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PubMed1989

Effect of the time of administration of calcium acetate on phosphorus binding.

Phosphorus binders are given to patients with renal failure to increase gastrointestinal excretion of phosphorus. To determine the relative importance of the binding of dietary as compared with endogenous phosphorus and to determine the optimal dose schedule, we gave either 4.4 g of calcium acetate (25 mmol of calcium) or a placebo to six normal subjects on each of seven different schedules in a randomized sequence. The net gastrointestinal balance of phosphorus and calcium was determined by a one-day lavage technique. After a meal containing approximately 12 mmol of phosphorus, the mean phosphorus absorption (+/- SE) measured 9.17 +/- 0.36 mmol (78 percent) with placebo but decreased to 3.81 +/- 0.58 mmol (31 percent) when calcium acetate was given immediately before the meal (representing binding of 5.36 +/- 0.77 mmol of phosphorus). Similar binding was observed when calcium acetate was given immediately after the meal and when half the dose was given before and half after the meal. In contrast, when calcium acetate was given two hours after the meal or while the subject was fasting, phosphorus binding was reduced to 2.00 +/- 0.52 mmol and 1.81 +/- 0.84 mmol, respectively. Calcium absorption from calcium acetate averaged 21 +/- 1 percent when the binder was given with a meal; absorption from calcium acetate averaged 40 +/- 4 percent when the binder was given while the subject was fasting. We conclude that calcium acetate increases fecal excretion of phosphorus by binding both dietary and endogenous phosphorus, but the binding of dietary phosphorus is quantitatively much more important. For the most efficient phosphorus binding, calcium (and presumably other phosphorus-binding cations) should be given with meals.

Acetates↗
PubMed1991

The treatment of uraemic hyperphosphataemia with calcium acetate and calcium carbonate: a comparative study.

A comparative study of long-term haemodialysis patients investigated the effects of calcium acetate and calcium carbonate on concentrations of serum phosphate, calcium, and parathyroid hormone. It was demonstrated that both substances led to a significant decrease in phosphate and serum parathyroid hormone. Administration of calcium acetate reduced the serum phosphate concentration in 7 weeks from an initial value of 2.08 +/- 0.53 mmol/l to 1.51 +/- 0.39 mmol/l (P less than 0.01). Following a 1-week wash-out period, calcium carbonate reduced the serum phosphate concentration in the same patients from 1.99 +/- 0.62 mmol/l to 1.34 +/- 0.40 mmol/l (P less than 0.01). Of particular significance, however, is the fact that in relation to daily elementary calcium intake, calcium acetate was a considerably more effective binder of intestinal phosphate than calcium carbonate. During administration of calcium acetate only 1.02 g of elementary calcium were required daily in order to reduce the serum phosphate concentration. The same patients, however, required 1.88 g of elementary calcium during calcium carbonate therapy. Complementary studies investigated the influence of an accompanying calcitriol medication. In this instance, too, calcium acetate was shown to be more effective; although the patients developed hypercalcaemia with calcium acetate, this happened more often with calcium carbonate. In summary it can be said that daily calcium loading of the uraemic organism under calcium acetate therapy is reduced by nearly half as compared to calcium carbonate therapy, and that this can be achieved with the same effective decrease of the serum phosphate concentration.

Acetates↗
PubMed1989

Acetate and arachidonate incorporations into lipids of ovine chorioallantoic tissue at day 24 of pregnancy.

Incorporation of acetate and arachidonic acid into lipid classes was examined in chorioallantoic membranes obtained from sheep at Day 24 of pregnancy. Conceptus tissues were incubated in vitro with 5 mM acetate, 0.042 mM arachidonate, 0.45 muCi [1-14C]acetate, and 5.0 muCi [5,6,8,9,11,12,14,15-3H]arachidonate for 3 and 6 h. After incubation, tissue lipid fractions were extracted, isolated, and examined for radiolabel incorporations. Medium was extracted and analyzed for radiolabeled metabolites. Metabolic pathways commonly associated with fatty acid metabolism were confirmed to be present. Acetate was utilized for de novo synthesis of free cholesterol and free fatty acid. Fatty acids containing radiolabel from both acetate and arachidonate were mainly esterified in phospholipid and triglyceride, major lipid classes found in chorioallantoic tissue. Labeled metabolites of acetate were not sufficient for analytical measurement in medium. Metabolites of arachidonic acid from lipoxygenase and cyclooxygenase pathways were determined in medium after incubation. Results suggest that, within Day 24 ovine chorioallantoic tissue, utilization of exogenous arachidonate and de novo lipogenesis from acetate function in a parallel and anabolic mode appropriate for membrane expansion.

