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PubMed1997

Effects of methylmalonate and propionate on [3H]glutamate binding, adenylate cyclase activity and lipid synthesis in rat cerebral cortex.

The effects of methylmalonic (MMA) and propionic acid (PPA), metabolites that accumulate in methylmalonic and propionic acidemia respectively, on [3H]glutamate binding, adenylate cyclase activity and [U-14C]acetate incorporation into lipids were investigated in rat cerebral cortex. Neither acid effected [3H]glutamate binding, regardless of the presence of sodium in the incubation medium. Also, the acids had no effect on basal or GMP-PNP-stimulated adenylate cyclase activity. These results suggest that MMA and PPA do not interact with glutamate binding sites and have no effect on basal or guanine nucleotide-stimulated adenylate cyclase activity. In contrast, [U-14C]acetate incorporation into brain lipids was significantly blocked by both acids, the effects being more pronounced with PPA, indicating an inhibition of brain lipid biosynthesis caused by MMA and PPA. These results may explain at least in part the hypomyelinization and/or demyelinization characteristic of patients affected by methylmalonic acidemia and propionic acidemia.

Acetates↗
PubMed2004

Kinetics of LCFA inhibition on acetoclastic methanogenesis, propionate degradation and beta-oxidation.

Kinetics of long-chain fatty acids (LCFAs) inhibition on acetoclastic methanogenesis, propionate degradation and beta-oxidation were studied with granular sludge under mesophilic batch conditions. Mathematical expressions used for reaction rates were as shown below: [formula: see text]. The simulated results revealed that the methane production rates from acetate decreased with an increase in both concentration and the number of double bonds of LCFAs. The concentrations of oleate (C18:1), linoleate (C18:2), palmitate (C16:0), and stearate (C18:0) were 0.54 mM, 0.11 mM 1.62 mM, and 2.58 mM, respectively, at which the methane production rates from acetate dropped 10%, and 3.10 mM, 0.72 mM, 5.71 mM, and 5.37 mM, respectively, at which the rates dropped 50%. The inhibitory effects of LCFAs on propionate degradation showed a similar tendency with acetoclastic methanogenesis; however, were less severe. The concentrations of oleate, linoleate, palmitate, and stearate were 1.02 mM, 0.18 mM, 2.34 mM, and 1.92 mM, respectively, at which the propionate degradation rates dropped 10%, and 4.38 mM, 1.17 mM, 5.88 mM, and 5.18 mM, respectively, at which the rates dropped 50%. The observed maximum beta-oxidation rates of oleate, linoleate, palmitate, and stearate were 0.21 mmol (gVSS)(-1) d(-1), 0.09 mmol (gVSS)(-1) d(-1), 0.12 mmol (gVSS)(-1) d(-1), and 0.08 mmol (gVSS)(-1) d(-1), respectively. The lag-phase times in beta-oxidation were also dependent on LCFA concentrations. The concentrations of oleate, linoleate, palmitate, and stearate, at which the lag-phase times became 5 days, were 5.93 mM, 2.24 mM, 4.02 mM, and 2.81 mM, respectively.

Fatty Acids↗
PubMed1980

Effects of intravenous infusions of glucose, lactate, propionate or acetate on the induction of lipogenesis in bovine adipose tissue.

Crossbred steers (seven to nine per treatment) fed a pelleted alfalfa hay diet were biopsied (preinfusion) to obtain subcutaneous adipose tissue (SAT). Five days later a continuous intravenous infusion was begun of either 0.9% NaCl, glucose (2.75 moles/day), DL-lactate (5.5 moles/day of L-lactate), propionate (5.5 moles/day) or acetate (8.25 moles/day); after infusion for 14 days, a second biopsy sample of SAT was obtained. Glucose and DL-lactate infusion increased acetyl-CoA carboxylase activity about 12-fold compared to preinfusion activity of 5.3 +/- 4.2 nmoles/minute/g of wet weight. Glucose infusion induced activities of fatty acid synthetase (2.6 fold) and NADP+-malate dehydrogenase (7-fold) relative to preinfusion activities of 26.8 +/- 5.2 and 30.3 +/- 15.5 nmoles/minute/g of wet weight, respectively. Glucose, DL-lactate and propionate infusion increased NADP-isocitrate dehydrogenase activity 20-30% compared to preinfusion activity. Activity of NAD-malate dehydrogenase was not altered by any infusion treatment (P > 0.05). Activity of ATP-citrate lyase was decreased 48% by lactate infusion. Glucose, lactate and propionate infusion increased the rates of lactate and glucose incorporation into fatty acids in SAT incubated in vitro three to fourfold over preinfusion incorporation rates. Increased availability of glucose or gluconeogenic precursors may be responsible for induction of lipogenesis in steers fed high concentrate diets.

