Oxidation of acetaldehyde molecules adsorbed on Na- and Mg-Wyoming montmorillonite at room temperature (20-25°C) and in N2 atmosphere has been studied by I.R. spectroscopy, A comparison between clay-acetic acid complex and that prepared from acetaldehyde is given. The influence of the nature of the saturating cation as well as the clay pretreatment on this oxidation process are discussed and reaction pathways are proposed. Acetic acid directly adsorbed on the clay surface is almost removed at 110°C, while that produced from the oxidation of the adsorbed acetaldehyde appears to be strongly held. Within a temperature range 180-230°C, the fixed acetic acid molecules dissociate to acetate form; then occurs an interaction of the acetate and the residual acid with the lattice OH of the clay at 200–300°C. This interaction involves the loss of the structural OH and deposition of carbon on the clay surfaces. The thermal decomposition of the residual complex is almost completed at 500–600°C

This research communication investigated the role and the underlying mechanism of sn-1-acylglycerol-3-phosphate O-acyltransferase 6 (AGPAT6) in acetate-induced mTORC1 signaling activation and milk fat synthesis in dairy cow mammary epithelial cells. The data showed AGPAT6 knockdown significantly decreased acetate-induced phosphorylation of mTORC1 signaling molecules and intracellular triacylglycerol (TAG) content, whereas this inhibition effect was reversed after the addition of 16:0,18:1 phosphatidic acid (PA), suggesting that AGPAT6 could generate PA in response to acetate simulation, that in turn activates mTORC1 signaling. PPARγ is the upstream regulator of AGPAT6 upon acetate stimulation. Luciferase assay with clones containing various deletions and mutation in AGPAT6 promoter showed that there is a RXRα binding sequence located at −96 bp of AGPAT6 promoter. Acetate stimulation significantly increased the interaction between PPARγ and AGPAT6 via this RXRα binding site. Taken together, our data indicated that AGPAT6 could activate mTORC1 signaling by producing PA during acetate-induced milk fat synthesis, and PPARγ acts as a transcription factor to mediate the effect of acetate on AGPAT6 via RXRα.

We aimed to evaluate the effect of replacing corn silage by orange peel silage on nutrient intake, ruminal parameters and milk production of multiparous lactating Holstein cows. Eight fistulated Holstein cows averaging 587.5 ± 39.6 kg and 111 ± 22 d in milking were randomly assigned to a double 4 × 4 Latin square design carried out two times to determine the effects of feeding with orange peel silage (OPS) in substitution of whole plant corn silage (WPCS). The treatments were a control diet with WPCS only or diets with OPS replacing WPCS in the total mixed diet (250, 500, or 750 g/kg DM). All cows were fed the same 750 : 250 g/kg roughage : concentrate ratio. The DM intake and milk production were reduced with the OPS inclusion, with decreases in consumption of neutral detergent fibre and increased consumption of non-fibrous carbohydrates. Diets with 250 and 500 g/kg OPS showed similar milk production and protein content in milk to the standard WCPS diet, whilst 750 g/kg orange peel silage as roughage increased fat and protein contents significantly. The orange peel silage as a substitute for corn silage for feeding dairy cows did not show adverse changes in the rumen environment and showed promising results in the increase of fat in milk of Holstein cows.

The experiments reported in this research paper aimed to determine the effect of supplementing different forms of L-methionine (L-Met) and acetate on protein synthesis in immortalized bovine mammary epithelial cell line (MAC-T cells). Treatments were Control, L-Met, conjugated L-Met and acetate (CMA), and non-conjugated L-Met and Acetate (NMA). Protein synthesis mechanism was determined by omics method. NMA group had the highest protein content in the media and CSN2 mRNA expression levels (P < 0.05). The number of upregulated and downregulated proteins observed were 39 and 77 in L-Met group, 62 and 80 in CMA group and 50 and 81 in NMA group from 448 proteins, respectively (P < 0.05). L-Met, NMA and CMA treatments stimulated pathways related to protein and energy metabolism (P < 0.05). Metabolomic analysis also revealed that L-Met, CMA and NMA treatments resulted in increases of several metabolites (P < 0.05). In conclusion, NMA treatment increased protein concentration and expression level of CSN2 mRNA in MAC-T cells compared to control as well as L-Met and CMA treatments through increased expression of milk protein synthesis-related genes and production of the proteins and metabolites involved in energy and protein synthesis pathways.

