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PubMed1973

Propionate formation from cellulose and soluble sugars by combined cultures of Bacteroides succinogenes and Selenomonas ruminantium.

Succinate is formed as an intermediate but not as a normal end product of the bovine rumen fermentation. However, numerous rumen bacteria are present, e.g., Bacteroides succinogenes, which produce succinate as a major product of carbohydrate fermentation. Selenomonas ruminantium, another rumen species, produces propionate via the succinate or randomizing pathway. These two organisms were co-cultured to determine if S. ruminantium could decarboxylate succinate produced by B. succinogenes. When energy sources used competitively by both species, i.e. glucose or cellobiose, were employed, no succinate was found in combined cultures, although a significant amount was expected from the numbers of Bacteroides present. The propionate production per S. ruminantium was significantly greater in combined than in single S. ruminantium cultures, which indicated that S. ruminantium was decarboxylating the succinate produced by B. succinogenes. S. ruminantium, which does not use cellulose, grew on cellulose when co-cultured with B. succinogenes. Succinate, but not propionate, was produced from cellulose by B. succinogenes alone. Propionate, but no succinate, accumulated when the combined cultures were grown on cellulose. These interspecies interactions are models for the rumen ecosystem interactions involved in the production of succinate by one species and its decarboxylation to propionate by a second species.

Acetates↗
PubMed2003

Propionyl coenzyme A is a common intermediate in the 1,2-propanediol and propionate catabolic pathways needed for expression of the prpBCDE operon during growth of Salmonella enterica on 1,2-propanediol.

The studies reported here identify propionyl coenzyme A (propionyl-CoA) as the common intermediate in the 1,2-propanediol and propionate catabolic pathways of Salmonella enterica serovar Typhimurium LT2. Growth on 1,2-propanediol as a carbon and energy source led to the formation and excretion of propionate, whose activation to propionyl-CoA relied on the activities of the propionate kinase (PduW)/phosphotransacetylase (Pta) enzyme system and the CobB sirtuin-controlled acetyl-CoA and propionyl-CoA (Acs, PrpE) synthetases. The different affinities of these systems for propionate ensure sufficient synthesis of propionyl-CoA to support wild-type growth of S. enterica under low or high concentrations of propionate in the environment. These redundant systems of propionyl-CoA synthesis are needed because the prpE gene encoding the propionyl-CoA synthetase enzyme is part of the prpBCDE operon under the control of the PrpR regulatory protein, which needs 2-methylcitrate as a coactivator. Because the synthesis of 2-methylcitrate by PrpC (i.e., the 2-methylcitrate synthase enzyme) requires propionyl-CoA as a substrate, the level of propionyl-CoA needs to be raised by the Acs or PduW-Pta system before 2-methylcitrate can be synthesized and prpBCDE transcription can be activated.

Acyl Coenzyme A↗
PubMed2006

Reconstruction and regulation of the central catabolic pathway in the thermophilic propionate-oxidizing syntroph Pelotomaculum thermopropionicum.

Obligate anaerobic bacteria fermenting volatile fatty acids in syntrophic association with methanogenic archaea share the intermediate bottleneck step in organic-matter decomposition. These organisms (called syntrophs) are biologically significant in terms of their growth at the thermodynamic limit and are considered to be the ideal model to address bioenergetic concepts. We conducted genomic and proteomic analyses of the thermophilic propionate-oxidizing syntroph Pelotomaculum thermopropionicum to obtain the genetic basis for its central catabolic pathway. Draft sequencing and subsequent targeted gap closing identified all genes necessary for reconstructing its propionate-oxidizing pathway (i.e., methylmalonyl coenzyme A pathway). Characteristics of this pathway include the following. (i) The initial two steps are linked to later steps via transferases. (ii) Each of the last three steps can be catalyzed by two different types of enzymes. It was also revealed that many genes for the propionate-oxidizing pathway, except for those for propionate coenzyme A transferase and succinate dehydrogenase, were present in an operon-like cluster and accompanied by multiple promoter sequences and a putative gene for a transcriptional regulator. Proteomic analysis showed that enzymes in this pathway were up-regulated when grown on propionate; of these enzymes, regulation of fumarase was the most stringent. We discuss this tendency of expression regulation based on the genetic organization of the open reading frame cluster. Results suggest that fumarase is the central metabolic switch controlling the metabolic flow and energy conservation in this syntroph.

