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PubMed1983

Citrate uptake by basolateral and luminal membrane vesicles from rabbit kidney cortex.

The mechanisms of tubular transport of citrate in renal basolateral and luminal membrane vesicles were studied under various experimental conditions. Both membrane preparations take up citrate by a Na+-dependent transport system, although with different characteristics. The uptake of citrate by basolateral membrane vesicles was insensitive to changes in membrane potential, which is indicative of electroneutral transport of the anion. The Na+-dependent uptake of citrate by luminal membrane vesicles was influenced by the presence of Na+salt anions of different permeabilities in the order: chloride greater than sulfate greater than gluconate. Furthermore, addition of citrate to membrane vesicle-potential-sensitive dye suspensions resulted in optical changes of the dye, indicative of electrogenic transfer of this compound. The apparent affinity of the citrate transport system located in luminal membrane vesicles, in contrast to basolateral membrane vesicles, was sensitive to changes in medium pH and was higher than that of basolateral membrane vesicles in the pH range studied. On the basis of these results a model for the transport of citrate by rabbit kidney proximal tubule is proposed.

Anaerobiosis↗
PubMed1990

Gallstone decalcification and dissolution using chenodeoxycholate and citrate.

Gallstone dissolution may be possible only in selected patients. Patients with calcified or large gallstones are not suitable for dissolution. Citrate is normally present in bile and an oral citrate load can increase biliary citrate. A combination of chenodeoxycholic acid (C.D.C.A.) and citrate has been shown to dissolve calcified cholesterol gallstones in vitro. Patients with calcified or large gallstones were treated with a combination of C.D.C.A. and citrate. Partial decalcification was achieved in seven out of twenty patients with calcified stones (35%) and complete decalcification in four patients (20%). One of the patients with large stones had complete dissolution. Five patients who were suitable for C.D.C.A. treatment but did not respond were also treated with C.D.C.A. and citrate. One of the patients in this latter group had complete dissolution. Oral citrate can decalcify some calcified gallstones.

Adult↗
PubMed1994

Citrate anticoagulation and divalent cations in hemodialysis.

Anticoagulation with citrate in combination with a calcium-free, magnesium-containing dialysate (Ca-Mg+) and intravenous supplementation of calcium is a safe procedure in renal failure patients at high risk of bleeding. Since magnesium may antagonize the anticoagulant effect of citrate by forming complexes with citrate, we studied the in vitro and in vivo interactions of calcium and magnesium on citrate anticoagulation. In the in vitro studies the activated partial thromboplastin time (APTT) was 88 s, both after addition of 3.0 mumol magnesium and after addition of 1.0 mumol calcium. The combination of 2.4 mumol magnesium and 1.0 mumol calcium achieved similar APTT values of about 35 s as 3.5 mumol calcium alone. Moreover, in a Lee-White blood clotting time, the anticoagulant effect of 7 mumol citrate was neutralized by either 10.5 mumol of a mixture of the two cations or 10.5 mumol calcium chloride alone. In 6 chronic hemodialysis patients the in vivo interactions of calcium and magnesium on citrate were measured. At the dialyzer outlet, the whole blood activated clotting time (ACT) was significantly (p < 0.05) shorter during dialysis with a Ca-Mg+ dialysate than during dialysis with a calcium- and magnesium-free dialysate (Ca-Mg-). With the Ca-Mg- dialysate the ACT at the dialyzer outlet was still significantly longer than the ACT in the arterial line before citrate infusion. We also compared the serum concentrations of calcium and magnesium during the Ca-Mg- dialysate which was used in combination with intravenous calcium and magnesium supplementation - 0.18 and 0.08 mmol/min respectively--and during a conventional calcium- and magnesium-containing dialysate (Ca+Mg+).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Plaque inhibition by a combination of zinc citrate and sodium lauryl sulfate.

