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Association of dietary fatty acids with urinary oxalate excretion in calcium oxalate stone-formers in their fourth decade.

OBJECTIVE: To examine the influence of the dietary intake of fatty acid on urinary oxalate excretion in calcium oxalate stone-formers in their fourth decade, as previous reports show that animal fat intake is associated with urinary oxalate excretion. PATIENTS AND METHODS: The dietary intake of 58 idiopathic stone-formers in their fourth decade was recorded using the dietary-record method. The patients collected 24-h urine samples at home and their urinary oxalate excretion was measured in a clinical biochemistry laboratory. The results were used to determine the relationship between the dietary intake of fatty acids and urinary oxalate excretion. Associations between urinary oxalate excretion and dietary contents of animal fat, animal protein and various fatty acids were assessed using Spearman's correlation coefficient and multiple regression. RESULTS: The dietary content of arachidonic acid was positively correlated with urinary oxalate excretion, as assessed by univariate and multivariate analysis. CONCLUSION: The association between arachidonic acid and oxalate excretion suggests that arachidonic acid increases the intestinal absorption of oxalate and increases the clearance of oxalate in the kidneys.

Adult↗

gamma-L-glutamyl-L-DOPA inhibits Na(+)-phosphate cotransport across renal brush border membranes and increases renal excretion of phosphate.

BACKGROUND: For treatment of phosphate (Pi) overload in various pathophysiological states, an agent that selectively increases renal Pi excretion would be of major value. Previously, we have shown that dopamine (DA) inhibits Na(+)-Pi cotransport in renal epithelia. However, the administration of DA or its immediate precursor L-DOPA increases DA in multiple tissues. Synthetic dipeptide gamma-L-glutamyl-L-DOPA (gludopa) can serve as an inactive precursor (pro-pro-drug) of DA. This study tested the hypothesis that, because of the unique colocalization of gamma-glutamyltransferase (gamma-GT), aromatic amino acid decarboxylase, Na(+)-Pi cotransporter, and Na(+)-L-DOPA cotransporter in brush border membrane (BBM) of proximal tubular cells, gludopa may elicit phosphaturia by action of DA generated within the kidney. METHODS: Thyroparathyrectomized rats were given placebo, or gludopa, or gludopa + gamma-GT inhibitor acivicin. Urinary excretion of Pi, Ca2+, Na+, K+, DA, cAMP, and cGMP was determined, and Na(+)-Pi cotransport was measured in BBM prepared from kidneys of rats at the end of the experiment. RESULTS: The administration of gludopa resulted in: (a) an inhibition of Na(+)-Pi cotransport, but not cotransport of Na(+)-proline and Na(+)-alanine in BBM; (b) an increase (+300%) of fractional excretion (FE) of Pi and a drop (-35%) of plasma Pi, whereas the plasma levels and FEs of Ca2+, Na+, and K+ were unchanged; (c) an increase in urinary excretion of cAMP. but not cGMP; (d) a 1000-fold increase of urinary excretion of DA, without a change in excretion of norepinephrine; and (e) an incubation of gludopa with BBM in vitro, which caused a release of L-DOPA, and the in vivo administration of acivicin, which blocked actions of gludopa to inhibit Na(+)-Pi cotransport and to increase urinary excretions of Pi and DA. CONCLUSIONS: We conclude that colocalization of enzymes of biotransformation, BBM transporters, and the autocrine/paracrine DA system in cells of proximal tubules constitutes a cellular basis for the potent and specific phosphaturic action of gludopa.

Alanine↗

Contribution of dietary oxalate to urinary oxalate excretion.

BACKGROUND: The amount of oxalate excreted in urine has a significant impact on calcium oxalate supersaturation and stone formation. Dietary oxalate is believed to make only a minor (10 to 20%) contribution to the amount of oxalate excreted in urine, but the validity of the experimental observations that support this conclusion can be questioned. An understanding of the actual contribution of dietary oxalate to urinary oxalate excretion is important, as it is potentially modifiable. METHODS: We varied the amount of dietary oxalate consumed by a group of adult individuals using formula diets and controlled, solid-food diets with a known oxalate content, determined by a recently developed analytical procedure. Controlled solid-food diets were consumed containing 10, 50, and 250 mg of oxalate/2500 kcal, as well as formula diets containing 0 and 180 mg oxalate/2500 kcal. Changes in the content of oxalate and other ions were assessed in 24-hour urine collections. RESULTS: Urinary oxalate excretion increased as dietary oxalate intake increased. With oxalate-containing diets, the mean contribution of dietary oxalate to urinary oxalate excretion ranged from 24.4 +/- 15.5% on the 10 mg/2500 kcal/day diet to 41.5 +/- 9.1% on the 250 mg/2500 kcal/day diet, much higher than previously estimated. When the calcium content of a diet containing 250 mg of oxalate was reduced from 1002 mg to 391 mg, urinary oxalate excretion increased by a mean of 28.2 +/- 4.8%, and the mean dietary contribution increased to 52.6 +/- 8.6%. CONCLUSIONS: These results suggest that dietary oxalate makes a much greater contribution to urinary oxalate excretion than previously recognized, that dietary calcium influences the bioavailability of ingested oxalate, and that the absorption of dietary oxalate may be an important factor in calcium oxalate stone formation.