Acyl Coenzyme A↗
PubMed1962

Conversion of lactate-C14 to propionate by the rumen microflora.

Baldwin, R. L. (Michigan State University, East Lansing), W. A. Wood, and R. S. Emery. Conversion of lactate-C(14) to propionate by the rumen microflora. J. Bacteriol. 83:907-913. 1962.-Rumen microflora enriched on five different diets calculated to present increasing carbohydrate or lactate availability were used to determine the contribution of the randomizing (succinate) and nonrandomizing (acrylate) routes to propionate with lactate-2-C(14) and -3-C(14) as substrates. Propionate was labeled as though 70 to 90% was formed via the nonrandomizing route. This percentage was highest on diets containing high levels of carbohydrate or lactate or both. Evidence for the presence of succinic dehydrogenase, acetokinase, phosphotransacetylase, and coenzyme A transphorase was obtained with cell-free extracts. Propionate-2-C(14) and lactate-2-C(14) were converted by extracts to the activated derivatives of acrylate, lactate, propionate, and acetate.

Acetates↗
PubMed1969

Divergent metabolic pathways for propane and propionate utilization by a soil isolate.

The metabolism of propane and propionate by a soil isolate (Brevibacterium sp. strain JOB5) was investigated. The presence of isocitrate lyase in cells grown on isopropanol, acetate, or propane and the absence of this inducible enzyme in n-propanol- and propionate-grown cells suggested that propane is not metabolized via C-terminal oxidation. Methylmalonyl coenzyme A mutase and malate synthase are constitutive in this organism. The incorporation of (14)CO(2) into pyruvate accumulated during propionate utilization suggests that propionate is metabolized via the methyl-malonyl-succinate pathway. These results were further substantiated by radiorespirometric studies with propionate-1-(14)C, -2-(14)C, and -3-(14)C as substrate. Propane -2-(14)C was shown, by unlabeled competitor experiments, to be oxidized to acetone; acetone and isopropanol are oxidized in this organism to acetol. Cleavage of acetol to acetate and CO(2) would yield the inducer for the isocitrate lyase present in propane-grown cells.

Alkanes↗
PubMed1985

Electrophysiological effects of propionate and bicarbonate on gallbladder epithelium.

The effects of propionate and HCO3- on cell membrane potentials in Necturus gallbladder epithelium were investigated using microelectrode techniques in vitro. Bilateral exposure to either propionate or HCO3- (25 mM each) hyperpolarized both cell membranes by about 12 mV. Mucosal addition of either substance produced cyclic changes in voltage of both cell membranes, which attenuated spontaneously, whereas serosal addition caused sustained hyperpolarization. By intraepithelial cable analysis it was shown that both cell membrane conductances rose during the hyperpolarization. Experiments using substitution of mucosal K+ for Na+ revealed that the relative K+ permeability (PK) of the apical membrane was enhanced during the hyperpolarization induced by mucosal (or serosal) propionate (or HCO3-). These effects are mediated by increases in PK at both membranes, with a larger basolateral effect. We suggest that this mechanism accounts for the higher cell membrane potential values measured in epithelia bathed in HCO3--or propionate-containing solutions. Inasmuch as both propionate and HCO3- stimulate fluid absorption in gallbladder epithelium, the increase in cell membrane PK may represent an adaptive response of the cells to regulate their solute content.

Animals↗
PubMed1993

Propionate activates multiple ion transport mechanisms in the HT29-18-C1 human colon cell line.

