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PubMed2003

Analysis of total propionic acid in feed using headspace solid-phase microextraction and gas chromatography.

A method is described to analyze total propionic acid content (free propionic acid + sodium, ammonium, calcium salts, etc.) in feed, using headspace solid-phase microextraction (HS-SPME) of a feed suspension in salted and acidified water. Optimization of the extraction variables was done by simplex method after choosing a polyacrilate fiber to enhance the response of this acid. Separation was made by capillary gas chromatography (GC), using a special free fatty acid phase (FFAP) column for acids and a flame ionization detector (FID). Some of the chromatograms were also done, injecting the SPME fiber in a GC-mass spectrometry (MS) system, working with some specific ions for propionic acid, to be selective enough to avoid confusing the propionic acid peak with interferences of those complex matrixes. The method was tested for linearity and repeatability. Detection and quantification limits were also calculated. The method was applied to commercial feed samples, very variable in composition, quantifying by standard addition method. No major interferences were observed.

Animal Feed↗
PubMed2006

A Salmonella-based, propionate-inducible, expression system for Salmonella enterica.

The expression and regulatory properties of a propionate-regulated overexpression system (Salmonella enterica prpBCDE promoter (P(prpB)) and positive regulator (prpR)) were evaluated in wild-type S. enterica serovar Typhimurium TR6583 and prpB(-) or prpD(-) versions of this strain and compared with the arabinose-regulated T7 expression system. The wild-type strain showed low expression in the absence of propionate and high expression in the presence of propionate under all growth conditions. In 96-well plates and culture tubes, the wild-type strain exhibited a long delay before full induction; the time delay was significantly shorter in shake flasks. The prpD(-) strain exhibited low expression in the presence of glucose, highly regulatable expression over a wide range of propionate concentrations, and, in contrast to the wild-type strain, fast induction to full expression under all growth conditions. In contrast, the prpB(-) strain showed very high background expression in both culture tubes and shake flasks.

Arabinose↗
PubMed2004

Interspecies electron transfer in methanogenic propionate degrading consortia.

Propionate is a key intermediate in the conversion of complex organic matter under methanogenic conditions. Oxidation of this compound requires obligate syntrophic consortia of acetogenic proton- and bicarbonate reducing bacteria and methanogenic archaea. Although H(2) acts as an electron-carrier in these consortia, evidence accumulates that formate plays an even more important role. To make energy yield from propionate oxidation energetically feasible for the bacteria and archaea involved, the concentrations of H(2) and formate have to be extremely low. On the other hand, the diffusion distance of these carriers has to be small to allow high propionate conversion rates. Accordingly, the high conversion rates observed in methanogenic bioreactors are due to the fact that the propionate-oxidizing bacteria and their methanogenic partners form micro-colonies within the densely packed granules.

Bacteria↗
PubMed2002

Esterification of the propionate groups promotes alpha/beta hemoglobin chain homogeneity of CN-hemin binding.

This study examines the post-translational role of peripheral propionate groups in the incorporation of the Fe-protoporphryin IX heme into nascent alpha- and beta-globin chains. Human apohemoglobin (a heme-free alpha/beta dimer) in 0.05 M potassium phosphate buffer, pH 7, at 20 degrees C was titrated with either CN-protohemin (native heme with two peripheral propionate groups), or CN-dimethylester hemin (a modified heme with two methyl ester groups in place of the propionate groups). Soret spectrophotometric CN-hemin titrations confirmed that a spectral shift resulted upon binding of protohemin, but no spectral shift occurred upon binding the dimethylester derivative. Recent studies have correlated a Soret spectral shift with the preferential heme binding to the alpha subunit of apohemoglobin. The absence of a Soret wavelength shift (in conjunction with molecular modeling) presented here suggested that the modification of heme propionate groups prevented the formation of an alpha-heme/beta-globin intermediate, a requisite step in the normal assembly of functional hemoglobin.