Adult↗

Urinary excretion of LH and testosterone from male rats during exposure to increased gravity: post-spaceflight and centrifugation.

A dissociation between plasma luteinizing hormone (LH) and testosterone (T) appears to exist during exposure to altered gravity. The pulsatile nature of LH release and the diurnal variability of T secretion may mask or bias the effects of altered gravity on the pituitary-gonadal axis when analyzing plasma concentrations. Therefore, we examined the relationship between the excretion of urinary LH and T in male Sprague-Dawley rats during exposure to increased gravity upon return to Earth following a 14-day spaceflight (n = 6) and by 12 days of centrifugation at 2g (n = 8). Excreted LH and T were elevated on the first 3 days postflight. Excreted T was elevated between Days 1 and 8 of centrifugation; however, excreted LH was reduced on Days 2 and 3 compared with control animals. Excreted LH and T were significantly correlated (R = 0.731 and 0.706, respectively) in postspaceflight and centrifuged animals. Correlation curves had similar slopes (0.0213 and 0.023, respectively), but different y-intercepts (-1.43 and 3.32, respectively). The sustained increase in excreted T during centrifugation suggests that the pituitary-gonadal axis in postspaceflight animals may adapt quicker to increased gravity. The upward shift in the correlation curve exhibited by the centrifuged animals suggests that the sensitivity of LH-induced T release is increased in these animals. The previous dissociation between plasma LH and T during altered gravity was not observed in the present study in which excreted LH and T were measured.

Adaptation, Physiological↗

Influence of nutritional status on the daily patterns of nitrogen excretion in the carp (Cyprinus carpio L.) and the rainbow trout (Salmo gairdneri R.).

Nitrogen (ammonia and/or urea) excretion in carp and rainbow trout kept under different feeding regimes was continuously monitored over 24-hr cycles. The daily nitrogen excretion patterns resulting from these feeding regimes were studied over several days after a change from one made to another. Constant levels of endogenous nitrogen excretion were reached about one week after the start of a fasting period; almost one week was needed for the daily nitrogen excretion pattern to stabilize after the feeding rhythm was changed. Overall daily nitrogen excretion rates were directly related to nitrogen consumption in carp as well as in trout. The rate of ammonia excretion increased immediately after each meal; the maximum rate occurred at different intervals, depending on the amount of nitrogen intake as well as on the time-lapse after a particular feeding regime was initiated. Contrary to data on sockeye salmon, post-digestive nitrogen excretion rate was distinctly different from the ENE rates observed during fasting in carp and rainbow trout.

Ammonia↗

Creatinine excretion in continuous peritoneal dialysis: a systematic error of the Cockroft-Gault formula.

We investigated the hypothesis that the rate of loss of creatinine excretion with age in peritoneal dialysis (PD) patients differs from the rate predicted from the Cockroft-Gault formula (Cr(Pred)) by analyzing creatinine excretion data obtained from clearance studies of 925 patients on continuous ambulatory PD therapy with an age range of 12 to 91 years. Measured creatinine generation (Cr(Meas)) is the sum of creatinine excretion in urine plus dialysate (Cr(Excr)) plus an estimated metabolic degradation of creatinine. The effect of age on Cr(Excr) and the differences Cr(Excr) - Cr(Pred) and Cr(Meas) - Cr(Pred) were analyzed by linear regression. In 373 women, Cr(Excr) = W(16.9360 - 0.084A), r = -0.342, P < 0.001 (where W is weight in kilograms and A is age in years). The regression slope was one half of the slope in the Cockroft-Gault formula. Cr(Excr) - Cr(Pred) = -413.91 + 4.78A, r = 0.300, P < 0.001. Cr(Meas) - Cr(Pred) = -176.36 + 4.37A, r = 0.278, P < 0.001. In 552 men, Cr(Excr) = W(21.079 - 0.108A), r = -0.338, P < 0.001. The regression slope was approximately one half of the slope in the Cockroft-Gault formula. Cr(Excr) - Cr(Pred) = -493.25 + 6.28A, r = 0.267, P < 0.001. Cr(Meas) - Cr(Pred) = -66.41 + 3.63A, r = 0.143, P = 0.001. The rate of loss of creatinine excretion with age is one half of the rate predicted by the Cockroft-Gault formula in both women and men on PD therapy. Therefore, the difference between excretion (or measured generation) of creatinine and creatinine generation predicted by the Cockroft-Gault formula is not constant, but increases with age. The Cockroft-Gault formula systematically overestimates the effect of age on creatinine excretion in PD patients and is not suitable for predicting creatinine excretion in these subjects.