Experiments to explore the dissolution behaviour of Pb-rich orthoclase (1% PbO) and quartz have been carried out in the presence of pH buffered and unbuffered potassium acetate and lithium acetate solutions at 150°C and 50 MPa (500 bars). In pH-unbuffered potassium acetate solutions Pb and Na solubilities (and pH) increase with increasing fluid acetate content, reflecting increased bulk dissolution of the feldspar; silica solubility decreases despite an increase in measured pH from 7.5 to 8.9. Similarly, in experiments at pH 6 using a potassium acetate pH buffer, quartz solubility decreases with increasing acetate content. The use of lithium acetate pH buffers (pH 6 at 25°C) in experiments with orthoclase plus quartz results in the precipitation of the lithium chlorite cookeite, complicating interpretation of the fluid chemistry. It is also apparent that in the presence of orthoclase plus quartz (but not albite alone) acetate decarboxylation takes place at much higher rates than expected for the experimental configuration used. The observed effects are unlikely to be due to the presence of acetate alone; the influence of species produced by acetate decay (especially carbonate) must also be considered. This study provides little support for models which call upon acetate to enhance the solubility of aluminosilicate minerals, and suggests that acetate decarboxylation in nature may limit its involvement in dissolution processes. It emphasises the potential of feldspars as sources of elements for mineralisation, such as Pb.

Hoganite, copper(II) acetate monohydrate, and paceite (pronounced ‘pace-ite’), calcium(II) copper(II) tetraacetate hexahydrate, occur as isolated crystals embedded in ferruginous gossan from the Potosi Pit, Broken Hill, New South Wales, Australia. They are associated with goethite, hematite, quartz, linarite, malachite, azurite, cerussite and cuprian smithsonite. Hoganite is bluish green with a pale blue streak and a Mohs hardness of 1½; it possesses perfect {001} and distinct {110} cleavages and has a conchoidal fracture. Chemical analysis of hoganite gave (wt.%) C 23.85; H 3.95; Cu 31.6; Fe 0.4; O (by difference) 40.2, yielding an empirical formula of C4H7.89O5.07Cu1.00Fe0.01. The simplified formula is C4H8O5Cu or Cu(CH3COO)2.H2O, the mineral being identical to the synthetic compound of the same formula. Single-crystal X-ray data for hoganite are: monoclinic, space group C2/c, a = 13.162(3), b = 8.555(2), c = 13.850(3)Å, β = 117.08(3)°, Z = 8. The density, calculated from single-crystal data, is 1.910 g cm−3. The strongest lines in the X-ray powder pattern are [dobs (Iobs) (hkl)] 6.921 (100) (011); 3.532 (28) (202); 6.176 (14) (200); 3.592 (11) (22); 5.382 (10) (11); 2.278 (10) (204); 5.872 (9) (002). Hoganite (orientation presently unknown) is biaxial positive with α = 1.533(2), β = 1.541(3), γ = 1.554(2), 2V(meas.) = 85(5)°, 2V(calc.) = 76.8°, dispersion is r < v, medium (white light); it is strongly pleochroic with X = blue, Y = pale bluish, Z = pale bluish green and absorption X > Y > Z. The mineral is named after Graham P. Hogan of Broken Hill, New South Wales, Australia, a miner and well-known collector of Broken Hill minerals.

