971

Glucose and lipid homeostasis in the absence of human growth hormone.

To clarify the role of insulin and growth hormone (HGH) in regulating substrate production for body fuel during prolonged starvation, 6 normal subjects and 10 HGH-deficient dwarfs were fasted for 6 days. Four of these dwarfs received HGH during the fast. Blood glucose concentration decreased a mean 15 mg/100 ml in both controls and HGH-treated dwarfs, but decreased 50 mg/100 ml in untreated dwarfs. The final level at which the blood glucose stabilized was significantly higher in the former two groups (65 +/-1.0 mg/100 ml and 88 +/-19 mg/100 ml, respectively, versus 39.0 +/-4.0 mg/100 ml in the untreated dwarfs). The decline in plasma insulin concentration showed a comparable pattern, decreasing from a similar basal level to 7.7 +/-0.4 muU/ml in controls, 8.8 +/-1.1 muU/ml in dwarfs treated with HGH, and to a significantly lower level of 3.8 +/-1.1 muU/ml in untreated dwarfs. When glucose concentrations were plotted against paired insulin values, the correlation in both dwarfs and normals was significant. In normals, no correlation existed at any time between plasma HGH levels and plasma concentration of either glucose or free fatty acid. Free fatty acid, beta-hydroxybutyrate, and acetoacetate increased respectively in normals to peak concentrations in plasma of 1.55 +/-0.11, 2.87 +/-0.23, and 0.77 +/-0.09 mmoles/liter. Untreated dwarfs had significantly greater values of all three (mean maximal concentration: FFA = 2.16 +/-0.17 mmoles/liter, beta-hydroxybutyrate = 4.11 +/-0.34 mmoles/liter, and acetoacetate = 1.16 +/-0.10 mmoles/liter). Values returned toward normal in HGH-treated dwarfs. The cahnges in plasma concentrations of beta-hydroxybutyrate and acetoacetate were not due to changes in renal excretion. In starvation, the relation between insulin on the one hand and glucose and free fatty acid on the other hand is maintained in the absence of HGH. However, the setting of blood glucose concentration at which this relation takes place is decreased in the absence of HGH. This results in a lower than normal insulin level and, consequently, in a higher than normal free fatty acid concentration.

Acetoacetates↗
PubMed1974

Ketone-body production and oxidation in fasting obese humans.

Rates of plasma acetoacetate and total ketone-body production and oxidation to CO2 were determined by an isotope tracer technique in eight obese subjects undergoing progressive starvation. After a brief fast and under conditions of mild ketonemia and minimal ketonuria, rates of acetoacetate and total ketone-body production and oxidation were directly related to the increasing plasma concentration. After a longer fast and with severer ketonemia, acetoacetate and total ketone-body production and oxidation rates were higher but became constant and unrelated to the plasma concentrations. The maximum rates of total ketone-body production and oxidation were about 150 g/24 h and 129 g/24 h, respectively. Although an increased ketone-body production was the primary factor responsible for the hyperketonemia, an imbalance between production and removal of the ketone bodies cannot be excluded. Such an imbalance could account, at least in part, for the developing hyperketonemia and for the lack of relationship between production rates and plasma concentrations.

Acetoacetates↗
PubMed1976

The rate of cerebral utilization of glucose, ketone bodies, and oxygen: a comparative in vivo study of infant and adult rats.

Cerebral blood flow (CBF) was measured by means of Celabeled microspheres in infant (20-day-old) and adult (3-month-old) rats, anesthetised with Na-5-ethyl-5-(1-methylpropyl)2-thiobarbituric acid. Cerebral arteriovenous differences of acetoacetate, D-beta-hydroxybutyrate, glucose, lactate, and oxygen and brain DNA content were determined in other groups of similarly treated infant and adult animals fed or starved for 48 or 72 hr. The mean CBF values of 0.48+/-0.04 and 0.62+/-0.07 ml/(g X min), +/- SEM, in infant and adult animals, respectively, were not significantly different. CBF was unaffected by starvation. At any given arterial concentration the cerebral arteriovenous difference of acetoacetate was significantly higher in infant than adult rats. The same was true for D-beta-hydroxybutyrate at arterial concentrations above 1 mmol/liter. There was an approximately linear relationship between arterial concentration of acetoacetate and its cerebral arteriovenous difference in both infant and adult rats. A similar relationship was found for D-beta-hydroxybutyrate only in infant animals. In the fed state, the cerebral uptake of glucose and ketone bodies (micromoles per (mg DNA X min)) was not different in infant and adult rats. During starvation, cerebral uptake of ketone bodies expressed as micromoles per (mg DNA X min) was higher in infant than adult rats, indicating a higher rate of utilization of ketone bodies per cell in these animals. For glucose, no such difference was found in either fed or starved groups (Table 3). The average percentage of the total cerebral uptake of substrates (micromoles per min) accounted for by ketone bodies increased in both infant and adult rats during starvation. This percentage value was clearly higher in infant than adult rats during starvation. After 72 hr of starvation the values were 38.8% and 15.2% in infant and adult rats, respectively (Fig. 3). Calculated cerebral metabolic rate for oxygen (CMRO2), assuming complete oxidation of glucose and ketone bodies and expressed as micromoles per (mg DNA X min), was similar in fed and starved rats of both age groups (Table 3), indicating that ketone bodies serve as an alternative substrate for glucose during starvation. Calculated CMRO2 for glucose plus ketone bodies was similar to the measured CMRO2 in adult rats both in the fed and the starved groups. For infant rats, calculated CMRO2 for glucose plus ketone bodies was higher than measured CMRO2, indicating that in this age group a portion of substrate was used for synthesis or storage rather than for complete oxidation.