Acetates↗
PubMed1995

Effect of acetate on sorbitol fermentation by oral lactobacilli.

The rate of acid production and end-products from sorbitol were measured under anaerobic conditions in washed-cell suspensions of oral strains of Lactobacillus casei subsp. casei and Lactobacillus casei subsp. rhamnosus. The enzymatic activities were assayed in cell extracts of these strains. The cells fermented sorbitol to lactate, formate, ethanol and acetate under anaerobic conditions. Exposure of the cells to air (oxygen) led to inactivation of pyruvate formate-lyase and inhibition of anaerobic sorbitol fermentation. In the presence of acetate, air-exposed cells fermented sorbitol with a concomitant consumption of acetate and production of ethanol and lactate. Acetate also enhanced acid production from sorbitol in cells kept under anaerobic conditions and resulted in formation of lactate and ethanol. Cell extracts of all the strains had NADH-coupled acetate-reducing activity, which consisted of sequential reactions of acetate kinase, phosphotransacetylase, acylating aldehyde dehydrogenase and alcohol dehydrogenase. These findings indicate that oral lactobacilli can utilize acetate as an electron acceptor for maintaining their intracellular redox balance during anaerobic sorbitol fermentation in the absence of pyruvate formate-lyase activity.

Acetate Kinase↗
PubMed1991

Misoprostol attenuates acetic acid-induced increases in mucosal permeability and inflammation: role of blood flow.

The objectives of this study were 1) to quantify the effects of misoprostol (Miso; prostaglandin E1 analogue) on acetic acid-induced increases in mucosal permeability and inflammation; 2) to determine what effect acetic acid, Miso, or the combination of Miso plus acetic acid has on colonic blood flow; and 3) to assess whether the protective effect of Miso may be attributable to its vasodilatory properties. We found that intrarectal administration of acetic acid produced a 6.4-fold increase in colonic myeloperoxidase activity (an index of granulocyte infiltration), an 8.2-fold increase in mucosal permeability, a 1.6-fold increase in colonic weight, and a 6.8% decrease in body weight 48 h after enema. Miso pretreatment significantly attenuated the increases in colonic myeloperoxidase activity, mucosal permeability, and colon weight as well as prevented the loss of body weight. In a different series of experiments, we found that blood flow in the descending, transverse, and ascending colon increased 2.5- to 3.5-fold immediately after the acetic acid enema; however, it returned to control values at 1 and 4 h after enema. Miso pretreatment, followed by acetic acid, resulted in a further increase (2.5-fold) in blood flow in the descending colon 1 h after enema compared with acetic acid alone. This Miso-induced increase in blood flow at 1 h could not account for its protective effect inasmuch as colonic mucosal permeability (i.e., injury) in Miso-pretreated animals was not significantly different from values obtained in animals pretreated with vehicle and then given the enema.

Acetates↗
PubMed1992

Acetic acid-induced colitis in the rat: a reproducible experimental model for acute ulcerative colitis.

There exists no ideal model for experimental ulcerative colitis in common laboratory animals. Therefore, we tried in the present study to establish a reproducible model for inducing colitis in rats by using acetic acid. A blind loop of the colon including the cecum, ascending colon and part of the transverse colon, was brought out through two colostomies. After mechanical washing with warm normal saline, acetic acid was instilled at different doses (4, 6 and 8%) for different exposure times (10, 15, 20, 25 and 30 s). The excluded colon was examined by light microscopy on the 1st, 2nd, 3rd, 4th, 7th and 14th days after operation and acetic acid instillation. We found that 4% acetic acid for 15 s produced a moderate, superficial colitis on the 1st day after operation, whereafter a uniform colitis evolved in all rats on the 4th day after operation. The developed colitis showed morphological similarities with human ulcerative colitis. Signs of healing and regeneration of the mucosa were seen on the 7th day, and the mucosa became almost normal at the 14th day after operation. 6 or 8% acetic acid solution or exposure times exceeding 15 s resulted in severe, deep colitis with a concomitant high mortality rate. In contrast, at exposure times less than 15 s, acetic acid induced only mild superficial colitis. We conclude that by using 4% acetic acid for 15 s in the excluded colon a uniform and reproducible colitis pathologically resembling human ulcerative colitis could be achieved. Furthermore, no mortality was encountered and the general health of the rats was similar to that of the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗
PubMed1985