Paceite is dark blue with a pale blue streak and a Mohs hardness of 1½; it possesses perfect {100} and {110} cleavages and has an uneven fracture. Chemical analysis of paceite gave (wt.%) C 21.25; H 5.3; Ca 9.0; Cu 14.1; O (by difference) 50.35, yielding an empirical formula of C8H23.77O14.23Ca1.02-Cu1.00. The simplified formula is C8H24O14CaCu or CaCu(CH3COO)4.6H2O, the mineral being identical to the synthetic compound of the same formula. Unit-cell data (refined from X-ray powder diffraction data) for paceite are: tetragonal, space group I4/m, a = 11.155(4), c = 16.236(17)Å, Z = 4. The density, calculated from refined cell data, is 1.472 g cm−3. The strongest lines in the X-ray powder pattern are [dobs (Iobs) (hkl)] 7.896 (100) (110); 3.530 (20) (310); 5.586 (15) (200); 8.132 (8) (002); 9.297 (6) (101); 2.497 (4) (420); 3.042 (3) (321). Paceite is uniaxial positive with ω = 1.439(2) and ɛ = 1.482(3) (white light); pleochroism is bluish with a greenish tint (O), pale bluish with a greyish tint (E), and absorption O ⩾ E. The mineral is named after Frank L. Pace of Broken Hill, New South Wales, Australia, an ex-miner and well-known collector of Broken Hill minerals.

An experiment was conducted to investigate the effect of acetate treatment on lipid metabolism in rabbits. New Zealand Rabbits (30 days, n=80) randomly received a subcutaneous injection (2 ml/injection) of 0, 0.5, 1.0 or 2.0 g/kg per day body mass acetate (dissolved in saline) for 4 days. Our results showed that acetate induced a dose-dependent decrease in shoulder adipose (P<0.05). Although acetate injection did not alter the plasma leptin and glucose concentration (P>0.05), acetate treatment significantly decreased the plasma adiponectin, insulin and triglyceride concentrations (P<0.05). In adipose, acetate injection significantly up-regulated the gene expression of peroxisome proliferator-activated receptor gamma (PPARγ), CCAAT/enhancer-binding protein α (C/EBPα), differentiation-dependent factor 1 (ADD1), adipocyte protein 2 (aP2), carnitine palmitoyltransferase 1 (CPT1), CPT2, hormone-sensitive lipase (HSL), G protein-coupled receptor (GPR41), GPR43, adenosine monophosphate-activated protein kinase α1 (AMPKα1), adiponectin receptor (AdipoR1), AdipoR2 and leptin receptor. In addition, acetate treatment significantly increased the protein levels of phosphorylated AMPKα, extracellular signaling-regulated kinases 1 and 2 (ERK1/2), p38 mitogen-activated protein kinase (P38 MAPK) and c-jun amino-terminal kinase (JNK). In conclusion, acetate up-regulated the adipocyte-specific transcription factors (PPARγ, C/EBPα, aP2 and ADD1), which were associated with the activated GPR41/43 and MAPKs signaling. Meanwhile, acetate decreased fat content via the upregulation of the steatolysis-related factors (HSL, CPT1 and CPT2), and AMPK signaling may be involved in the process.

Chlorimuron antagonized the activity of quizalofop on broadleaf signalgrass when applied in greenhouse studies as a postemergence tank mix. In vitro leaf disc assays utilizing 14C-acetate or 14C-pyruvate as substrates were conducted to ascertain the effect of clorimuron and quizalofop on fatty acid biosynthesis and to determine if antagonism between the two herbicides occurs at the biochemical sites of action. Incorporation of 14C-acetate in control treatments was linear with time to 120 min. Acetate incorporation in the presence of quizalofop (1.1 μM) was also linear but was inhibited 30 min after initialization of the reaction. The concentration of quizalofop that inhibited 14C-acetate incorporation 50% (I50) was 0.54 μM. Chlorimuron, up to 155 μM, had no effect on 14C-acetate incorporation. A mixture of quizalofop (1.1 μM) and chlorimuron (4.8 μM) inhibited 14C-acetate incorporation similar to that of quizalofop alone at 1.1 μM. Quizalofop I50 for incorporation of 14C-pyruvate was 1.1 μM, and clorimuron at 4.8 μM decreased incorporation 15%. Excess unlabeled pyruvate (5 μM) had no effect on either 14C-acetate or 14C-pyruvate incorporation in the presence of both herbicides. It is believed that antagonism of quizalofop by clorimuron is not due to an excess pool of pyruvate resulting from inhibition of acetolactate synthase by chlorimuron.