Apoproteins↗
PubMed1997

Detection and discrimination of propionic acid after removal of its 2-DG identified major focus in the olfactory bulb: a psychophysical analysis.

Prior 2-deoxyglucose and c-fos studies have demonstrated increased metabolic activity in a rostral dorsomedial area of the olfactory bulb in response to the vapor of propionic acid. We used psychophysical tests to assess the effect of removing this area of the bulb on odor sensitivity and discrimination. Normal rats, those with lesions of the rostral dorsomedial bulb or with control lesions of the lateral olfactory bulb were tested for propionic acid absolute detection and intensity difference thresholds and ability to discriminate propionic acid from other odors. There were no differences among groups for absolute or intensity difference threshold or on simple 2-odor discrimination tests but both groups with bulbar lesions made more errors than controls on a relatively difficult odor-mixture task. The results demonstrate that removal of an area of the bulb identified as responsive to propionic acid is essentially without effect on sensitivity to that odor or ability to discriminate it from other odors.

Animals↗
PubMed1998

Chronic administration of propionic acid reduces ganglioside N-acetylneuraminic acid concentration in cerebellum of young rats.

Elevated levels of propionate comparable to those of human propionic acidaemia were achieved in the blood of young rats by injecting subcutaneously buffered propionic acid (PPA) twice a day at 8-h intervals from the 6th to the 28th day of life. A matched group of animals (controls) was treated with the same volumes of saline. The animals were weighed and sacrificed by decapitation at 28, 35 or 60 days of age. Cerebellum and cerebrum were weighed and their protein and ganglioside N-acetylneuraminic acid (G-NeuAc) contents determined. Body, cerebral and cerebellar weights were similar in both groups, suggesting that PPA per se neither alters the appetite of the rats nor causes malnutrition. Brain protein concentration was also not affected by chronic administration of PPA, in contrast to G-NeuAc concentration which was significantly reduced in the cerebellum. Since ganglioside concentration is closely related to the dendritic surface and indirectly reflects synaptogenesis, our results of an important ganglioside deficit in the brain of PPA-treated animals may be related to the neurologic dysfunction characteristic of propionic acidaemic patients.

Animals↗
PubMed2003

Optic nerve atrophy in propionic acidemia.

OBJECTIVE: Propionic acidemia is a rare metabolic disorder that is diagnosed in the early neonatal period. The disorder is characterized by life-threatening ketoacidosis, lethargy, failure to thrive, and developmental delay. Herein we report the ocular findings in a prospective series of six patients with propionic acidemia. DESIGN: Prospective case series. PARTICIPANTS: Six children (three male and three female) between the ages of 2 and 10 years with propionic acidemia who were examined at Children's Hospital Los Angeles. METHODS: A complete ophthalmic examination was performed on each of the six children. The examination included visual acuity testing, ocular motility, anterior segment examination, and funduscopic evaluation. Emphasis was placed on the function of the optic nerve and on the appearance of the optic disc, looking for possible atrophic changes. MAIN OUTCOME MEASURES: The clinical appearance of the optic disc and evidence of optic neuropathy. RESULTS: Optic nerve atrophy was present exclusively in all of the male patients in the series; none of the female patients demonstrated any detectable impairment of optic nerve function. The optic nerve atrophy was symmetric and age dependent and varied from moderate to severe. There were no other anterior or posterior segment abnormalities, other than one case of unilateral morning glory syndrome, diagnosed at birth. There was no correlation between metabolic control and the development and progression of optic nerve atrophy. CONCLUSIONS: Males with propionic acidemia have moderate to severe bilateral optic atrophy.

Amino Acid Metabolism, Inborn Errors↗
PubMed2001

Stable performance of anaerobic digestion in the presence of a high concentration of propionic acid.