A mechanism of hypoxemia during hemodialysis. Consumption of CO2 in metabolism of acetate.

The present study is an investigation of the role of acetate metabolism in dialysis-induced hypoxemia and of the relative roles of acetate metabolism, bicarbonate loss, and CO2 gas (g) loss in causation of hypoxemia. The loss of CO2 (g) measured in 23 patients during acetate dialysis was found to be negligible (0.21 +/- 0.01 mmol/min). The HCO-3 loss was substantial (3.4 +/- 0.5 mmol/min), but its predicted effect on dialysis hypoxemia was modest. The infusion of acetate at 4 mmol/min into 6 normal volunteers decreased the respiratory exchange ratio (R) from 0.83 +/- 0.06 to 0.71 +/- 0.06 with constant O2 consumption (VO2) and reduced net CO2 production (VCO2). In another experiment, the infusion of sodium acetate into 9 normal volunteers resulted in a similar reduction in R (from 0.82 +/- 0.04 to 0.71 +/- 0.04) and arterial pO2 (from 92.3 +/- 1.1 to 78.3 +/- 1.7 mm Hg). The results indicate that acetate metabolism can lead to reduction in R and hypoxemia and suggest that the same mechanism is responsible for hypoxemia during hemodialysis using acetate dialysate.

Acetates↗
PubMed1988

Radiolabeled acetate as a tracer of myocardial tricarboxylic acid cycle flux.

The kinetics of [1-14C]acetate oxidation in isolated perfused rat hearts have been determined over a range of perfusion conditions. Effluent measurements demonstrated that 14CO2 cleared biexponentially over 50 minutes after bolus injection of [1-14C]acetate into normoxic hearts perfused with 5 mM glucose and 10 mU/ml insulin. The clearance half-time (t1/2) for the predominant initial clearance phase was 3.1 +/- 0.5 minutes (n = 4). MVO2 was varied over a fourfold range by hypoxia and phenylephrine stimulation (t1/2, 7.2 +/- 1.2 and 2.2 +/- 0.2 minutes, respectively) and in the presence of alternate substrates (lactate, 2 mM; DL-3-hydroxybutyrate, 20 mM; and palmitate, 0.1 mM), which did not modify either tricarboxylic acid (TCA) cycle flux or acetate kinetics. A good correlation (r = 0.93) was observed between k, the rate constant for the initial phase of 14CO2 clearance, and TCA cycle flux, estimated from oxygen consumption. In contrast to results with [1-14C]acetate, lactate (2 mM) increased t1/2 for 14CO2 clearance from a bolus injection of [1-14C]palmitate from 3.0 +/- 0.4 minutes (n = 3) at control to 4.3 +/- 0.2 minutes (n = 3, p less than 0.01). Addition of acetate in nontracer amounts (0.5 or 5 mM) caused significant underestimation of TCA cycle flux when estimated with [1-14C]acetate. 14CO2 clearance accounted for 88-98% of total effluent 14C between 10 and 20 minutes after [1-14C]acetate bolus injection; rate constants for clearance of 14CO2 and total 14C clearance were very similar during this period, and these two rate constants did not differ significantly from each other under any conditions tested.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗
PubMed2005

Acetate and ethanol production from H2 and CO2 by Moorella sp. using a repeated batch culture.