Short-chain fatty acids (SCFAs) are the major solutes and the major anions in the colonic lumen. We studied the response of suspended HT29-18-C1 cells (an epithelial cell line derived from a human colon carcinoma) to SCFA exposure. Cellular response was evaluated by measurement of cell volume (Coulter counter), intracellular pH [pHi; measured fluorometrically with 2',7'-bis(2-carboxyethyl)-5-(6)-carboxyfluorescein (BCECF)], and intracellular Na+, K+, and Cl- content (flame photometry and chloride titrator). Exposure to 130 mM propionate in isosmotic medium causes a rapid decrease in pHi and activates pHi recovery via amiloride-sensitive Na-H exchange. In the presence of propionate, Na-H exchange also causes cell swelling to a peak volume 11% above control cells and causes a 2.8-fold increase in intracellular Na+ content. After peak swelling, a regulatory-volume decrease (RVD) significantly reduced volume and intracellular Na+ returned to baseline. Other SCFAs (acetate, butyrate, and valerate) also elicit swelling and RVD. Activation of the Na(+)-K(+)-adenosinetriphosphatase (ATPase) is required to return Na+ to normal levels and to indirectly provide ion gradients required for propionate-induced RVD, but Na(+)-K(+)-ATPase activity does not directly mediate RVD. When 1 mM 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS) is added in the presence of propionate, RVD was inhibited and cell Na+ content increased. Cl- depletion inhibited propionate-induced RVD and diminished the effect of SITS.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1984

Effects of glucagon, insulin, propionate, acetate, and HCO3 on K excretion in sheep.

The effects on renal K excretion of 1 h intravenous infusion of glucagon, insulin, Na propionate, Na acetate, or NaHCO3 were studied in mature, conscious fasted ewes. These treatments were compared with the fasted state without treatment (control) and with feeding a single daily meal. Renal K excretion was increased by feeding and by Na propionate and Na acetate treatments but not by infusion of glucagon, insulin, and NaHCO3. Since hormone levels were elevated more by specific hormone infusions than by feeding or Na propionate infusions, these results do not support a role for glucagon and insulin in mediating the increases in renal K excretion that occurred after meals or during acetate and propionate infusions. The mechanisms responsible for the acetate- and propionate-induced kaliuresis are not clear but do not appear to include changes in plasma K (PK), glucagon, and insulin (Pinsulin) or in urine flow and urine Na excretion. However, a relation between insulin and K was observed during infusion of KCl in fasting sheep. Above a PK threshold of 4 meq/l, Pinsulin (ng/ml) = 1.52 PK (meq/l) - 5.89. In other experiments, K excretion increased after an intravenous bolus injection of 1 mg of glucagon, indicating that sheep, like humans and dogs, respond to pharmacologic doses of glucagon with kaliuresis.

Acetates↗
PubMed1990

Increased urinary metabolite excretion during fasting in disorders of propionate metabolism.

Odd-chain fatty acids are recognized precursors of propionate in man, but their clinical significance in disorders of propionate metabolism has not been well studied. Urinary excretion of methylmalonate, methylcitrate, propionylglycine, and 3-hydroxypropionate was measured in five children with methylmalonic acidemia and three with propionic acidemia during frequent or continuous feeding and after 10-18 h of fasting. There was a significant (p less than 0.01) increase in the mean total measured metabolite excretion during fasting (fed 38.1 mumol/kg/h, fasting 54.6 in methylmalonic acidemia, fed 1.45, fasting 2.98 in propionic acidemia). Percentage rises in each subject were similar for all measured metabolites. These increases in metabolite excretion are most easily explained by mobilization and oxidation of odd-chain fatty acids in the fasting state. Prolonged fasting should be avoided in children with disorders of propionate metabolism.

Adult↗
PubMed2005

Acetate and propionate short chain fatty acids stimulate adipogenesis via GPCR43.

It has recently been discovered that G protein-coupled receptors (GPCR) 41 and 43 are characterized by having the short chain fatty acids acetate and propionate as their ligands. The objective of this study was to investigate the involvement of GPCR41, GPCR43, and their ligands in the process of adipogenesis. We measured the levels of GPCR41 and GPCR43 mRNA in both adipose and other tissues of the mouse. GRP43 mRNA expression was higher in four types of adipose tissue than in other tissues, whereas GPCR41 mRNA was not detected in any adipose tissues. A high level of GPCR43 expression was found in isolated adipocytes, but expression level was very low in stromal-vascular cells. Expression of GPCR43 was up-regulated in adipose tissues of mice fed a high-fat diet compared with those fed a normal-fat diet. GPCR43 mRNA could not be detected in confluent and undifferentiated 3T3-L1 adipocytes; however, the levels rose with time after the initiation of differentiation. GPCR41 expression was not detected in confluent and differentiated adipocytes. Acetate and propionate treatments increased lipids present as multiple droplets in 3T3-L1 adipocytes. Propionate significantly elevated the level of GPCR43 expression during adipose differentiation, with up-regulation of PPAR-gamma2. Small interfering RNA mediated a reduction of GPCR43 mRNA in 3T3-L1 cells and blocked the process of adipocyte differentiation. In addition, both acetate and propionate inhibited isoproterenol-induced lipolysis in a dose-dependent manner. We conclude that acetate and propionate short chain fatty acids may have important physiological roles in adipogenesis through GPCR43, but not through GPCR41.