An automatically controlled, glucose-fed, anaerobic digester was deliberately inhibited by addition of phenol. To overcome the phenol inhibition the feed dilution rate was lowered in such a way that the methane yield from glucose was kept the same as that under normal conditions. The concentrations of acetic and butyric acids remained below 100 mg/l, however, propionic acid accumulated to 2,750 mg/l. Phenol apparently inhibited all tropic groups of organisms and it was shown that the propionic acid was formed from the metabolism of phenol. From the nature of the operating strategy, it was deduced that the digester continued to convert all the glucose that was supplied to methane showing that propionic acid accumulation did not inhibit conversion of glucose to methane. Therefore, propionic acid accumulation may be an effect and not a cause of inhibition of the anaerobic digestion process.

Anaerobiosis↗
PubMed1999

Structure of a Michaelis complex analogue: propionate binds in the substrate carboxylate site of alanine racemase.

The structure of alanine racemase from Bacillus stearothermophilus with the inhibitor propionate bound in the active site was determined by X-ray crystallography to a resolution of 1.9 A. The enzyme is a homodimer in solution and crystallizes with a dimer in the asymmetric unit. Both active sites contain a pyridoxal 5'-phosphate (PLP) molecule in aldimine linkage to Lys39 as a protonated Schiff base, and the pH-independence of UV-visible absorption spectra suggests that the protonated PLP-Lys39 Schiff base is the reactive form of the enzyme. The carboxylate group of propionate bound in the active site makes numerous interactions with active-site residues, defining the substrate binding site of the enzyme. The propionate-bound structure therefore approximates features of the Michaelis complex formed between alanine racemase and its amino acid substrate. The structure also provides evidence for the existence of a carbamate formed on the side-chain amino group of Lys129, stabilized by interactions with one of the residues interacting with the carboxylate group of propionate, Arg136. We propose that this novel interaction influences both substrate binding and catalysis by precisely positioning Arg136 and modulating its charge.

Alanine Racemase↗
PubMed2000

Structural determinants of AMPA agonist activity in analogues of 2-amino-3-(3-carboxy-5-methyl-4-isoxazolyl)propionic acid: synthesis and pharmacology.

We have previously shown that the 2-amino-3-(3-hydroxy-5-methyl-4-isoxazolyl)propionic acid (AMPA) receptor agonist, 2-amino-3-(3-carboxy-5-methyl-4-isoxazolyl)propionic acid (ACPA, 2), binds to AMPA receptors in a manner different from that of AMPA (1) itself and that 2, in contrast to 1, also binds to kainic acid receptor sites. To elucidate the structural requirements for selective activation of the site/conformation of AMPA receptors recognized by 2, a number of isosteric analogues of 2 have now been synthesized and pharmacologically characterized. The compound 2-amino-3-(5-carboxy-3-methoxy-4-isoxazolyl)propionic acid (3a) (IC(50) = 0.11 microM; EC(50) = 1.2 microM), which is a regioisostere of 2 with a methoxy group substituted for the methyl group, was approximately equipotent with 2 (IC(50) = 0.020 microM; EC(50) = 1.0 microM) as an inhibitor of [(3)H]AMPA binding and as an AMPA agonist, respectively, whereas the corresponding 3-ethoxy analogue 3b (IC(50) = 1.0 microM; EC(50) = 4.8 microM) was slightly weaker. The analogues 3c-e, containing C3 alkoxy groups, were an order of magnitude weaker than 3b, whereas the additional steric bulk of the alkoxy groups of 3f-i or the presence of an acidic hydroxyl group at the 3-position of the isoxazole ring of 3j prevented interaction with AMPA receptor sites. The 2-amino-3-(2-alkyl-5-carboxy-3-oxo-4-isoxazolyl)propionic acids 4a,b, i, which are regioisosteric analogues of 3a,b,i, showed negligible interaction with AMPA recognition sites. Similarly, replacement of the carboxyl group of 3b by isosteric tetrazolyl or 1,2,4-triazolyl groups to give 5 and 6, respectively, or conversion of 3b into analogue 7, in which the diaminosquaric acid group has been bioisosterically substituted for the alpha-aminocarboxylic acid unit, provided compounds completely devoid of effect at AMPA receptors. In contrast to the parent compound ACPA (2) (IC(50) = 6.3 microM), none of the analogues described showed detectable inhibitory effect on [(3)H]kainic acid receptor binding.