Acetoacetates↗
PubMed1984

On the state of calcium ions in isolated rat liver mitochondria. II. Effects of phosphate and pH on Ca2+-induced Ca2+ release.

At high K+ concentration, the effect of phosphate on Ca2+ uptake and release was studied in isolated rat liver mitochondria. Phosphate stimulated uptake at moderately high Ca2+ concentration, and inhibited release at high pH. At low pH, phosphate accelerated Ca2+ release. Ca2+ was released after a lag phase. The time of onset and the velocity of Ca2+ release depended on Ca2+ concentration. Ca2+ release was associated with mitochondrial swelling and destruction of the permeability barrier for sucrose and for chloride. Mg2+ inhibited Ca2+ release and the accompanying events. Ruthenium red and EGTA protected mitochondria from the destructive Ca2+ release and induced an immediate, slow release of Ca2+ and phosphate. Destructive Ca2+ release depended on the time of preincubation of respiration-inhibited mitochondria in the presence of Ca2+, prior to respiration-initiated Ca2+ uptake. The presence of phosphate and mitochondrial energization antagonized the destructive effect of calcium ions. Ca2+ release by acetoacetate also depended on pH. At pH 6.8, phosphate-stimulated Ca2+ release by acetoacetate, while it inhibited the acetoacetate effect at pH 7.6. The results suggest that an essential cause for the destruction of mitochondrial integrity is an increase in the intramitochondrial concentration of free calcium ions under the influence of phosphate.

Acetoacetates↗
PubMed2005

Quantitative measurement of ketone bodies in urine using reflectometry.

BACKGROUND: Recently, automated urine test strip readers became available that can report quantitative data. We explored the possibility of measuring all ketone bodies (acetone, acetoacetate, 3-hydroxybutyrate) in urine with these test strips. Monitoring urinary ketone concentrations could offer the advantages of measuring higher values (due to the low renal thresholds) and being less sensitive to fluctuations. METHODS: We evaluated URISYS 2400 (Roche) quantitative reflectance data for the ketone reflectance field and compared it with biochemical data from urine samples. Using an easy sample pre-treatment with 3-hydroxybutyrate dehydrogenase, we were able to assay 3-hydroxybutyrate as well, which normally does not react on urine test strips. RESULTS: Within- and between-run reproducibility of the reflectance signal for high- and low-concentration urine pools was 11.0-3.6% and 11.0-5.8% for aceto-acetate, 8.2-9.2% and 10.4-16.1% for acetone, and 5.1-3.0% and 5.6-3.5% for 3-hydroxybutyrate, respectively. The lower limit of detection for acetoacetate was 0.13 mmol/L (CV=3.6%). Fair agreement was obtained between test strip data for ketones andcolorimetrically determined acetoacetate values (r=0.90). CONCLUSIONS: In urine test strip analysis, quantitative ketone reflectance data allow a simple and fast analysis, offering affordable screening for the detection of ketone body production in diabetes, especially in emergency settings.

3-Hydroxybutyric Acid↗
PubMed1987

Effects of hyperglycemia and ketone bodies on the in vitro development of early somite rate embryos.

The teratogenic effects of diabetes are attributed to the influence of hyperglycemia and hyperketonemia as well as to other metabolic factors. We studied the effects of ketone bodies and glucose on the development of early somite rat embryos (day 10 1/2 of gestation) cultured in vitro. D-glucose was added to normal rat serum in concentrations of 2, 5, and 10 mg/ml. Ketone bodies (acetoacetate and beta-hydroxybutyrate, B-HOB) were individually added to normal or to hyperglycemic sera (total glucose concentrations of 3 mg/ml) in the following concentrations: acetoacetate--5, 10, 20, and 40 micrograms/ml; B-HOB--2, 5, and 8 mg/ml. The higher concentrations of each of the substances induced growth retardation and abnormalities. The growth-retarding and teratogenic effects of a combination of the substances, glucose and B-HOB, glucose and acetoacetate, on the development of 10 1/2 day embryos were greater than when each substance was added separately, even at relatively low doses. The greatest teratogenic effects were observed when low concentrations of all three substances were added simultaneously to the culture medium. These results may have direct relevance to human diabetes since diabetes is characterized by a simultaneous elevation of serum levels of all these substances.