Adolescent↗

Conjugated bile acid replacement therapy reduces urinary oxalate excretion in short bowel syndrome.

BACKGROUND: Patients with short bowel syndrome (SBS) have steatorrhea, in part because of bile acid malabsorption that causes decreased bile acid secretion into the duodenum and consequent fat maldigestion. In SBS patients with colon in continuity, luminal calcium forms calcium fatty acid soaps rather than precipitating as insoluble calcium oxalate. Soluble oxalate is hyperabsorbed by the colon leading to hyperoxaluria and an increased risk for renal calcium oxalate stones and deposits. The authors hypothesized that oral ingestion of conjugated bile acids would increase fat absorption and thereby decrease calcium fatty acid soap formation and oxalate hyperabsorption. METHODS: The effect of conjugated bile acid replacement therapy (9 g/d) on fecal fat excretion and urine oxalate excretion was measured in an appropriate patient, utilizing the metabolic balance technique. The effects of chronic bile acid replacement therapy on oxalate excretion and nutritional status also were measured in a 3-month outpatient study. RESULTS: Natural conjugated bile acid replacement therapy reduced fecal fat excretion from 119 to 79 g/d (Delta40 g/d), and urinary oxalate excretion from 87 to 64 mg/d (966 to 710 micromol/d; Delta23 mg/d). Cholylsarcosine, a synthetic conjugated bile acid, had similar but less powerful effects. During a 3-month outpatient trial of natural conjugated bile acids (9 g/d), urine oxalate decreased to normal levels (27 mg/d) in association with weight gain, decreased hunger, and decreased hyperphagia. CONCLUSION: Conjugated bile acid replacement therapy reduced fecal fat excretion, reduced urinary oxalate excretion, and improved nutritional status in a patient with SBS with colon in continuity, hyperoxaluria, and oxalate nephrolithiasis.

Administration, Oral↗

Decreased urinary peptide excretion in patients with renal disease.

BACKGROUND: Normal urine contains low-molecular-weight peptides or protein fragments that have been poorly studied, primarily because of the technical difficulty of measuring peptides in the presence of proteins. We studied these substances in healthy subjects and patients with renal disease and varying degrees of proteinuria to understand the factors that determine their excretion. METHODS: We estimated these substances as the difference between results using the Lowry method (which detects both proteins and peptides) and those obtained using the dye-binding Bradford (Biorad) method (Biorad Laboratories Inc, Hercules, CA; which detects only proteins). RESULTS: We validated this 2-assay approach to measure peptide levels by showing that such proteins as immunoglobulin G, albumin, and lysozyme were measured equally by the Lowry and Biorad methods, whereas degraded proteins were recognized by the Lowry method only, but not by the Biorad method. We found that healthy subjects excreted less than 200 mg of protein, but 3 to 4 g of peptides/g creatinine; thus, peptides constituted approximately 95% of total protein material excreted in urine. Patients with renal disease and proteinuria had a progressive decrease in peptide excretion, ranging from 3 to 0 g/g creatinine. Twenty-five percent of nephrotic patients (18 of 72 patients) excreted very small amounts of peptides in urine (0% to 10% of total protein material). CONCLUSION: We found that healthy persons excrete substantial amounts of peptides in urine, and this excretion decreases in the presence of proteinuric renal disease. It is possible that these peptides in urine arise from the tubular degradation of filtered proteins and exocytosis of protein fragments toward the urinary side, a process that becomes increasingly impaired as proteinuria increases.

Humans↗

Fermentable carbohydrate supplementation alters nitrogen excretion in chronic renal failure.