Animals↗
PubMed2003

(S)-2-Amino-3-(3-hydroxy-7,8-dihydro-6H-cyclohepta[d]isoxazol-4-yl)propionic acid, a potent and selective agonist at the GluR5 subtype of ionotropic glutamate receptors. Synthesis, modeling, and molecular pharmacology.

We have previously described (RS)-2-amino-3-(3-hydroxy-7,8-dihydro-6H-cyclohepta[d]isoxazol-4-yl)propionic acid (4-AHCP) as a highly effective agonist at non-N-methyl-d-aspartate (non-NMDA) glutamate (Glu) receptors in vivo, which is more potent than (RS)-2-amino-3-(3-hydroxy-5-methylisoxazol-4-yl)propionic acid (AMPA) but inactive at NMDA receptors. However, 4-AHCP was found to be much weaker than AMPA as an inhibitor of [(3)H]AMPA binding and to have limited effect in a [(3)H]kainic acid binding assay using rat cortical membranes. To shed light on the mechanism(s) underlying this quite enigmatic pharmacological profile of 4-AHCP, we have now developed a synthesis of (S)-4-AHCP (6) and (R)-4-AHCP (7). At cloned metabotropic Glu receptors mGluR1alpha (group I), mGluR2 (group II), and mGluR4a (group III), neither 6 nor 7 showed significant agonist or antagonist effects. The stereoisomer 6, but not 7, activated cloned AMPA receptor subunits GluR1o, GluR3o, and GluR4o with EC(50) values in the range 4.5-15 microM and the coexpressed kainate-preferring subunits GluR6 + KA2 (EC(50) = 6.4 microM). Compound 6, but not 7, proved to be a very potent agonist (EC(50) = 0.13 microM) at the kainate-preferring GluR5 subunit, equipotent with (S)-2-amino-3-(5-tert-butyl-3-hydroxyisothiazol-4-yl)propionic acid [(S)-Thio-ATPA, 4] and almost 4 times more potent than (S)-2-amino-3-(5-tert-butyl-3-hydroxyisoxazol-4-yl)propionic acid [(S)-ATPA, 3]. Compound 6 thus represents a new structural class of GluR5 agonists. Molecular modeling and docking to a crystal structure of the extracellular binding domain of the AMPA subunit GluR2 has enabled identification of the probable active conformation and binding mode of 6. We are able to rationalize the observed selectivities by comparing the docking of 4 and 6 to subtype constructs, i.e., a crystal structure of the extracellular binding domain of GluR2 and a homology model of GluR5.

Alanine↗
PubMed2002

Ganglioside alterations in the central nervous system of rats chronically injected with methylmalonic and propionic acids.

Neurological dysfunction and structural cerebral abnormalities are commonly found in patients with methylmalonic and propionic acidemia. However, the mechanisms underlying the neuropathology of these disorders are poorly understood. We have previously demonstrated that methylmalonic and propionic acids induce a significant reduction of ganglioside N-acetylneuraminic acid in the brain of rats subjected to chronic administration of these metabolites. In the present study, we investigated the in vivo effects of chronic administration of methylmalonic (MMA) and propionic (PA) acids (from the 6th to the 28th day of life) on the distribution and composition of gangliosides in the cerebellum and cerebral cortex of rats. Control rats were treated with the same volumes of saline. It was first verified that MMA and PA treatment did not modify body, cerebellum, or cortical weight, nor the ganglioside concentration in the cerebral cortex of the animals. In contrast, a significant reduction in total ganglioside content in the cerebellum of approximately 20-30% and 50% of control levels occurred in rats injected with MMA and PA, respectively. Moreover, chronic MMA and PA administration did not interfere with the ganglioside pattern in the cerebral cortex, whereas the distribution of individual gangliosides was altered in the cerebellum of MMA- and PA-treated animals. Rats injected with MMA demonstrated a marked decrease in GM1 and GD3, whereas chronic PA treatment provoked a significant reduction of all ganglioside species, with the exception of an increase in GM2. Since gangliosides are closely related to the dendritic surface and other neural membranes, indirectly reflecting synaptogenesis, these ganglioside abnormalities may be associated with the brain damage found in methylmalonic and propionic acidemias.