Bacteriological tests demonstrated an additive inhibitory effect of ZnCl2 and sodium lauryl sulfate (SLS) on in vitro growth of Streptococcus sobrinus OMZ 176 and of Streptococcus sanguis ATCC 10556. As measured by atomic absorption spectrophotometry, the solubility of zinc citrate increased in the presence of SLS. After 48 h, the concentration of solubilized zinc from aqueous solutions of 5.0 mM zinc citrate was 12.0 mM versus 14.4 mM in the presence of 34.7 mM SLS. The plaque-inhibiting properties of aqueous solutions of 12.0 mM Zn2+ from zinc citrate, 34.7 mM SLS, and 14.4 mM Zn2+ from zinc citrate in combination with 34.7 mM SLS were examined in 7 volunteers. Plaque accumulations were assessed by using a method earlier described after 3 days of twice daily mouthrinses with 10 ml test solution, during which period no mechanical oral hygiene was performed. Compared to placebo, SLS and zinc citrate increased the frequency of plaque index score 0 by 52.9 and 98.3%, respectively, and SLS gave 36.9% and zinc citrate 55.7% less surfaces with scores 2 or 3 (p less than 0.05 in all cases). The combination of zinc citrate and SLS gave a threefold increase of plaque index score 0 and a 70.5% reduction of scores 2 or 3 (p less than 0.05).

Chemical Phenomena↗
PubMed1993

The effect of different concentrations of citrate in drinks on plaque pH.

The effect of 0.1, 0.2 and 0.4% citrate in 10% sucrose solutions on the plaque pH in vivo was tested in 20 volunteers using the plaque harvesting technique. Results showed that the pH response for the three test solutions with citrate was significantly less compared with that for 10% sucrose (positive control) alone (p < 0.05). Mean areas under the pH curve were: sorbitol (negative control) 0.02, citrate 0.2% 5.30, citrate 0.4% 6.24, citrate 0.1% 6.94 and 10% 12.69. The cariogenic potential index of all the citrate test drinks was almost half compared with a 10% sucrose solution (p < 0.05). It was concluded that the addition of relatively low levels of citrate in a sucrose solution reduces the acidogenic response in the plaque.

Adolescent↗
PubMed1995

Effect of addition of 0.103% citrate to a blackcurrant drink on plaque pH in vivo.

The aim of the present study was to investigate whether the addition of a small amount of citrate to infant fruit drinks resulted in a similar beneficial effect to that reported recently with 10% sucrose solution. A popular blackcurrant drink was tested with and without added 0.103% citrate by measuring its ability to depress plaque pH in 20 adult subjects using the plaque-harvesting technique. Solutions of 10% sucrose and 10% sorbitol were used as positive and negative controls, respectively. The results showed that the blackcurrant drink with added citrate had a significantly weaker plaque pH response as compared with the blackcurrant drink without added citrate and 10% sucrose (positive control). The mean areas enclosed by the pH curve below pH 6.0 (+/- SD) were 10% sorbitol (negative control) 0.00, blackcurrant with 0.103% citrate 1.85 +/- 1.07, plain blackcurrant 4.65 +/- 2.11, and 10% sucrose 6.25 +/- 2.35. The acidogenic potential of the blackcurrant drink with added citrate was less than half as compared with the plain blackcurrant drink. It was concluded that the addition of relatively low levels of citrate to a blackcurrant drink reduces the acidogenic response in plaque.

Adolescent↗
PubMed1995

Aluminium deposition in liver and kidney following acute intravenous administration of aluminium chloride or citrate in conscious rats.