3-Hydroxybutyric Acid↗
PubMed2001

Ketone bodies in milk and blood of dairy cows: relationship between concentrations and utilization for detection of subclinical ketosis.

The objective of this study was to investigate the relationship between the concentrations of the different ketone bodies in milk and blood and to evaluate these concentrations for the detection of subclinical ketosis. A total of 60 multiparous cows were used. Concentrations of acetone, acetoacetate, and beta-hydroxybutyrate were analyzed quantitatively in blood and milk, and the Ketolac strip test was used for semiquantitative determination of beta-hydroxybutyrate in milk. Cows were defined subclinically ketotic when their concentration of blood beta-hydroxybutyrate was over 1200 micromol/L. High correlation coefficients were observed between blood acetone and blood acetoacetate, and between blood and milk acetone. On the contrary, concentrations of milk and blood beta-hydroxybutyrate were poorly correlated with the other concentrations of ketone bodies. The Ketolac strip test overestimated the concentrations of beta-hydroxybutyrate in milk. For the detection of subclinical ketosis, the best sensitivity-specificity combination was obtained with the determination of acetoacetate in blood or milk, with threshold concentrations of 125 and 50 micromol/L, respectively. Determination of beta-hydroxybutyrate in the milk via an enzymatic analysis or via the Ketolac strip test provided valuable results, with threshold concentrations of 70 and 100 micromol/L, respectively. The simplicity of use of the Ketolac strip test makes it a valuable way to investigate subclinical ketosis.

3-Hydroxybutyric Acid↗
PubMed1986

Autoregulation of alimentary and hepatic ketogenesis in sheep.

To determine the mechanism of autoregulation of ketogenesis, beta-hydroxybutyrate was infused into 5 normal; 3 diabetic, insulin-treated; and 3 diabetic, untreated anesthetized sheep. Net flux of fatty acids, acetoacetate, beta-hydroxybutyrate, and insulin were measured across splanchnic tissues by multiplying venoarterial differences by blood flow. beta-hydroxybutyrate depressed fatty acid concentrations and hepatic uptake. This decrease in hepatic uptake was not due solely to decreased concentrations, because hepatic extraction decreased 40% in normal and insulin-treated sheep. Portal-drained visceral release of acetoacetate was increased by beta-hydroxybutyrate infusion in normal and insulin-treated sheep, but this was associated with even larger increases in hepatic uptake, resulting in decreased total splanchnic release. Portal-drained viscera switched from release to uptake of beta-hydroxybutyrate in both normal and insulin-treated animals, but hepatic release increased slightly in normal sheep. beta-hydroxybutyrate increased insulin concentration, pancreatic production, and hepatic uptake. Because effects of ketone infusion on net fluxes of fatty acids, acetoacetate, and beta-hydroxybutyrate were similar in normal and diabetic, insulin-treated sheep but were diminished or totally absent in diabetic, untreated animals, the mechanism of autoregulation of ketogenesis may be mediated at the insulin receptor or at the site of hepatic fatty acid uptake.

3-Hydroxybutyric Acid↗
PubMed1992

Etiology of acetonemia in Norwegian cattle. 2. Effect of butyric acid, valeric acid, and putrescine.

A feeding experiment was performed on 16 cows in order to test the effect of naturally occurring substances in silage on forage intake, ketonemia, and milk yield. The cows were divided into a control group and three experimental groups. The cows in the three experimental groups were fed 100 g/d of putrescine, 200 g/d of valeric acid, or 200 g/d of butyric acid through a ruminal tube for 3 d. Butyric acid increased plasma acetoacetate; the effect was largest in high yielding cows. Putrescine influenced both milk yield and forage intake and may possibly be a contributory factor, alone or combined with other amines, for the development of ketonemia. Valeric acid did not influence feed intake or plasma acetoacetate concentration. A rapid method for acetoacetate analysis also is described.

Acetoacetates↗
PubMed2000

[Metabolic acidosis and ketone body in severely head-injured patients].