Most athletic horses are fed a high-starch diet despite the risk of health problems. Replacing starch concentrate with high-energy forage would alleviate these health problems, but could result in a shift in major substrates for muscle energy supply from glucose to short-chain fatty acids (SCFA) due to more hindgut fermentation of fibre. Dietary fat inclusion has previously been shown to promote aerobic energy supply during exercise, but the contribution of SCFA to exercise metabolism has received little attention. This study compared metabolic response with exercise and lactate threshold (VLa4) in horses fed a forage-only diet (F) and a more traditional high-starch, low-energy forage diet (forage–concentrate diet - FC). The hypothesis was that diet F would increase plasma acetate concentration and increase VLa4 compared with diet FC. Six Standardbred geldings in race training were used in a 29-day change-over experiment. Plasma acetate, non-esterified fatty acids (NEFA), lactate, glucose and insulin concentrations and venous pH were measured in samples collected before, during and after a treadmill exercise test (ET, day 25) and muscle glycogen concentrations before and after ET. Plasma acetate concentration was higher before and after exercise in horses on diet F compared with diet FC, and there was a tendency (P = 0.09) for increased VLa4 on diet F. Venous pH and plasma glucose concentrations during exercise were higher in horses on diet F than diet FC, as was plasma NEFA on the day after ET. Plasma insulin and muscle glycogen concentrations were lower for diet F, but glycogen utilisation was similar for the two diets. The results show that a high-energy, forage-only diet alters the metabolic response to exercise and, with the exception of lowered glycogen stores, appears to have positive rather than negative effects on performance traits.

Based on their proposed metabolic effects, we examined whether fish oil (FO) and SCFA, alone or in combination, accelerate weight loss and the resultant metabolic improvements. Obesity was induced in male C57BL/6J mice by high-energy feeding for 10 weeks. The mice were transferred to a low-fat diet (2·5w%) for 4 weeks, the source of fat being either FO, a lard–safflower oil mix (control), or both types combined with SCFA. Weight, fasting insulin, tissue and serum lipid concentrations, as well as mRNA amount of genes related to adipose inflammation and hepatic fat oxidation were determined. All groups lost weight and showed reduced fasting insulin concentrations and reduced liver TAG. However, weight loss on the control-fat diet caused significant increase in hepatic and cardiac NEFA. Substituting 20 % of the fat with SCFA increased weight loss by 48 % and reduced fasting insulin 1·5-fold more than the no-SCFA diets. It furthermore significantly increased the amount of mRNA for PPAR-α, and decreased the mRNA amount for NF-κB in the liver and white adipose tissue. The FO diets enhanced improvement of tissue lipid levels. Thus, FO improved liver TAG and NEFA levels compared with weight loss on the control diet. Combining FO and SCFA further reduced tissue NEFA accumulation. In conclusion, we found that dietary SCFA had a significant impact on gene expression in the liver and adipose tissue, and that the effect of FO on tissue NEFA content was modified by SCFA. Thus, interactions between fatty acids should be considered when studying the effects of specific fatty acids.