1. Plasma, urinary, liver and kidney cell aluminium (Al) levels were monitored in the rat, 1h after intravenous administration of 29630 nmol (800 micrograms) Al as either Al chloride or as Al citrate (Al chloride plus excess sodium citrate). Al levels were measured in plasma, urine and liver by atomic absorption spectroscopy (AAS). Liver and kidney Al content was measured at the cellular and subcellular level by electron probe X-ray microanalysis (EPXMA). 2. Urinary excretion of Al was significantly higher (P < 0.01), when Al was given as the citrate than as the chloride. After 1h, plasma Al levels were significantly lower in the Al citrate group than the Al chloride group (59 +/- 3.7 vs 877 +/- 214 nmol ml-1, respectively; P < 0.01). 3. Al concentrations were significantly higher in the livers of rats receiving Al chloride (818 +/- 252 nmol g-1 wet weight; P < 0.05), than in either control or Al citrate groups (122 +/- 41 and 107 +/- 26 nmol g-1 wet weight, respectively). Al concentrations derived from EPXMA measurements were in agreement with AAS values for the three groups, with significantly higher Al concentrations in the Al chloride group (1.7 +/- 0.4 nmol mg-1 dry weight; P < 0.05) than in the control or Al citrate groups, where Al was not detectable. EPXMA analysis showed that Al was distributed in all liver organelles analysed (cytoplasm, mitochondria, nucleus, ER) and was not preferentially taken up by any one organelle in Al chloride treated rats. 4. Significant amounts of Al were found in cytoplasm and mitochondria of proximal tubule cells of rats given Al citrate (0.64 +/- 0.15 and 0.80 +/- 0.11 nmol mg-1 dry weight, respectively), but not in nuclei or lysosomes of these cells. Al levels were not detectable in control kidneys, in proximal tubule cells after Al chloride administration or distal tubule cells after either Al treatment.

Aluminum↗
PubMed1975

Effect of 2-methylcitrate on citrate metabolism: implications for the management of patients with propionic acidemia and methylmalonic aciduria.

2-Methylcitrate was tested in vitro on enzymes which interact with citrate and isocitrate. It was found to inhibit citrate synthase, aconitase, the NAD+- and NADP+-linked isocitrate dehydrogenase. This inhibition was competitive in nature except in the case of aconitase, and the Ki for all the enzymes was in the range of 1.5-7.6 mM. Phosphofructokinase was also inhibited by 2-methylcitrate with 50% inhibition achieved at 1 mM. ATP-citrate lyase and acetyl-CoA carboxylase were not inhibited by this compound. 2-Methylcitrate was not a substrate for ATP-citrate lyase. Acetyl-CoA carboxylase was activated by 2-methylcitrate with a Ka of 2.8 mM. The apparent Km (3.3 mM) for 2-methylcitrate for the mitochondrial citrate transporter was about 10-fold higher than the apparent Km (0.26 mM) for citrate. The tricarboxylase carrier can also be inhibited by low concentrations (0.2 mM) of 2-methylcitrate when the concentration of citrate is close to the apparent Km. Accumulation of 2-methylcitrate inside the mitochondrion, therefore, might lead to inhibition of enzymes in the citric acid cycle and thereby contribute to the ketogenesis and hypoglycemia seen under these conditions.

Animals↗
PubMed1976

Effects of parathormone and calcitonin on citrate and hyaluronate metabolism in cultured bone.

Two metabolic correlates of parathormone-induced bone resorption are increased synthesis of hyaluronate and decreased production of CO2 from citrate. We have examined these phenomena simultaneously with calcium release in cultured mouse calvaria and fetal rat radii and ulnae treated with parathormone and calcitonin, separately or in combination. In both types of tissue the parathormone dose-response curves for inhibition of citrate decarboxylation, enhanced hyaluronate synthesis, and increased release of calcium were identical when measured 48 h after treatement. In each case a minimum response occurred at approximately 0.01 mug parathormone per ml and a maximum response at about 0.1 mug per ml. The time courses of these responses to parathromone were different. Hyaluronate synthesis increased within 1 h after treatment and peaked at 6 h; decarboxylation of citrate declined after 3 h; demineralization of the bone was not detected until 24 h. When parathormone-treated bones were placed in parathormone-free medium, citrate decarboxylation returned to control levels within 24 h, but increased synthesis of hyaluronate and demineralization persisted for at least 24 h more. When calcitonin was added to bones which were treated with parathormone, the parathormone-induced inhibition of citrate metabolism did not change, but both hyaluronate synthesis and demineralization rapidly declined. Subsequently the rate of hyaluronate synthesis increased, and this was followed several hours later by an increase in demineralization. These data suggest that citrate and hyaluronate metabolism are involved in the overall response of bone to parathormone but are only loosely coupled to one another. Synthesis of hyaluronate appears to be more closely related to subsequent calcium release than is citrate metabolism.