Animals↗
PubMed2003

Effect of propionic and methylmalonic acids on the in vitro phosphorylation of intermediate filaments from cerebral cortex of rats during development.

In this study we investigated the in vivo and in vitro effects of methylmalonic (MMA) and propionic acids (PA), at concentrations usually found in methylmalonic acidemia and propionic acidemia respectively, on the phosphorylation of intermediate filament proteins in cerebral cortex of rats during development. Rats of 9, 12, and 17 days were acutely injected with the acids and sacrificed 90 min after injection. The cerebral cortex was dissected, and slices were incubated with 32P-orthophosphate. The cytoskeletal fraction was extracted and the radioactivity incorporated into intermediate filament subunits was measured. In addition, cortical slices from nontreated rats of 9, 12, 15, 17, 21, and 60 days of life were incubated with the acids in the presence of 32P-orthophosphate, the cytoskeletal fraction was extracted and the radioactivity was measured. Results demonstrated that MMA and PA significantly decreased the radioactivity incorporated into intermediate filament proteins at day 12, both in vivo and in tissue slices. In contrast, PA increased the in vitro phosphorylation of the cytoskeletal proteins in slices of 21-day-old animals. It acts through PP2A and PP2B in 12-day-old rats and through PKA and PKCaMII in 21-day-old animals. We propose that alteration of cytoskeletal protein phosphorylation caused by methylmalonic and propionic acids may be related to the neurological dysfunction characteristic of propionic and methylmalonic acidemia.

Animals↗
PubMed1967

Rates of entry and oxidation of acetate, glucose, D(-)-beta-hydroxybutyrate, palmitate, oleate and stearate, and rates of production and oxidation of propionate and butyrate in fed and starved sheep.