The growth inhibition of Moorella sp. HUC22-1 by undissociated acetic acid was analyzed using a non-competitive inhibition model coupled with a pH inhibition model. In the cells grown on H2 and CO2, the inhibition constant, K(p) of the undissociated acetic acid was 6.2 mM (164 mM as the total acetate at pH 6.2, pKa = 4.795, 55 degrees C), which was 1.5-fold higher than that obtained in cells grown on fructose. When a pH-controlled batch culture was performed using a fermentor at pH 6.2 with H2 and CO2, a maximum of 0.92 g/l of dry cell weight and 339 mM of acetate were produced after 220 h, which were 4.4- and 6.8-fold higher than those produced in the pH-uncontrolled batch culture, respectively. In order to reduce acetate inhibition in the culture medium, a repeated batch culture with cell recycling was performed at a constant pH with H2 and CO2. At a pH of 6.2, the total acetate production reached 840 mmol/l-reactor with 4.7 mmol/l-reactor of total ethanol production after 420 h. When the culture pH was maintained at 5.8, which was the optimum for ethanol production, the total ethanol production reached 15.4 mmol/l-reactor after 430 h, although the total acetate production was decreased to 675 mmol/l-reactor.

Acetates↗
PubMed1992

Calcium acetate as a phosphorus binder in hemodialysis patients.

Much interest is currently centered on the use of calcium acetate as a phosphorus binder in patients with renal failure. Therefore, this compound in subjects previously stable on calcium carbonate and undergoing high-efficiency hemodialysis with a dialysate calcium of 2.5 mEq/L was evaluated. Twenty subjects were switched from generic calcium carbonate to a single calcium carbonate preparation for a period of 2 months. This was followed by a phase (1 month) in which calcium acetate was substituted for calcium carbonate at a dose containing half the amount of elemental calcium. Subjects then continued calcium acetate for 6 months. It was found that calcium acetate allowed comparable control of immunoreactive parathyroid hormone, calcium, and phosphorus levels compared with calcium carbonate. This occurred with half the amount of elemental calcium ingested in the form of calcium acetate (349 +/- 25 versus 699 +/- 75 mmol/day; P less than 0.001). With this lower dose, the overall incidence of hypercalcemia was the same with each formulation. In the eight subjects concurrently receiving i.v. calcitriol, the incidence of hypercalcemia was significantly higher during the first month of calcium acetate compared with that in those not receiving this compound (P less than 0.05). Of those four subjects receiving the high dose of calcitriol (2 micrograms thrice weekly), all required either reduction in the dose or discontinuation of the drug. Thus, mineral metabolism could be controlled adequately with calcium acetate despite using half as much elemental calcium compared with calcium carbonate. This, however, did not result in a lower incidence of hypercalcemia, particularly in those receiving i.v. calcitriol.

Acetates↗
PubMed1989

Metabolic effects of acetate on the heart.

The effects of various substrates (15 mM glucose, 5 mM glucose, 20 mM acetate, or a combination of these substrates) on the coronary blood flow and on the energetic status of myocytes were studied in isolated perfused rat hearts. We demonstrate that low level glucose (5 mM) or high concentration of acetate (20 mM) leads to a simultaneous fall in tissue ATP, rise in tissue adenosine, and significant increment in coronary blood flow. The latter effect is especially marked with 20 mM acetate. Dipyridamole (10(-6) M) does not enhance the vasodilatation induced by acetate. The provision of 15 mM glucose together with 20 mM acetate fully prevents these changes, indicating that the vasodilatation induced by acetate is probably mediated by metabolic changes. The evidence supports the concept that a redistribution of blood flow together with a fall in tissue ATP may explain some of the adverse effects of acetate dialysis in man, and suggests that the provision of glucose may alleviate these changes.

Acetates↗
PubMed1995

Effect of acetate and propionate on fasting hepatic glucose production in humans.