Animals↗
PubMed2002

Potassium citrate prevents increased urine calcium excretion and bone resorption induced by a high sodium chloride diet.

The amount of sodium chloride in the diet of industrialized nations far exceeds physiological requirements. The impact of abundant dietary salt on skeletal health has yet to be established, but is potentially detrimental through increased urinary calcium losses. We examined the effect of increased dietary sodium chloride on urine calcium excretion and bone turnover markers in postmenopausal women and, further, whether potassium citrate attenuates the effects of increased dietary salt. Postmenopausal women (n = 60) were adapted to a low-salt (87 mmol/d sodium) diet for 3 wk, then randomized to a high-salt (225 mmol/d sodium) diet plus potassium citrate (90 mmol/d) or a high-salt diet plus placebo for 4 wk. Urine calcium, urine N-telopeptide, urine cAMP, serum osteocalcin, and fasting serum PTH were measured at the end of the low- and high-salt diets. On the high salt plus placebo diet, urine calcium increased 42 +/- 12 mg/d (mean +/- SEM), but decreased 8 +/- 14 mg/d in the high salt plus potassium citrate group (P = 0.008, potassium citrate vs. placebo, unpaired t test). N-telopeptide increased 6.4 +/- 1.4 nanomoles bone collagen equivalents per millimole creatinine in the high salt plus placebo group and 2.0 +/- 1.7 nanomoles bone collagen equivalents per millimole creatinine in the high salt plus potassium citrate group (P < 0.05, potassium citrate vs. placebo, unpaired t test). Osteocalcin, PTH, and cAMP were not significantly altered. The addition of oral potassium citrate to a high-salt diet prevented the increased excretion of urine calcium and the bone resorption marker caused by a high salt intake. Increased intake of dietary sources of potassium alkaline salts, namely fruit and vegetables, may be beneficial for postmenopausal women at risk for osteoporosis, particularly those consuming a diet generous in sodium chloride.

Aged↗
PubMed1993

Efficacy of 1.4 percent sodium citrate in maintaining arterial catheter patency in patients in a medical ICU.

PURPOSE: The primary purpose of this study was to compare the efficacy of 1.4 percent sodium citrate with heparin, 4 U/ml, for maintaining radial artery catheter patency in patients in the medical ICU. PATIENTS AND METHODS: Patients in the medical ICU (n = 40) were randomized to either a 1.4 percent sodium citrate or heparin 4 U/ml arterial line flush solution in a double-blind, parallel fashion. The flush solutions were continuously infused at approximately 3 ml/h over a maximum of 96 h. Catheter survival rates were compared using Kaplan-Meier survival curves. The frequency of catheter malfunctions and corrective manipulations were recorded and compared. Coagulation status (APTT, PT) and ionized calcium values were monitored to evaluate the systemic effects of sodium citrate. RESULTS: Ninety-four percent of catheters flushed with sodium citrate were functional at 48 h compared with 88 percent for heparin (p > 0.05). At 96 h, 80 percent vs 88 percent of the catheters were functional in the citrate and heparin groups, respectively (p > 0.05). Frequency of catheter malfunctions did not differ between the two groups. No systemic effects of sodium citrate were observed. CONCLUSION: Arterial catheter flush solutions containing sodium citrate (1.4 percent) are an effective and safe alternative to heparin in patients requiring peripheral arterial catheterization.

Adult↗
PubMed1978

Plasma citrate during submaximal and intermittent supramaximal exercise.