1. Rates of entry and oxidation of a range of metabolites have been measured in tracheostomized sheep (diet, 800g. of lucerne chaff and 100g. of maize/day) by combining isotope-dilution techniques with the continuous measurement of total respiratory gas exchange, and (14)CO(2) production during the intravenous or intraruminal infusion of (14)C-labelled substrates. 2. Mean entry rates in fed and starved (24hr.) sheep respectively, expressed as mg./min./kg. body wt.(0.75), were: glucose, 5.0 (range 4.8-5.1, 2 observations) and 3.8 (3.2-4.2, 4); acetate, 10.8 (9.1-13.5, 4) and 5.8 (1); d(-)-beta-hydroxybutyrate, 1.4 (1) and 1.5 (0.8-2.4, 4); palmitate, oleate and stearate (starved sheep only) 1.0 (0.6-1.9, 7), 0.9 (0.2-1.6, 10) and 0.9 (0.5-1.1, 11) respectively. 3. Production rates of propionate and butyrate in continuously feeding sheep were 6.4 (4.7-8.3, 4) and 4.3 (3.4-6.1, 4) mg./min./kg.(0.75) respectively, and in starved (24hr.) sheep were 2.5 (2.2-2.9, 2) and 1.0 (0.8-1.2, 2) mg./min./kg.(0.75) respectively. 4. Calculated terminal values for the specific radioactivity of respiratory (14)CO(2) during measurements of entry rates and production rates were used to calculate the contributions of individual substrates to overall oxidative metabolism. Mean values for fed and starved sheep respectively were: glucose, 9.1 (8.6-9.6, 2) and 11.2 (5.9-15.1, 4)%; acetate, 31.6 (26.8-38.1, 4) and 22.1 (1)%; d(-)-beta-hydroxybutyrate, 10.4 (1) and 4.8 (1.9-7.7, 4)%; propionate, 23.0 (13.8-29.9, 4) and 7.1 (6.8-7.4, 2)%; butyrate, 16.5 (13.7-20.5, 4) and 5.3 (5.2-5.3, 2)%; palmitate, oleate and stearate (starved sheep only), 4.7 (2.0-7.7, 7), 4.0 (1.2-6.6, 10) and 4.4 (3.8-5.8, 9)% respectively. The sum of these values for individual substrates in fed and starved sheep, excluding that of beta-hydroxybutyrate and after correction of the glucose value for the known interrelations of this substrate with propionate, accounted for 76% and 58% respectively of total production of carbon dioxide. 5. Calculations based on the proportion of substrate entry directly oxidized indicated that the substrates studied accounted for 63% (fed sheep) and 43% (starved sheep) of total energy expenditure measured by oxygen uptake. The contribution of beta-hydroxybutyrate was excluded, and corrections were made for glucose-propionate interrelations, and for the different rates of oxidation of the methyl and carboxyl fragments of acetate. 6. The present results have been combined with those obtained earlier in this Laboratory to examine the relationships between rates of substrate entry and oxidation, and concentrations of substrate in blood. Rates of entry of acetate, glucose, d(-)-beta-hydroxybutyrate, palmitate and oleate (but not stearate) were well correlated with concentration in blood, and substrate contribution to production of carbon dioxide showed a similar correlation to blood concentration, except with glucose. 7. It was concluded that the general technique is of potential value in providing valid quantitative parameters of animal metabolism.

Acetates↗
PubMed2002

Oxidation of propionate to pyruvate in Escherichia coli. Involvement of methylcitrate dehydratase and aconitase.

The pathway of the oxidation of propionate to pyruvate in Escherichia coli involves five enzymes, only two of which, methylcitrate synthase and 2-methylisocitrate lyase, have been thoroughly characterized. Here we report that the isomerization of (2S,3S)-methylcitrate to (2R,3S)-2-methylisocitrate requires a novel enzyme, methylcitrate dehydratase (PrpD), and the well-known enzyme, aconitase (AcnB), of the tricarboxylic acid cycle. AcnB was purified as 2-methylaconitate hydratase from E. coli cells grown on propionate and identified by its N-terminus. The enzyme has an apparent Km of 210 micro m for (2R,3S)-2-methylisocitrate but shows no activity with (2S,3S)-methylcitrate. On the other hand, PrpD is specific for (2S,3S)-methylcitrate (Km = 440 micro m) and catalyses in addition only the hydration of cis-aconitate at a rate that is five times lower. The product of the dehydration of enzymatically synthesized (2S,3S)-methylcitrate was designated cis-2-methylaconitate because of its ability to form a cyclic anhydride at low pH. Hence, PrpD catalyses an unusual syn elimination, whereas the addition of water to cis-2-methylaconitate occurs in the usual anti manner. The different stereochemistries of the elimination and addition of water may be the reason for the requirement for the novel methylcitrate dehydratase (PrpD), the sequence of which seems not to be related to any other enzyme of known function. Northern-blot experiments showed expression of acnB under all conditions tested, whereas the RNA of enzymes of the prp operon (PrpE, a propionyl-CoA synthetase, and PrpD) was exclusively present during growth on propionate. 2D gel electrophoresis showed the production of all proteins encoded by the prp operon during growth on propionate as sole carbon and energy source, except PrpE, which seems to be replaced by acetyl-CoA synthetase. This is in good agreement with investigations on Salmonella enterica LT2, in which disruption of the prpE gene showed no visible phenotype.