3T3-L1 Cells↗
PubMed2002

Metabolism of propionate and 1,2-propanediol absorbed from the washed reticulorumen of lactating cows.

To investigate the metabolism of 1,2-propanediol (PPD) in lactating cows independently of normal rumen microbial metabolism, three ruminally cannulated lactating Holstein cows were subjected to three experimental infusion protocols under washed reticulo-ruminal conditions in a Latin square design. Reticulo-ruminal absorption rates were maintained for 420 min by continuous intraruminal infusion of VFA and PPD. With the control treatment, 1,246 +/- 39 mmol/ h of acetate and 213 +/- 5 mmol/h of butyrate were absorbed from the reticulorumen. With the propionate treatment, 1,148 +/- 39 mmo/h of acetate, 730 +/- 23 mmol/h of propionate and 196 +/- 5 mmol/h of butyrate were absorbed from the reticulorumen. With PPD treatment, 1,264 +/- 39 mmol/h of acetate, 220 +/- 5 mmol/h of butyrate and 721 +/- 17 mmol/h of PPD were absorbed from the reticulorumen. Glucose irreversible loss rate (ILR), as well as the relative enrichment of plasma lactate and alanine, were determined by primed continuous infusion of [U-13C]glucose in a jugular vein. Treatments did not affect (P > 0.10) the plasma concentrations of glucose (4.2 +/- 0.1 mmoVL), alanine (0.14 +/- 0.01 mmol/L), or insulin (80 +/- 25 pmol/L). The plasma concentration of lactate was higher (P < 0.05) with both propionate (0.84 +/- 5 mmol/L) and PPD treatment (0.81 +/- 5 mmol/ L) compared with the control treatment (0.29 +/- 0.5 mmol/L). The plasma concentration of pyruvate was higher (P < 0.05) with the propionate treatment (0.09 +/- 0.01 mmol/L) compared with the control treatment (0.03 +/- 0.01 mmol/L). The plasma concentration of 3-hydroxybutyrate was lower (P < 0.05) with the propionate treatment (0.15 +/- 0.03 mmol/L) compared with the control treatment (0.40 +/- 0.03). With the PPD treatment, the plasma concentrations of pyruvate and 3-hydroxybutyrate were in between the other treatments and tended (P < 0.10) to be different from both. The plasma concentration of PPD increased throughout the infusion period with the PPD treatment and reached a concentration of 4.9 +/- 0.6 mmol/L at 420 min. The ILR of glucose was not affected (P > 0.10) by treatments (441 +/- 35 mmol/h). The relative 13C enrichment of plasma lactate compared with that of glucose decreased (P < 0.05) with the PPD treatment compared with the control treatment (44 to 21 +/- 3%). It was concluded that PPD has a low rate of metabolism in cows without a normal functioning rumen, although about 10% of the absorbed PPD was metabolized into lactate.

Absorption↗
PubMed2005

Effects of feeding propionate and calcium salts of long-chain fatty acids on transition dairy cow performance.