Acetates↗
PubMed1991

High propionic acid fermentations and mineral accumulation in the cecum of rats adapted to different levels of inulin.

The digestive and metabolic effects of inulin (from chicory) were studied in rats adapted to semipurified diets containing 0, 5, 10 or 20% inulin (wt/wt). Moderate levels of inulin (5-10%) did not significantly affect food intake or body weight gain. Dietary inulin resulted in considerably greater cecal fermentation and a significantly greater intraluminal concentration of propionate (peaking at 58.4 mmol/L). A lower concentration of acetate (42.6 mmol/L) was observed in rats fed 20% inulin. Lactic fermentations were observed in rats fed the 10 or 20% inulin diets. The cecal pool of volatile fatty acids tended to reach a plateau in rats fed diets containing more than 10% inulin (up to 600-700 mumol), but volatile fatty acid absorption was a slightly hyperbolic function of the dietary inulin level. Butyrate absorption was proportionally lower than that of propionate. Inulin-containing diets induced an enlargement of the cecal pool of calcium, phosphate and (to a lesser extent) magnesium. There was also an enhanced absorption of these divalent cations. The cecal pool of bile acids was greater in rats fed inulin, and this oligosaccharide displayed a slight hypocholesterolemic effect, even in rats fed the 5% inulin diet. However, plasma triglycerides were depressed only in rats fed the 20% inulin diet. In conclusion, inulin seems very effective in promoting propionic fermentation and in enhancing the calcium content of the large intestine. However, high levels of inulin (greater than 10%) may affect growth in rats and lead to acidic (pH 5.65) cecal fermentation.

Adaptation, Physiological↗
PubMed2000

In vitro fermentation of swine ileal digesta containing oat bran dietary fiber by rat cecal inocula adapted to the test fiber increases propionate production but fermentation of wheat bran ileal digesta does not produce more butyrate.

This experiment evaluated three hypotheses: i) production of propionate is increased during fermentation of substrate containing oat bran (OB)(6); ii) production of butyrate is increased during fermentation of substrate containing wheat bran (WB) and iii) results of in vitro fermentations using physiological substrates and inocula agree with in vivo data. Ileal digesta collected from swine fed OB and WB were the substrates. Digesta was fermented for 0-96 h in an anaerobic in vitro system using inocula prepared from ceca of rats fed the same fiber sources. Carbohydrate and short-chain fatty acid (SCFA) contents in the fermentations were measured by gas chromatography. Fermentation of WB digesta did not produce more n-butyrate (P > 0.05) and was significantly slower (P < 0.05) than fermentation of OB digesta. OB digesta fermentation produced a significantly greater (P < 0.05) molar proportion of SCFA as propionate. Bacterial mass increased more and was maintained longer during fermentation of OB digesta than the WB digesta. Our results indicate that dilution of undigested WB fiber and not n-butyrate production is one mechanism by which WB may protect colonic mucosa; propionate production is increased during fermentation of beta-glucan in OB; and an in vitro system using physiological sources of inoculum and substrate containing WB and OB yields results that agree with in vivo findings in humans and rats.

Analysis of Variance↗
PubMed2000

Propionic and L-methylmalonic acids induce oxidative stress in brain of young rats.

The in vitro effects of propionic and L-methylmalonic acids on some parameters of oxidative stress were investigated in the cerebral cortex of 21-day-old rats. Chemiluminescence, thiobarbituric acid-reactive substances (TBA-RS) and total radical-trapping antioxidant capacity (TRAP) were measured in brain tissue homogenates in the presence of propionic or L-methylmalonic acids at concentrations ranging from 1 to 10mM. Both acids significantly increased chemiluminescence and TBA-RS and decreased TRAP, indicating a simulation of lipid peroxidation and a reduction of tissue antioxidant potential. Other organic acids tested which accumulate in some organic acidemias (suberic, sebacic, adipic, 3-methylglutaric and 4-hydroxybutyric acids) did not affect these parameters. This study provides evidence that free radical generation may participate in the neurological dysfunction of propionic and methylmalonic acidemias.