The recently discovered SCFA-activated G-coupled protein receptors FFA receptor 2 and FFA receptor 3 are co-localised in l-cells with the anorexigenic ‘ileal brake’ gut hormone peptide YY, and also in adipocytes, with activation stimulating leptin release. Thus, SCFA such as acetate and propionate show promise as a candidate to increase satiety-enhancing properties of food. We therefore postulate SCFA may have a role in appetite regulation and energy homeostasis. SCFA can be delivered either directly within food, or indirectly via the colon by the provision of fermentable non-digestible carbohydrates. A review of studies investigating the effects of oral SCFA ingestion on appetite suggests that while oral SCFA ingestion is associated with enhanced satiety, this may be explained by product palatability rather than a physiological effect of SCFA. Colon-derived SCFA generated during microfloral fermentation have also been suggested to explain satiety-enhancing properties of non-digestible carbohydrates. However, findings are mixed from investigations into the effects of the prebiotic inulin-type fructans on appetite. Overall, data presented in this review do not support a role for SCFA in appetite regulation.

In animals, colonic infusion of SCFA does not affect glucagon-like peptide-1 (GLP-1) release whereas intravenous infusion does and SCFA may directly stimulate peptide YY (PYY) release. It is unknown whether SCFA and their route of administration affect human blood concentrations of GLP-1 and PYY. Our aim was to conduct a pilot study to determine the effects of intravenous and rectal acetate on blood concentrations of GLP-1, PYY, ghrelin, adiponectin and TNF-α in hyperinsulinaemic human subjects. Six hyperinsulinaemic female subjects were given 20 mmol sodium acetate intravenously, 60 mmol acetate rectally, or normal saline rectally or intravenously on four separate occasions in randomised order, with blood samples collected at 0, 10, 15, 30, 45 and 60 min. Change in plasma PYY was significantly higher after acetate and rectal infusions (9·69 and 13·78 pg/ml) compared with saline and intravenous (0·60 and − 3·1 pg/ml; P < 0·01), respectively. Change in plasma GLP-1 was increased by rectal and acetate infusions (0·25 and 0·23 mmol/l) v. intravenous and saline ( − 0·26 and − 0·19 mmol/l; P < 0·01). Acetate decreased TNF-α v. saline ( − 0·8 and 0·15 pg/ml; P < 0·05). Rectal infusions increased TNF-α and ghrelin (0·2 and 98·27 pg/ml) v. intravenous ( − 0·9 and − 40 pg/ml; P < 0·01). There was no effect of treatment on plasma adiponectin. These preliminary results suggest that acetate raises plasma PYY and GLP-1, and suppresses TNF-α. Also, distending the rectum increases PYY, GLP-1, TNF-α and ghrelin in hyperinsulinaemic females. Increasing colonic fermentation products, particularly acetate, could yield a new mechanism for modifying weight gain.

The oxidation of fatty acids, carbohydrates and amino acids can be measured by quantifying the rate of excretion of labelled CO2 following administration of 14C- or 13C-labelled substrates at whole-body and tissue level. However, there is a theoretical need to correct the oxidation rates for the proportion of labelled CO2 that is produced via oxidation but not excreted. Furthermore, depending on the substrate and position of the C label(s), there may also be a need to correct for labelled C from the metabolized substrate that does not appear as CO2, but rather becomes temporarily fixed in other metabolites. The bicarbonate correction factor is used to correct for the labelled CO2 not excreted. Recently, an acetate correction factor has been proposed for the simultaneous correction of CO2 not excreted and label fixed in other metabolites via isotopic exchange reactions, mainly in the tricarboxylic acid cycle. Changes in metabolic rate induced, for example, by feeding, hormonal changes and physical activity, as well as infusion time, have been shown to affect both correction factors. The present paper explains the theoretical and physiological basis of these correction factors and makes recommendations as to how these correction factors should be used in various physiological conditions.