Plasma citrate was determined in seven subjects working 45 min at 50-60% of their maximal aerobic power and in six subjects who were exercised intermittently for five periods of 1 min at supramaximal work loads. Determinations of plasma lactate, glucose, free fatty acids and insulin were carried out simultaneously. During submaximal work the mean plasma citrate concentration decreased from 116 +/- 4 mumol/1 at rest to 108 +/- 5 mumol/1 after 10 min exercise (P less than 0.05) and increased above resting level to 136 +/- 5 mumol/1 40 min after cessation of work (P less than 0.05). During intermittent supramaximal exercise, mean plasma citrate concentration rose after the third work period and during recovery from 117 +/- 6 mumol/1 at rest to 181 +/- 9 mumol/1 40 min after last work period (P less than 0.05). Plasma citrate varied similarly to variations in plasma free fatty acids and inversely to changes of lactate concentrations during submaximal exercise. Opposite interrelationships were demonstrated during intermittent supramaximal exercise. Plasma citrate concentration varied in the same way as might be expected for changes in cytosolic citrate levels of muscle from in vitro knowledge of the regulatory role of citrate on glucose oxidation.

Adult↗
PubMed1991

Effects of egg yolk-citrate and milk extenders on chromatin structure and viability of cryopreserved bull sperm.

Semen from four Holstein bulls was evaluated to compare effects of four extender treatments on postthaw semen quality. Extender fractions A and B, either heated whole milk or 20% egg yolk-citrate, were combined to yield the extender treatments 1) milk and milk, 2) milk and egg yolk-citrate, 3) egg yolk-citrate and milk, and 4) egg yolk-citrate and egg yolk-citrate. Semen was evaluated at thawing and after 30, 60, 120, and 180 min of incubation at 38.5 degrees C. Flow cytometry showed that acridine orange-stained sperm were most susceptible to in situ DNA denaturation when fraction A was milk. For sperm stained with rhodamine 123, flow cytometry showed that the proportion with intact mitochondrial membrane potential was lowest of all treatments at thawing but greatest at 180-min incubation with milk and milk extender. Flow cytometry of propidium iodine-stained sperm showed greatest proportion of cell membrane intact sperm when fraction A was egg yolk-citrate. Light microscopy showed the lowest proportion of cell membrane intact sperm with milk and milk extender after eosin-aniline blue vital staining. Postthaw motility scores tended to be reduced when both extender fractions were egg yolk-citrate. Results demonstrate differential extender effects on postthaw semen quality and indicate that altering extender composition or sequence of adding extender components may improve postthaw quality of cryopreserved sperm.

Analysis of Variance↗
PubMed1999

99Tcm-citrate: a new bone imaging radiopharmaceutical.

99Tcm-citrate has been shown to incorporate irreversibly in the skeleton with a biodistribution different to that on a conventional bone scan. The aims of this study were to confirm the bone-imaging properties of 99Tcm-citrate, to identify the variabilities influencing its skeletal uptake, to compare its uptake in bone with that of 99Tcm-MDP and to assess its possible role in bone scintigraphy. Appropriate animal and human studies (n = 45) were conducted. The 3 h lesion-to-bone ratio of 99Tcm-citrate was compared with that of 99Tcm-MDP in more than 150 lesions, including osteoblastic sites (Group A), lesions undergoing treatment or healing (Group B), and degenerative or old healed lesions (Group C). The uptake ratio was classified as concordant (< 20% variation), mildly discordant (20-50% variation) or significantly discordant (> 50% variation). Animal experiments showed most bone uptake of 99Tcm-citrate when prepared at a pH of 6.0-6.5. The two radiopharmaceuticals appeared to compete for bone uptake, suggesting related but different sites of bone accumulation. The 99Tcm-citrate/99Tcm-MDP uptake ratio in Group A was concordant (mean +/- S.D. = 0.92 +/- 0.15), while Group C lesions had a significantly lower 99Tcm-citrate/99Tcm-MDP uptake ratio (0.34 +/- 0.24, P < 0.01). A comparison of Group B lesions showed wide variation in intensity and area of involvement in many lesions (uptake ratio < 0.5 or > 1.5 in 13 of 30 sites). We conclude that 99Tcm-citrate has a different site of bone localization than phosphonates, possibly in the organic matrix. Although its skeletal uptake is lower than that of 99Tcm-MDP, it may have better specificity in differentiating osteoblastic from degenerated or healed bony lesions, and therefore be useful in predicting healing of bone secondaries, fractures or osteomyelitic lesions.