Animals↗
PubMed1998

Syntrophobacter fumaroxidans sp. nov., a syntrophic propionate-degrading sulfate-reducing bacterium.

A syntrophic propionate-oxidizing bacterium, strain MPOBT, was isolated from a culture enriched from anaerobic granular sludge. It oxidized propionate syntrophically in co-culture with the hydrogen- and formate-utilizing Methanospirillum hungateii, and was able to oxidize propionate and other organic compounds in pure culture with sulfate or fumarate as the electron acceptor. Additionally, it fermented fumarate. 16S rRNA sequence analysis revealed a relationship with Syntrophobacter wolinii and Syntrophobacter pfennigii. The G + C content of its DNA was 60.6 mol%, which is in the same range as that of other Syntrophobacter species. DNA-DNA hybridization studies showed less than 26% hybridization among the different genomes of Syntrophobacter species and strain MPOBT. This justifies the assignment of strain MPOBT to the genus Syntrophobacter as a new species. The name Syntrophobacter fumaroxidans is proposed; strain MPOBT (= DSM 10017T) is the type strain.

Anaerobiosis↗
PubMed2004

Characterization of the marine propionate-degrading, sulfate-reducing bacterium Desulfofaba fastidiosa sp. nov. and reclassification of Desulfomusa hansenii as Desulfofaba hansenii comb. nov.

A rod-shaped, slightly curved sulfate reducer, designated strain P2(T), was isolated from the sulfate-methane transition zone of a marine sediment. Cells were motile by means of a single polar flagellum. The strain reduced sulfate, thiosulfate and sulfite to sulfide and used propionate, lactate and 1-propanol as electron donors. Strain P2(T) also grew by fermentation of lactate. Propionate was oxidized incompletely to acetate and CO(2). The DNA G+C content was 48.8 mol%. Sequence analysis of the small-subunit rDNA and the dissimilatory sulfite reductase gene revealed that strain P2(T) was related to the genera Desulfonema, Desulfococcus, Desulfosarcina, 'Desulfobotulus', Desulfofaba, Desulfomusa and Desulfofrigus. These genera include incomplete as well as complete oxidizers of substrates. Strain P2(T) shared important morphological and physiological traits with Desulfofaba gelida and Desulfomusa hansenii, including the ability to oxidize propionate incompletely to acetate. The 16S rRNA gene similarities of P2(T) to Desulfofaba gelida and Desulfomusa hansenii were respectively 92.9 and 91.5 %. Combining phenotypic and genotypic traits, we propose strain P2(T) to be a member of the genus Desulfofaba. The name Desulfofaba fastidiosa sp. nov. (type strain P2(T)=DSM 15249(T)=ATCC BAA-815(T)) is proposed, reflecting the limited number of substrates consumed by the strain. In addition, the reclassification of Desulfomusa hansenii as a member of the genus Desulfofaba, Desulfofaba hansenii comb. nov., is proposed. A common line of descent and a number of shared phenotypic traits support this reclassification.

DNA, Bacterial↗
PubMed2006

Anaerobic and aerobic metabolism of glycogen-accumulating organisms selected with propionate as the sole carbon source.

In the microbial competition observed in enhanced biological phosphorus removal (EBPR) systems, an undesirable group of micro-organisms known as glycogen-accumulating organisms (GAOs) compete for carbon in the anaerobic period with the desired polyphosphate-accumulating organisms (PAOs). Some studies have suggested that a propionate carbon source provides PAOs with a competitive advantage over GAOs in EBPR systems; however, the metabolism of GAOs with this carbon source has not been previously investigated. In this study, GAOs were enriched in a laboratory-scale bioreactor with propionate as the sole carbon source, in an effort to better understand their biochemical processes. Based on comprehensive solid-, liquid- and gas-phase chemical analytical data from the bioreactor, a metabolic model was proposed for the metabolism of propionate by GAOs. The model adequately described the anaerobic stoichiometry observed through chemical analysis, and can be a valuable tool for further investigation of the competition between PAOs and GAOs, and for the optimization of the EBPR process. A group of Alphaproteobacteria dominated the biomass (96 % of Bacteria) from this bioreactor, while post-fluorescence in situ hybridization (FISH) chemical staining confirmed that these Alphaproteobacteria produced poly-beta-hydroxyalkanoates (PHAs) anaerobically and utilized them aerobically, demonstrating that they were putative GAOs. Some of the Alphaproteobacteria were related to Defluvicoccus vanus (16 % of Bacteria), but the specific identity of many could not be determined by FISH. Further investigation into the identity of other GAOs is necessary.