Aconitate Hydratase↗
PubMed2000

Resting energy expenditure in disorders of propionate metabolism.

OBJECTIVES: During intercurrent illness children with methylmalonic acidemia were found to have increased resting energy expenditure (REE). We measured REE in children with disorders of propionate metabolism (methylmalonic and propionic acidemia) when they were well and compared the values with those predicted by the Schofield equation. STUDY DESIGN: Prospective study in tertiary care facility. REE was measured with open-circuit indirect calorimetry under standardized conditions. Predicted REE values were calculated with the Schofield equation. Fourteen subjects with propionic acidemia (n = 3) and methylmalonic acidemia (n = 11) were studied. RESULTS: The median REE was 690 kcal/d (range 186 to 1687 kcal/d), which is significantly reduced, representing 80% +/- 18% of that predicted by the Schofield height and weight equation (P <.01). REE was significantly lower in female compared with male patients for unknown reasons. There were no differences with age or neurologic state. REE was not further reduced in those with chronic renal failure. CONCLUSION: REE in patients with disorders of propionate metabolism is reduced when they are well.

Amino Acid Metabolism, Inborn Errors↗
PubMed1980

Effects of somatostatin and glucagon on the utilization of [2-(14)C]propionate in glucose production in vivo in sheep.

This study examined the effects of hypoglucagonaemia and hyperglucagonaemia on the incorporation of 14C from [2-(14)C]propionate into plasma glucose of sheep in vivo. The sheep were adult ewes fed a maintenance diet of lucerne pellets delivered in equal aliquots hourly. The irreversible loss of glucose was determined by the continuous infusion of [6-(3)H]glucose. During the control period (the hour immediately preceding infusion of hormones) 63 +/- 2% of the propionate was converted to glucose, accounting for 30 +/- 2% of glucose production. Glucagon deficiency, induced by infusion of somatostatin (100 micrograms/h), did not affect gluconeogenesis and the irreversible loss of glucose significantly. However, glucagon infusion at 11.5 +/- 0.6 micrograms/h significantly increased the irreversible loss of glucose, with the greatest increase occurring in the first 15 min of infusion. The 14C specific radioactivity of glucose and the fraction of glucose derived from propionate decreased significantly during glucagon infusion. The data are consistent with glucagon have a marked glycogenolytic effect initially, but little or no selective effect in promoting the utilization of propionate for glucose synthesis in vivo in sheep.

Animals↗
PubMed1978

The utilization of diets containing acetate, propionate or butyrate salts by growing lambs.

1. In a comparative slaughter experiment growing lambs were given concentrate diets in which 7, 15 or 22% of the metabolizable energy (ME) provided by barley was replaced by sodium and calcium salts of acetic acid, or 22% of ME was replaced by Na and Ca salts of propionic or butyric acids. 2. The efficiency of utilization for fattening (kf) of the diets containing 0, 7, 15 or 22% of ME as acetate was 57.2, 59.6, 54.1 and 48.8 (SE +/- 1.8) respectively, the last value being significantly lower (P less than 0.001) than the first. The kf for successive increments of acetate was 90, 37 and 19% (SE +/ 3), the decrease being significant (P less than 0.001). 3. The kf value of the diets containing 22% of ME as propionate or butyrate respectively were 48.7 and 50.6 (SE +/- 1.8), both values being significantly lower than the control (P less than 0.01). The partial kf of propionate was 19 +/- 13, and of butyrate 28 +/- 13%. 4. It is concluded that the experiment provided evidence that the efficiency with which acetateis utilized for energy retentionis not constant, but varies with its contribution to ME. The experiment also provided some evidence that large amounts of propionate and butyrate may be inefficiently utilized by growing lambs, although poor utilization of high levels of volatile fatty acid (VFA) salts per se cannot be entirely excluded.

Acetates↗