Multiparous Holstein cows (n = 40) were used in a randomized complete block design to determine the effects of feeding Ca and Na salts (1:1, wt/wt) of propionate and Ca salts of long-chain fatty acids (LCFA) on transition cow performance. All cows were fed the same basal diet once daily for ad libitum intake. Treatments (g/d) were 320 cornstarch (CS) as a control, 120 propionate (PRO), 120 propionate and 93 LCFA (PF1), and 178 propionate and 154 LCFA (PF2). Treatments were hand-mixed into the upper one-third of the TMR from 2 wk pre- through 3 wk postpartum. Intakes were recorded from 21 d pre- through 21 d postpartum. Energy density and crude protein were 1.54 and 1.65 Mcal/kg and 14.4 and 18.8% for pre- and postpartum diets, respectively. All cows received a common diet from 22 to 70 days in milk (DIM). Milk composition was analyzed on d 7, 14, and 21. Blood was sampled at 14, 7, and 2 d prepartum and 2, 7, 14, and 21 DIM. Pre- and postpartal dry matter intake (DMI) averaged 11.9 and 16.4 kg/d, respectively, and did not differ among treatments. A diet x week interaction for postpartal DMI was observed as cows fed PF2 consumed 2 kg/d less DM during wk 2 relative to other treatments. Milk yields from 22 to 70 DIM were 48.8, 48.5, 47.8, and 51.3 kg/d for CS, PRO, PF1, and PF2, respectively, and were not significantly affected by treatments. Milk true protein (3.32 vs. 3.16%) was increased and MUN (12.5 vs. 14.4 mg/dL) was decreased for CS relative to other treatments. Milk fat yield from cows fed PRO tended to be greater than those fed PF1 (1.58 vs. 1.29 kg/d). Plasma glucose, insulin, and beta-hydroxybutyrate were not affected by treatments. The PF2 treatment tended to decrease NEFA in plasma relative to PF1 over all times measured (492 and 670 muEq/L) and significantly decreased plasma NEFA relative to those fed PF1 postpartum (623 and 875 muEq/L). Relative to PF1, feeding propionate and LCFA at the higher level in this experiment improved energy balance postpartum as evidenced by decreased concentrations of plasma NEFA.

Animal Feed↗
PubMed1980

Mammary extraction of propionate in lactating cows.

Four cows with exteriorized carotid arteries were in an intensive study of concentrations in plasma and mammary extraction of propionate. A restricted-roughage, high-grain diet produced higher arterial propionate concentrations and larger carotid-subcutaneous abdominal vein (arteriovenous) differences that the control diet. Concomitant changes in acetate, beta-hydroxybutyrate, and glucose in plasma and in fat and protein in milk were measured. Mammary arteriovenous difference in propionate was correlated negatively with milk fat percentage. However, since arterial propionate and beta-hydroxybutyrate also were correlated negatively, evidence of a direct inhibitory effect of propionate in mammary gland is equivocal.

3-Hydroxybutyric Acid↗
PubMed1984

Effect of propionic acid on kinetics of acetate and oleate and on plasma and milk fatty acid composition of goats.

Entry rates of acetate and oleate and their incorporation into lipids of blood plasma and fatty acids of milk were studied in lactating goats fed a concentrate-roughage ration with propionic acid infused intraruminally at 0, 5.52, and 13.74 g/h by primed constant intravenous infusion of [1-carbon-14] acetate and [9, 10-hydrogen-3] oleate. Means for infusion rates were acetate, 60, 52, and 39 micrograms/ml blood plasma; propionate 9, 12, and 22 micrograms/ml; oleate, 19, 14, and 12 micrograms/ml; acetate entry rate, 3.9, 2.7, and 1.8 mmol/h per kg bodyweight; oleate entry rate, 47, 29, and 19 mumol/h per kg bodyweight; acetate oxidation rate, 2.0, 1.7, and 1.4 mmol/h per kg, and its contribution to the total carbon dioxide production, 16, 14, and 11%. Propionic acid increased incorporation of carbon-14 and hydrogen-3 into plasma lipids, elevated proportions of 7:0, 9:0, 11:0, 13:0, 15:0, and 17:0 fatty acids in milk, and tended to lower others. Specific radioactivities of milk fatty acids during infusion of propionic acid were elevated by 1.8 to 2.8 times, and total fatty acids in milk and plasma were lowered by 22 and 38%. Data support the glucogenic theory that propionic acid either directly or through gluconeogenesis stimulates insulin secretion, which in turn inhibits release of fatty acids from adipose tissue, resulting in milk fat depression.

Acetates↗
PubMed1984

Endocrine changes with infusion of propionate in the dairy cow.