OBJECTIVE: Short chain fatty acids (SCFA, e.g. acetate and propionate) produced from bacterial colonic fermentation may be involved in the improvement of fasting glucose concentration observed with high dietary fibre diets. Because fasting blood glucose is related to hepatic glucose production, we have tested the effect of propionate and acetate on hepatic glucose production. SETTING: The study was carried out in the Clinical Research Center for Human Nutrition. SUBJECTS: Six healthy young volunteers. INTERVENTIONS: The subjects received, in a random order: acetate (12 mmol/h), or propionate (4 mmol/h), or acetate+propionate (12 mmol/h + 4 mmol/h), or an isotonic sodium salt solution (saline) in 3 h gastric infusions. Blood glucose and plasma insulin was monitored. Hepatic glucose production was measured with an isotopic method using [6,6-2H2] glucose. RESULTS: No changes were observed in blood glucose, plasma insulin concentrations or hepatic glucose production with any of the infused solutions. An increase in free fatty acid (FFA) plasma concentration related to the fasting state was observed with the saline solution, but not with the SCFA infusions (P < 0.05). There was also an increase in beta-hydroxybutyrate concentration with the saline and the acetate solutions, but not with the propionate or acetate+propionate solutions. CONCLUSIONS: SCFA, administered at a rate calculated on the basis of a continuous daily fermentation of 30 g dietary fibres, do not change hepatic glucose production or fasting blood glucose. Propionate and acetate decrease plasma FFA, and further studies are needed to explore this effect on glucose tolerance and insulin sensitivity.

Acetates↗
PubMed1993

Acetate-induced adenosine mediated effects of ethanol.

Ethanol administration leads to a marked increase in hepatic blood flow, resulting from an increase in mesenteric blood flow. Studies presented indicate that the increase in portal blood flow induced by ethanol is mediated by acetate. Acetate infusion at rates which achieve blood concentrations equal to those following ethanol administration, fully reproduce this effect of ethanol. The adenosine receptor blocker 8-phenyltheophilline (8PT) fully abolishes the increase in portal blood flow induced by both ethanol and acetate. We have proposed that the extrahepatic metabolism of acetate into acetyl-CoA yields AMP and adenosine. Studies also indicate that adenosine receptor activation has a major contribution to the CNS depressant effects of ethanol at low concentrations of ethanol (below 1.5 g/kg) where the production of acetate is near maximal and the physico-chemical effects of ethanol are minor. Acetate significantly potentiates the CNS depressant effects of general anesthetics. Data to be presented indicate that for some behaviours, acetate through an adenosine-receptor activation potentiates the effects of ethanol while in other behavioural tests they antagonize ethanol effects.

Acetates↗
PubMed1984

Alternative induction and crossover schedules for methadyl acetate.

Various schedules exist for inducting heroin addicts newly admitted to treatment into methadyl acetate maintenance and crossover schedules for the transition from methadone maintenance to methadyl acetate maintenance. A sample of 255 street addicts was randomized to three induction schedules: methadyl acetate three times a week (tiw) with placebos on alternate days; methadyl acetate tiw supplemented with decreasing doses of methadone on alternate days; methadyl acetate six days a week with diminishing doses on three days. Treatment was double-blind for four weeks and single-blind for six. All schedules were considered feasible, but supplementation with methadyl acetate or methadone had no advantage. A sample of 310 patients receiving methadone maintenance was randomized to comparable supplementation groups, except that the group receiving supplementary methadyl acetate received it along with the regular dose. This schedule was not successful. Supplementing with methadone had no advantage.

Adolescent↗
PubMed1998

Proposed mechanism of acetate accumulation in two recombinant Escherichia coli strains during high density fermentation.

The productivity of Escherichia coli as a producer of recombinant proteins is affected by its metabolic properties, especially by acetate production. Two commercially used E. coli strains, BL21 (lambdaDE3) and JM109, differ significantly in their acetate production during batch fermentation at high initial glucose concentrations. E. coli BL21 grows to an optical density (OD, 600 nm) of 100 and produces no more than 2 g/L acetate, while E. coli JM109 grows to an OD (600 nm) of 80 and produces up to 14 g/L acetate. Even in fed-batch fermentation, when glucose concentration is maintained between 0.5 and 1.0 g/L, JM109 accumulates 4 times more acetate than BL21. To investigate the difference between the two strains, metabolites and enzymes involved in carbon utilization and acetate production were analyzed (isocitrate, ATP, phosphoenolpyruvate, pyruvate, isocitrate lyase, and isocitrate dehydrogenase). The results showed that during batch fermentation isocitrate lyase activity and isocitrate concentration were higher in BL21 than in JM109, while pyruvate concentration was higher in JM109. The activation of the glyoxylate shunt pathway at high glucose concentrations is suggested as a possible explanation for the lower acetate accumulation in E. coli BL21. Metabolic flux analysis of the batch cultures supports the activity of the glyoxylate shunt in E. coli BL21.