BACKGROUND: Considerable attention has been given to the impact of nutrition on kidney disease. Most dietary attempts to treat chronic renal failure (CRF) and to decrease uremia use a protein restriction. An alternative dietetic approach based on fermentable carbohydrate (FC) supplementation of the diet could lead to the same urea-lowering effect by increasing urea nitrogen (N) excretion in stool, with a concomitant decrease of the total N quantity excreted in urine. METHODS: In the present prospective study, the impact of FC (40 g/d) on uremia and on N excretion routes was investigated during 5 weeks in nine CRF patients in the presence of a moderated restrictive protein diet (0.8 g/kg/d). Patients were their own controls and were treated by the cross-over method after randomization (5 weeks with FC versus 5 weeks without FC). RESULTS: Feeding FC significantly increased the quantity of N excreted in stool from 2.1 +/- 0.8 to 3.2 +/- 1.1 g/d (+51%) (P < .01) and decreased, in parallel, the urinary N excretion from 9.4 +/- 1.7 to 8.3 +/- 1.4 g/d (-12%) (P < .01). The total N quantities excreted by the two routes were unchanged by the FC, which shows that the FC was efficient to shift N excretion from the urinary route toward the digestive route. As a result of the increase of urea transfer into the colon, the plasma urea concentration was significantly decreased from 26.1 +/- 8.7 to 20.2 +/- 8.2 mmol/L (-23%) (P < .05). CONCLUSIONS: These results show the same beneficial effects in CRF as those obtained with a restrictive protein diet without its nutritional drawbacks. This should be confirmed by other prospective works over a longer duration and a larger number of patients to study the effects of FC on CRF progression and on CRF terminal stage tolerance.

Adult↗

Hydroxylysine excretion does not indicate collagen damage with downhill running in young men.

The purpose of this study was to determine whether urinary excretion of hydroxylysine (HO-Lys) is increased following prolonged, predominantly downhill running. Such an increase would be evidence of exercise-induced collagen damage. Each of ten young men performed a treadmill running test to determine VO2peak (an approximation of VO2max) followed by 60 min of intermittent running on -10% slope. Total urine excreted from 48 h pre-exercise to 96h post-exercise was collected in 8-h samples for measurement of HO-Lys. In addition, both urinary 3-methylhistidine (3-MeHis) excretion and serum creatine kinase (SCK) activity were measured as indicators of muscle tissue damage. In no sampling period was post-exercise HO-Lys excretion altered compared with pre-exercise (e.g., pre-exercise: 82.2 +/- 9.6 mumol.24 h-1, mean +/- SE; 51.0 +/- 3.7 mumol.g creatinine-1; post-exercise: 72.9 +/- 2.0 mumol.24 h-1; 47.0 +/- 1.5 mumol.g creatinine-1). SCK activity was increased (346%) 24 h post-exercise, but not immediately, 48 h, or 72 h post-exercise. 3-MeHis excretion was not altered following exercise. There were no strong associations between HO-Lys excretion and either of the markers of muscle damage. We concluded that no evidence of exercise-induced collagen damage was provided by urinary HO-Lys excretion.

Adult↗

The effect of nifedipine on urinary excretion of calcium in preeclampsia.

Our objective was to determine if maternal urinary calcium excretion is altered during treatment of mild preeclampsia remote from term with the calcium channel blocker nifedipine. One hundred forty-eight women with mild preeclampsia were randomly allocated to treatment with either bed rest alone (n=64) or in combination with nifedipine (n=84) at 26-36 weeks' gestation. All women had 24 hr urine samples collected for creatinine clearance and calcium excretion determination prior to therapy and during treatment. There was no difference in gestational age at the time of urine collection between the two groups. There were no differences in 24-hr creatinine clearance and calcium excretion between the groups prior to therapy. When followed longitudinally, there was a significant reduction in calcium excretion within each group (p=0.0005 control group, p <0.0001 nifedipine group). Further, a significant reduction in calcium excretion was noted following nifedipine therapy (62+/-94 mg Ca/24 hr) compared to the control group (143+/-153 mg Ca/24 hr), p <0.001. Consistent with previous studies, we have shown that progressive hypocalciuria is a feature of preeclampsia. Further, urinary calcium excretion decreased despite nifedipine therapy. Altered urinary calcium excretion may be less reflective of the progression in severity of preeclampsia in patients treated with nifedipine.

Adolescent↗

Effect of control of blood glucose on urinary excretion of albumin and beta2 microglobulin in insulin-dependent diabetes.