Adult↗
PubMed2001

[Effect of potassium citrate in the prophylaxis of urinary lithiasis].

OBJECTIVE: The physiologic effects of potassium citrate on urinary solubility have led to their use to facilitate stone passage after lithotripsy. The aim of our study is to evaluate the foregoing effects and the efficacy of long-term treatment with potassium citrate to prevent stone recurrence in patients undergoing extracorporeal shock wave lithotripsy. METHODS: A prospective study was conducted on 100 patients with calcium oxalate or calcium phosphate nephrolithiasis that had undergone treatment by extracorporeal shock wave lithotripsy (ESWL). The patients were divided into 4 groups: patients that were stone-free treated with potassium phosphate (25 cases) or fluid diet (25 cases) and patients with persistent residual lithiasis treated with potassium citrate (25 cases) or fluid diet (25 cases). Calculi were classified according to the changes observed during the study compared with the pre-study status as stable (no changes from the pre-study status, with or without residual stone), increased (increase in number or size of the residual stone or recurrence), and decreased (decrease in number or size or passage of the residual stone). RESULTS: Of the 50 patients treated with potassium citrate, 35 (70%) remained stable, 10 cases (20%) showed a decrease and 5 (10%) showed an increase. Of the 50 patients on fluid diet, 19 (38%) remained stable throughout the study, 4 (8%) showed a decrease and 27 (54%) showed an increase in stone size or number. The number of stone recurrence throughout the study in the 100 patients was 25 (25%); of these, 8 were in patients treated with potassium citrate and 17 of those that did not receive potassium citrate. CONCLUSIONS: Potassium citrate therapy has been found to be statistically significantly effective in the control of post-lithotripsy residual stone and stone recurrence.

Adolescent↗
PubMed2003

Sildenafil citrate for the treatment of patients with cardiovascular diseases with exclusion of coronary artery disease and hypertrophic subaortic stenosis. Its beneficial effect on patients chronic Chagas's and diabetic cardioneuromyopathies, hypertensive and hypertrophic cardiomyopathies, with or without chronic congestive heart failure.

UNLABELLED: Sildenafil citrate is a potent donor of nitric oxide that has been proved to be effective for the treatment of male erectile dysfunction, but it has been contraindicated in patients with cardiovascular diseases, because of sudden death occurred to some of them. Based on the known vasodilator effect of nitrix oxide, effect that should be beneficial for some cardiomyopathies, this work was carried out in order to prove the cardiovascular effects of sildenafil citrate on: 1) heart rate, rhythm and repolarization changes on the ecg; 2) systolic and diastolic arterial blood pressure; 3) left ventricular systolic function and 4) right and left ventricular diastolic function in 26 patients suffering from the following cardiomyopathies: chronic Chagas's and diabetic cardioneuromyopathies, hypertensive and/or hypertrophic cardiomyopathies with or without chronic congestive heart failure. RESULTS: sildenafil citrate 50 mgr after a single oral dose: 1) improved the ecg findings in some patients, worsening the basal ecg in none of the studied patients; 2) significantly reduced systolic and diastolic arterial blood pressure being such reduction very strong in those with basal high level 3) significantly improved left ventricular systolic function in those patients with basal reduced function and 4) Right ventricular diastolic function evaluation: Sildenafil citrate 50 mgr significantly modified to normal pattern the E/A basal altered ratio in those patients with the inverted pattern as well as in those with restrictive pattern of tricupid diastolic influx to the right ventricle during the echo-duplex interrogation (p < 0.0001) 5) Left ventricular diastolic function evaluation: Sildenafil citrate 50 mgr significantly modified to normal pattern the E/A basal altered ratio in those patients with the inverted pattern as well as in those with restrictive pattern of mitral diastolic influx to the left ventricle, during the echo-duplex interrogation (p 0 <.0001). CONCLUSIONS: Based on the above findings it is feasible to propose the use of sildenafil citrate to treat patients with cardiovascular diseases, with exclusion of severe obstructive coronary artery disease, hypertrophic subaortic stenosis and patients with funduscopic alterations that may be affected by a significant and acute increase of flow within the ophthalmic arteries. The right ventricular diastolic changes observed with Sildenafil Citrate may be useful in patients with abnormal right ventricular compliance such as pulmonary stenosis or hypertension.