Increase of ketone body concentration in plasma is induced by various factors such as onset of diabetes. Secretion of excessive stress hormone including catecholamine is responsible for stimulation of lipolysis which increases plasma ketone body concentration. Catecholamine levels reflect the severity of the neurologic insult, so this is a basis for the use of catecholamine measurements as a physiological marker of patient outcome. Twenty-seven patients with severe head injury and twenty-five healthy volunteers were enrolled in this study, but patients with diabetes or liver dysfunction were excluded. The patients with severe head injury consisted of 19 with focal injury and 8 with diffuse injury. The outcome was as follows; 14 patients died and 13 patients survived. We collected arterial blood samples as promptly as possible after onset of severe head injury and measured the following: 1, base excess; 2, beta-hydroxybutyrate; 3, acetoacetate; 4, lactate; 5, epinephrine; 6, norepinephrine. The ketone body (beta-hydroxybutyrate + acetoacetate) concentration in plasma was significantly elevated in patients with severe head injury. The increment of beta-hydroxybutyrate levels was greater than that of acetoacetate levels, resulting decreased arterial ketone body ratio (AKBR; acetoacetate/beta-hydroxybutyrate). We demonstrated that plasma ketone body concentrations were elevated and the AKBR decreased in severe head-injured patients. Elevation of catecholamine has been reported as a stress reaction in severe head injury. Catecholamine is most potent in stimulating lipolysis, and ketogenesis. Therefore, the ketonemia observed in severe head injury is most likely to be induced by elevation of catecholamine levels. The degree of ketonemia may be an index of the severity of severe head injury.

3-Hydroxybutyric Acid↗
PubMed1992

Ketone body-induced dissociation between hepatocyte gluconeogenesis and ureagenesis in acutely uremic rats.

Ketone body production in isolated liver cells and the effect of ketone bodies on hepatocyte urea and glucose production were investigated in acutely uremic rats. Blood beta-hydroxybutyrate levels of starved acutely uremic rats were reduced compared to starved sham-operated controls, suggesting a failure to develop hyperketonemia. On the other hand, beta-hydroxybutyrate concentration is elevated in the liver. Hepatocyte beta-hydroxybutyrate production of acutely uremic animals is enhanced using serine as a substrate. Addition of ketone bodies abolishes this effect. Blood acetoacetate levels of starved acutely uremic rats are elevated compared to sham-operated controls. Liver acetoacetate concentration is unchanged in acute uremia. Hepatocyte acetoacetate production of acutely uremic rats is stimulated using serine and alanine as substrates. Again, this effect is reversed by addition of ketone bodies. Addition of ketone bodies does not affect enhanced glucose production from serine or alanine in hepatocytes of acutely uremic rats but decreases markedly enhanced urea production from serine (156 +/- 35.2 versus 27.4 +/- 7.1) and alanine (80.0 +/- 22.3 versus 42.0 +/- 4.4 nmol mg-1. 30 min-1), especially after bilateral nephrectomy. The data show that the two processes of gluconeogenesis and ureagenesis can be dissociated in hepatocytes of bilaterally nephrectomized rats by the addition of ketone bodies. The finding that ketone bodies decrease the rate of urea production may be worth further study.

3-Hydroxybutyric Acid↗
PubMed1991

[Lipolysis and ketosis during swimming in thermal water].

Plasma free fatty acids, blood glucose, beta-hydroxybutyrate and acetoacetate variations were studied in rats during swimming. Rats were forced to swim for 30 min in thermal water (source of Abano Terme) at 35 degrees and in normal water at 25 degrees. During swimming in thermal water plasma free fatty acids were increased, the glycemia remained unaffected, the beta-hydroxybutyrate and acetoacetate decreased. The swim in normal water induced a sharp increase of plasma free fatty acids, a decrease of blood glucose, an increase of blood beta-hydroxybutyrate and a marked decrease of acetoacetate. From these data, some indications of clinical interest are presented and discussed.

3-Hydroxybutyric Acid↗
PubMed1991

Effects of interferents on the kinetic Jaffé reaction and an enzymatic colorimetric test for serum creatinine concentration determination in cats, cows, dogs and horses.

The effects of acetoacetic acid, acetone, bilirubin, beta-carotene, three cephalospoprin antibiotics, glucose, hemoglobin and lipid on the kinetic Jaffé reaction and an enzymatic reaction for the determination of creatinine concentration were studied in bovine, canine, feline and equine serum. There were no obvious species' differences. The kinetic Jaffé reaction was unaffected by the addition of beta-carotene and hemoglobin. Acetone, cefazolin, cefoxitin, ceftiofur and glucose caused a positive bias while acetoacetic acid, bilirubin, and lipid caused a negative bias when added to the kinetic Jaffé reaction. The enzymatic reaction was unaffected by the addition of acetoacetic acid, acetone, beta-carotene, cefazolin, cefoxitin, glucose and hemoglobin while added lipid, bilirubin and ceftiofur caused a negative bias in the test results. Over all species and interferents, there was no difference in the precision of the two assay methods. In a series of sera from hospitalized patients, the two methods were highly correlated in a linear fashion. The enzymatic creatinine assay deals effectively with most interferents but has a greater cost and shorter shelf-life compared with the kinetic Jaffé reaction.

Acetoacetates↗