Aerobiosis↗
PubMed1990

Defective oxidation of pristanic acid by fibroblasts from patients with disorders in propionic acid metabolism.

The alpha-methyl fatty acid, pristanic acid (2, 6, 10, 14 tetramethylpentadecanoic acid) is oxidised rapidly by normal skin fibroblasts in culture to CO2 and to water-soluble metabolites. The latter are secreted into the culture medium. Fibroblasts from patients with propionyl CoA carboxylase, and to a lesser extent from patients with methylmalonyl CoA mutase defects, show reductions in the amount of CO2 released, although the production of water-soluble metabolites is not affected. Our data indicate that propionic acid is produced from pristanic acid, and ultimately from its immediate precursor phytanic acid. As phytanic and pristanic acids are significant components of diets rich in ruminant fats, it is likely that they may contribute to the accumulation of propionate and its metabolites in disorders of propionate metabolism.

Amino Acid Metabolism, Inborn Errors↗
PubMed1986

NH3 and propionate modulate the morphological response of aggregation-competent Dictyostelium discoideum to cAMP.

Two metabolites, NH3 and propionic acid, are known to act as morphogens during the development of Dictyostelium discoideum, specifically altering the course of morphogenesis and cytodifferentiation. They have also been shown to modulate the cAMP relay in this organism: NH3 by restricting intracellular accumulation, and propionate by inhibiting extracellular release. In the present study, we utilized the light-scattering properties of aggregation-competent cells in agitated suspension to demonstrate that the morphological responses of such cells to exogenous cAMP are also modulated by NH3 and propionate in a manner that has interesting implications for the overall control of morphogenetic movements in D. discoideum. Our experiments were conducted using a newly designed continuous-flow apparatus that represents a significant improvement in the technique. The apparatus is described in detail.

Ammonium Chloride↗
PubMed1976

A case of methylmalonic and propionic acidemia due to methulmalonyl-CoA carbonylmutase apoenzyme deficiency.

A patient presenting with a deep metabolic acidosis after birth is described. Gas chromatographic analysis of short chain fatty acid and non volatile organic acids revealed the presence of both propionic and methylmalonic acid. In plasma obtained immediately after death the propionic- and methylmalonic acid concentrations were measured after separation of both acids by thin layer chromatography. The propionic acid concentration was about 5 mM while the methylmalonic acid concentration was 2.6 mM. The methylmalonic acid concentration in urine was 6.8 mM. Propionyl-CoA carboxylase activity measured in leucocytes and liver-mitochondria revealed normal values (53 pmoles/min/mg protein and 6.5 nmoles/min/mg protein respectively). 2-14C-Methyl-malonate oxydation in intact fibroblasts was totally blocked in the patient's cells. The methylmalonyl-CoA carbonyl mutase activity was found to be absent in the patient's fibroblasts. Addition of vit. B12 coenzyme to the incubation mixture stimulated 14C-succinate formation in the control cells but not in the patient's cells.

Acidosis↗
PubMed1966

Transfer of propionate by rat small intestine in vitro.

1. The transfer of propionate by sacs of rat everted intestine has been investigated in relation to a number of physico-chemical factors which affect movement of weak electrolytes.2. Neither the observed movement nor the distribution of propionate can be accounted for by the theory of non-ionic diffusion or by modifications of it, such as the microclimate hypothesis or partial permeability to ions.3. It is not possible to account for the observed propionate movement by the electrical potential across the gut or by solvent drag.4. The most satisfactory explanation for the observations is a transfer process in the gut for volatile fatty acids, and some features of this are discussed.

Animals↗
PubMed1990

Effects of propionate and acetate additions on solvent production in batch cultures of Clostridium acetobutylicum.

Addition of acetate or propionate to uncontrolled-pH batch cultures does not affect the initiation of solventogenesis but does enhance final solvent concentrations compared with those of unchallenged cultures. This observation can be explained in terms of the increased buffering capacity of the medium brought about by the added acids, resulting in protection against premature growth inhibition due to low culture pH values at the end of the fermentation. The uptake of propionic acid from the medium does not proceed solely via the coenzyme A-transferase pathway, since less acetone than propanol is formed. Therefore, at least 50% of the propionic acid is taken up through the reversed kinase-phosphotransbutyrylase reaction pathway.