Sodium propionate (2.5 mmol/kg) was infused rapidly via a jugular vein into each of 13 multiparous Holstein cows at 7 wk postpartum for observation of clearance of propionate. Associated concentration changes of acetate and glucose in blood plasma and glucagon and insulin in blood serum were quantified. This dose elevated concentrations of propionate, which declined subsequently at an exponential rate (.108 min-1). Concentrations of glucagon and insulin were increased in the sampling immediately following infusion, yet subsequent decline of insulin concentrations acted to decrease the molar ratio of insulin:glucagon as propionate returned to preinfusion concentrations. Analysis of sample means disclosed a negative correlation -.82 between glucose and molar ratio of insulin:glucagon. These experimental observations suggest that a supraphysiological dose of propionate has an immediate effect on the pancreas to alter endocrine secretion in the lactating cow.

Animals↗
PubMed1985

Glucagon influence on gluconeogenesis and oxidation of propionic acid and threonine by perfused ovine liver.

An in situ ovine liver perfusion technique was developed and used to study glucagon effects on utilization of simultaneously infused propionic acid and amino acids. Physiological amounts of propionic acid and amino acids (hydrolyzed casein) were infused into livers along with carbon-14 propionic acid or carbon-14 threonine with and without glucagon. Glucagon (5 mg) caused a 75% increase of glucose synthesis and a 19% increase of labeled carbon dioxide production from carbon-14 propionic acid. There also was a decrease of perfusate urea nitrogen when glucagon was present. Glucagon caused a 76% decrease of carbon-14 threonine utilization by ovine livers, and labeled carbon dioxide production from carbon-14 threonine was only 38% of control when glucagon was infused. From these results, glucagon caused an increase of use of propionic acid and a decrease of use of threonine for energetic pathways in sheep liver. Therefore, glucagon directly or indirectly may mediate amino acid sparing by ruminant liver.

Animals↗
PubMed1986

Pancreatic amylase, plasma glucose, and insulin responses to propionate or monensin in sheep.

Yearling wethers fitted with reentrant bile-pancreatic duct cannulae were in a two-part study of effects of duodenal propionate infusions or increased ruminal propionate caused by dietary monensin on pancreatic alpha-amylase secretion and glucose and insulin in blood plasma. Continuous duodenal infusion of propionate increased concentrations of glucose and insulin in blood plasma of wethers fed alfalfa. Results supported a direct response of insulin secretion to propionate. Amylase secretion was not affected. Addition of monensin (22 ppm) to an 80% corn diet reduced the ratio of acetate:propionate in rumen, but bile-pancreatic flow and amylase activity were unaffected. Monensin supplementation had little influence on glucose and insulin in blood plasma. Pancreatic alpha-amylase secretion of ruminants seems to be a complex phenomenon that is not regulated strictly by fluctuations of glucose or insulin.

Amylases↗
PubMed1990

Metabolism of propionate, glucose, and carbon dioxide as affected by exogenous glucose in dairy cows at energy equilibrium.

In vivo kinetic techniques were used to quantify changes in metabolism of propionate, glucose, and blood CO2 when glucose was infused intravenously at 0, 342, or 737 g/d into four lactating cows. Neither production of milk or milk fat nor composition of milk was changed. Production of milk protein increased for the high glucose treatment. Isotope dilution data were used to calculate irreversible losses of rumen propionate, plasma glucose, and blood CO2 and to determine a unique solution for flux of C in this three-pool system. Irreversible losses of propionate and CO2 were not changed. Infusions of glucose increased irreversible loss of glucose in proportion to amounts infused, thus indicating there was no change in endogenous production of glucose. For the control, 52% of the C flux of blood glucose was derived directly from rumen propionate and another 26% came from other gluconeogenic substrates. Flux of C into glucose from exogenous sources increased in proportion to amounts of glucose infused. Flux of C from rumen propionate remained constant. The rate of C leaving the glucose pool, other than as CO2, tended to increase with infusion of glucose, and oxidation of glucose tended to increase for the high glucose treatment. High producing cows adjusted to increased exogenous glucose by increasing glucose utilization and without decreasing endogenous glucose production.

Animal Feed↗