Blood Pressure↗
PubMed1979

Acute control of fatty acid synthesis by cyclic AMP in the chick liver cell: possible site of inhibition of citrate formation.

Glucagon and N,(6)O(2)-dibutyryl cyclic adenosine 3',5'-cyclic monophosphate (Bt(2)cAMP) inhibit fatty acid synthesis from acetate by more than 90% and prevent citrate formation in chick hepatocytes metabolizing glucose. With substrates that enter glycolysis at or below triose-phosphates, e.g., fructose, lactate, or pyruvate, Bt(2)cAMP has no effect on the citrate level and its inhibitory effect on fatty acid synthesis is substantially reversed. Because acetyl-CoA carboxylase requires a tricarboxylic acid activator for activity, it is proposed that regulation of fatty acid synthesis by Bt(2)cAMP is due, in part, to changes in the citrate level. Reduced citrate formation appears to result from a cAMP-induced inhibition of glycolysis. Bt(2)cAMP inhibits (14)CO(2) production from [1-(14)C]-, [6-(14)C]-, and [U-(14)C]glucose and has little effect on (14)CO(2) formation from [1-(14)C]- or [2-(14)C]pyruvate or from [1-(14)C]fructose. [(14)C]Lactate formation from glucose is depressed 50% by Bt(2)cAMP. In the presence of an inhibitor of mitochondrial pyruvate transport lactate accumulation is enhanced, but continues to be lowered 50% by Bt(2)cAMP. The activity of phosphofructokinase is greatly decreased in Bt(2)cAMP-treated cells while the activities of pyruvate kinase and acetyl-CoA carboxylase are unaffected. It appears that decreased glycolytic flux and decreased citrate formation result from depressed phosphofructokinase activity. Fatty acid synthesis from [(14)C]acetate is partially inhibited by Bt(2)cAMP in the presence of fructose, lactate, and pyruvate despite a high citrate level. Incorporation of [(14)C]fructose, [(14)C]pyruvate, or [(14)C]lactate into fatty acids is similarly depressed by Bt(2)cAMP. Synthesis of cholesterol from [(14)C]acetate or [2-(14)C]pyruvate is unaffected by Bt(2)cAMP. These results implicate a second site of inhibition of fatty acid synthesis by Bt(2)cAMP that involves the utilization, but not the production, of cytoplasmic acetyl-CoA.-Clarke, S. D., P. A. Watkins, and M. D. Lane. Acute control of fatty acid synthesis by cyclic AMP in the chick liver cell: possible site of inhibition of citrate formation.

Animals↗
PubMed1989

Effects of citrate on urinary calcium excretion.

Thyroparathyroidectomized rats were studied during control, citrate infusion, and recovery periods to analyze the effects of citrate on urinary calcium excretion. The rats were infused with human PTH-(1-34) at a constant rate throughout the experiments that produced physiologic circulating PTH activity. Ultrafiltrable calcium was measured with a micropartition system while maintaining constant the pH and PCO2 of the sample. The plasma acid-base status, filtered load of calcium, and urinary sodium excretion rate did not vary during citrate infusion. The urinary calcium excretion rate increased from 71 +/- 9 nmol/min/g kidney during control period to 122 +/- 22 nmol/min/g kidney (p less than 0.05) during citrate infusion, and then returned below control levels during recovery period. A strong positive linear relationship was observed between the urinary excretion rates of calcium and citrate (r = 0.88; p less than 0.001). We conclude that tubular fluid citrate inhibits renal calcium reabsorption probably by forming calcium-citrate complexes.

Animals↗