1-Butanol↗
PubMed1996

Population dynamics of propionate-oxidizing bacteria under methanogenic and sulfidogenic conditions in anaerobic granular sludge.

Laboratory-scale upflow anaerobic sludge-bed reactors were inoculated with industrial granular sludge and fed with either propionate or propionate and sulfate. The population dynamics of the propionate-oxidizing bacteria Desulfobulbus sp. and the syntrophically growing strain SYN7 were studied in reactors by dot blot and in situ hybridization with 16S rRNA-based oligonucleotide probes.

Bacteria, Anaerobic↗
PubMed2002

Identification of the 2-methylcitrate pathway involved in the catabolism of propionate in the polyhydroxyalkanoate-producing strain Burkholderia sacchari IPT101(T) and analysis of a mutant accumulating a copolyester with higher 3-hydroxyvalerate content.

Burkholderia sacchari IPT101(T) induced the formation of 2-methylcitrate synthase and 2-methylisocitrate lyase when it was cultivated in the presence of propionic acid. The prp locus of B. sacchari IPT101(T) is required for utilization of propionic acid as a sole carbon source and is relevant for incorporation of 3-hydroxyvalerate (3HV) into copolyesters, and it was cloned and sequenced. Five genes (prpR, prpB, prpC, acnM, and ORF5) exhibited identity to genes located in the prp loci of other gram-negative bacteria. prpC encodes a 2-methylcitrate synthase with a calculated molecular mass of 42,691 Da. prpB encodes a 2-methylisocitrate lyase. The levels of PrpC and PrpB activity were much lower in propionate-negative mutant IPT189 obtained from IPT101(T) and were heterologously expressed in Escherichia coli. The acnM gene (ORF4) and ORF5, which are required for conversion of 2-methylcitric acid to 2-methylisocitric acid in Ralstonia eutropha HF39, are also located in the prp locus. The translational product of ORF1 (prpR) had a calculated molecular mass of 70,598 Da and is a putative regulator of the prp cluster. Three additional open reading frames (ORF6, ORF7, and ORF8) whose functions are not known were located adjacent to ORF5 in the prp locus of B. sacchari, and these open reading frames have not been found in any other prp operon yet. In summary, the organization of the prp genes of B. sacchari is similar but not identical to the organization of these genes in other bacteria investigated recently. In addition, this study provided a rationale for the previously shown increased molar contents of 3HV in copolyesters accumulated by a B. sacchari mutant since it was revealed in this study that the mutant is defective in prpC.

Amino Acid Sequence↗
PubMed2005

A propionate-inducible expression system for enteric bacteria.

A series of new expression vectors (pPro) have been constructed for the regulated expression of genes in Escherichia coli. The pPro vectors contain the prpBCDE promoter (P(prpB)) responsible for expression of the propionate catabolic genes (prpBCDE) and prpR encoding the positive regulator of this promoter. The efficiency and regulatory properties of the prpR-P(prpB) system were measured by placing the gene encoding the green fluorescent protein (gfp) under the control of the inducible P(prpB) of E. coli. This system provides homogenous expression in individual cells, highly regulatable expression over a wide range of propionate concentrations, and strong expression (maximal 1,500-fold induction) at high propionate concentrations. Since the prpBCDE promoter has CAP-dependent activation, the prpR-P(prpB) system exhibited negligible basal expression by addition of glucose to the medium.

Bacterial Proteins↗
PubMed1981

Butyrate and propionate: important components of toxic dental plaque extracts.

Extracts of in vitro-cultured human dental plaque contain factors toxic to mammalian cells. Previous studies demonstrated that those toxic factors most readily released from cultured plaque had very low molecular weights and were heat stable. Studies reported here demonstrate that metabolic end products including short-chain fatty acids were present in fractions containing the low-molecular-weight, heat-stable factors. The salts of two of these acids, butyrate and propionate, inhibited proliferation of both mouse L929 cells and human gingival fibroblasts. Furthermore, when tested at concentrations present in plaque extracts, the inhibitory effects of butyrate and propionate accounted for essentially all the inhibitory potential of the extracts. These findings, taken together with those of other groups, suggest that butyrate and propionate, end products of dental plaque metabolism, may have an etiological role in periodontal disease.

Animals↗