Acetic Acid↗
PubMed2001

Acetate-inducible protein overexpression from the glnAp2 promoter of Escherichia coli.

The Ntr regulon in Escherichia coli has previously been engineered to control the expression of a heterologous metabolic pathway. In this study, we reengineered the same system for protein production. In the absence of NRII (glnL gene product), we showed that glnAp2 can be an effective promoter for protein production that is inducible by exogenous acetate, but both the induction ratio and the range of modulation are low. To deal with this issue, we inactivated phosphotransacetylase (pta gene product), which disrupts the acetate pathway and denies the cell the ability to synthesize acetate. With this additional modification, gene expression from glnAp2 can be controlled by directly adding acetate into the growth medium. Using a lacZ reporter fusion, we found that glnAp2 induction was modulatable over a range of potassium acetate concentrations, and the induction/noninduction ratio increased to 77 in the absence of pta. The extracellular acetate required for maximal induction is lower than the concentration that causes toxicity, and thus growth inhibition by acetate addition was not a matter of concern. Furthermore, compared to the P(tac) promoter, overexpression of a model protein using the modified glnAp2 promoter system did not cause significant growth inhibition, although a higher level of protein expression was achieved.

Acetic Acid↗
PubMed2003

Down-regulation of acetate pathway through antisense strategy in Escherichia coli: improved foreign protein production.

A problem with the use of Escherichia coli to produce foreign proteins is that although endogenously produced acetate is physiologically indispensable, it inhibits protein expression. Here we firstly employed an antisense RNA strategy as an elaborate metabolic engineering tool to partially block biosynthesis of two major acetate pathway enzymes, phosphotransacetylase (PTA) and acetate kinase (ACK). Three recombinant plasmids containing antisense genes targeting either or both of pta and ackA were constructed, and their effects on the acetate pathway and foreign protein productivity compared to control plasmid without any antisense genes were determined in E. coli BL21. Green fluorescent protein (GFP) was employed as a model foreign protein, and timing of antisense expression was controlled by using the intrinsic ackA promoter. We found that the antisense method partially reduced mRNA levels of target enzyme genes and, over time, lowered the concentration of acetate in culture media in all antisense-regulated strains. Notably, total production of GFP was enhanced 1.6- to 2.1-fold in antisense-regulated strains, even though the degree of acetate reduction was not significantly large. It was revealed that the acetate pathway has more critical roles in cellular physiology than expected in the previous reports. When the scale of culture was increased, enhancement of protein production became larger, demonstrating that this antisense strategy can be successfully applied to practical large-scale protein production processes.

Acetates↗
PubMed1998

Prospective randomized controlled trial comparing percutaneous acetic acid injection and percutaneous ethanol injection for small hepatocellular carcinoma.

To assess whether ultrasound-guided percutaneous acetic acid injection is superior to percutaneous ethanol injection in the treatment of small hepatocellular carcinoma (HCC), 60 patients with one to four HCCs smaller than 3 cm were entered onto a randomized controlled trial. Thirty-one and 29 patients, respectively, were treated by percutaneous acetic acid injection using 50% acetic acid or by percutaneous ethanol injection using absolute ethanol. There were no significant differences in age, sex ratio, Child-Pugh class, size of tumors, or number of tumors between the two groups. When there was no evidence of viable HCC from biopsy, plain and helical dynamic computed tomography, or angiography, the treatment was considered successful and was discontinued. All original tumors were treated successfully by either therapy. However, 8% of 38 tumors treated with percutaneous acetic acid injection and 37% of 35 tumors treated with percutaneous ethanol injection developed a local recurrence (P < .001) during the follow-up periods of 29 +/- 8 months and 23 +/- 10 months, respectively. The 1- and 2-year survival rates were 100% and 92% in percutaneous acetic acid injection and 83% and 63% in percutaneous ethanol injection (P = .0017). A multivariate analysis of prognostic factors revealed that treatment was an independent predictor of survival. The risk ratio of percutaneous acetic acid injection versus percutaneous ethanol injection was 0.120 (range, 0.027-0.528; P = .0050). In conclusion, percutaneous acetic acid injection is superior to percutaneous ethanol injection in the treatment of small HCC.

Acetic Acid↗