Acetate is normally regarded as an endproduct of anaerobic fermentation, but butyrate-producing bacteria found in the human colon can be net utilisers of acetate. The butyrate formed provides a fuel for epithelial cells of the large intestine and influences colonic health. [1-13C]Acetate was used to investigate the contribution of exogenous acetate to butyrate formation. Faecalibacterium prausnitzii and Roseburia spp. grown in the presence of 60 mm-acetate and 10 mm-glucose derived 85–90 % butyrate-C from external acetate. This was due to rapid interchange between extracellular acetate and intracellular acetyl-CoA, plus net acetate uptake. In contrast, a Coprococcus-related strain that is a net acetate producer derived only 28 % butyrate-C from external acetate. Different carbohydrate-derived energy sources affected butyrate formation by mixed human faecal bacteria growing in continuous or batch cultures. The ranking order of butyrate production rates was amylopectin > oat xylan > shredded wheat > inulin > pectin (continuous cultures), and inulin > amylopectin > oat xylan > shredded wheat > pectin (batch cultures). The contribution of external acetate to butyrate formation in these experiments ranged from 56 (pectin) to 90 % (xylan) in continuous cultures, and from 72 to 91 % in the batch cultures. This is consistent with a major role for bacteria related to F. prausnitzii and Roseburia spp. in butyrate formation from a range of substrates that are fermented in the large intestine. Variations in the dominant metabolic type of butyrate producer between individuals or with variations in diet are not ruled out, however, and could influence butyrate supply in the large intestine.

A method for the measurement of the rate of lipogenesis in ruminants using a continuous intravenous infusion of [1-14C]acetate and measuring the rate of [1-14C]acetate incorporation into adipose tissue lipid was evaluated. Subcutaneous adipose tissue samples obtained by biopsy over the course of a 6 h continuous intravenous infusion of [1-14C]acetate into a wether and a steer maintained in a ‘metabolic steady state’ demonstrated that the incorporation of [1-14C]acetate into subcutaneous adipose tissue lipid was linear for the duration of the infusion period. Subsequent measures of rates of [1-14C]acetate incorporation into adipose tissue lipid were made on adipose tissue samples taken at a single time point during the infusion period. The technique was used to measure rates of lipogenesis in the subcutaneous adipose tissue of fourteen Hereford × Friesian steers that had been fed a pelleted diet of dried grass at a range of metabolizable energy (ME) intakes from 1·1 × ME requirement for maintenance to ad libitum for 11 weeks. Rates of lipogenesis increased linearly (P<0·001) with increasing ME intake. It was concluded that the method is an effective technique for measuring rates of lipogenesis in specific adipose tissue depots in vivo in ruminants.

In the present study the actual role of propionic acid in the control of fatty acid and cholesterol synthesis was investigated in isolated liver cells from fed rats maintained in the presence of near-physiological concentrations of glucose, glutamine and acetate. Using 3H2O for lipid labelling, propionate appears as an effective inhibitor of fatty acid synthesis and to a lesser extent of cholesterol synthesis, even at the lowest concentration used (0·6 mmol/l). Butyrate is a potent activator of both synthetic pathways, and the activating effect was not counteracted by propionate. Using 1-[14C]acetate, it was observed that propionate at a moderate concentration, or 1 mmol oleate/l, are both very effective inhibitors of 14C incorporation into fatty acid and cholesterol. This incorporation was drastically inhibited when propionate and oleate were present together in the incubation medium. The net utilization of acetate by rat hepatocytes was impaired by propionate, in contrast to oleate. 1-[14C]butyrate was utilized at a high rate for fatty acid synthesis, but to a lesser extent for cholesterol synthesis; both processes were unaffected by propionate. Intracellular citrate concentration was not markedly depressed by propionate, whereas it was strongly elevated by butyrate. In conclusion, propionate may represent an effective inhibitor of lipid synthesis when acetate is a major source of acetyl-CoA, a situation which is encountered with diets rich in readily-fermentable fibres. The present findings also suggest that propionate may be effective at concentrations close to values measured in vivo in the portal vein.