To study the effects of improved control of blood glucose on markers of renal glomerular and tubular function, we initially determined, by radioimmunoassay technics, urinary excretion rates of albumin and beta2 microglobulin in 17 nondiabetic subjects and in 43 insulin-dependent, clinically nonproteinuric diabetic patients. Duration of diabetes ranged from six months to 39 years, and the patients were studied while receiving conventional therapy. Mean urinary albumin excretion was significantly elevated in the diabetics, but beta2-microglobulin excretion rates were not different from those of the controls, suggesting that the increased albumin excretion was due to increased transglomerular loss of albumin. Seven patients with long-term diabetes (duration of six to 33 years), selected because of elevated albumin excretion, were studied before and during a continuous, subcutaneous insulin infusion for a period of one to three days. Urinary albumin excretion was significantly reduced during the insulin infusion, but mean beta2-microglobulin excretion did not change. Strict control of blood glucose, even in the short term, may reverse a functional renal abnormality in long-duration, insulin-dependent diabetes.

Adult↗

Glomerular lesions and urinary albumin excretion in type I diabetes without overt proteinuria.

Since several studies have suggested that a slight increase in urinary albumin excretion (microalbuminuria) is predictive of nephropathy in patients with diabetes mellitus, we studied the relation of albumin excretion to renal structure in patients with insulin-dependent (Type I) diabetes. Renal biopsy specimens were evaluated with light- and electron-microscopical morphometric techniques in 48 patients who had had diabetes for 5 to 40 years and who excreted less than 200 mg of urinary albumin per 24 hours. Patients in Group I (n = 26) had normal urinary albumin excretion, creatinine clearance, and blood pressure; those in Group II (n = 10) had increased urinary albumin excretion but normal creatinine clearance and blood pressure; those in Group III (n = 12) had increased urinary albumin excretion and hypertension, decreased creatinine clearance, or both. Glomerular structure varied similarly, ranging from normal to abnormal in Groups I and II, but was consistently abnormal in Group III. The thickness of the glomerular basement membrane, the fractional volume of the mesangium, and the mesangial volume per glomerulus in Group III exceeded the corresponding values in the other groups significantly. Thus, microalbuminuria, when present with hypertension, decreased creatinine clearance, or both, indicates established abnormalities of glomerular structure. Normal albumin excretion, or microalbuminuria without these other functional abnormalities, does not accurately predict the severity of the underlying glomerular lesions in patients with Type I diabetes.

Adolescent↗

Racial differences in aldosterone excretion and plasma aldosterone concentrations in children.

Blacks are more likely to have hypertension, have lower levels of plasma renin activity, and typically consume less potassium than whites. Whether blacks and whites secrete different amounts of aldosterone is less clear. We estimated aldosterone secretion indirectly in 715 children, 249 of whom were black, by measuring their nocturnal rates of urinary excretion of aldosterone. Dietary sodium and potassium intakes were estimated from their excretion rates. The mean (+/- SE) aldosterone-excretion rate was lower in the black children than in the white children (0.045 +/- 0.003 vs. 0.078 +/- 0.004 nmol per micromole of creatinine per kilogram of body weight; P less than 0.001). The potassium-excretion rate was also lower in the black children than in the white children (0.13 +/- 0.01 vs. 0.18 +/- 0.01 mmol per micromole of creatinine per kilogram; P less than 0.001). Aldosterone excretion was highly correlated with potassium excretion (P less than 0.001), but the lower aldosterone-excretion rate in blacks was explained only in part by their lower dietary intake of potassium. Systolic blood pressure was higher in black children (P less than 0.001), as was diastolic pressure (P = 0.037). In a second study of 99 children, the plasma aldosterone level was found to be significantly lower in black children than in white children (230 +/- 30 vs. 400 +/- 30 pmol per liter; P less than 0.001). Plasma renin activity and plasma cortisol levels were the same in both groups. In summary, we found that black children secrete about 40 percent less aldosterone than white children. The role of the lower aldosterone-secretion rate in the genesis of the higher blood pressures observed in black children is not known.

Aldosterone↗

Effect of plasma protein adsorption on protein excretion in kidney-transplant recipients with recurrent nephrotic syndrome.

BACKGROUND: Among patients with the idiopathic nephrotic syndrome who have focal and segmental glomerulosclerosis and undergo renal transplantation, 15 to 55 percent have recurrent nephrotic syndrome. The recurrence may be caused by a plasma factor or factors that increase glomerular permeability, because plasma exchange transiently decreases or abolishes proteinuria in some patients. We studied the effect on proteinuria of the removal of protein (mostly immunoglobulins) by adsorption onto protein A from the plasma of patients with recurrent nephrotic syndrome. METHODS: Eight patients were treated with one to three cycles of two to seven 1-day sessions of protein adsorption, and the patients' urinary protein excretion was measured repeatedly. Their immunosuppressive regimens were not changed during the treatment. The adsorbed proteins were eluted from the protein A and injected into rats, and the urinary albumin excretion of the rats was measured. RESULTS: The protein-adsorption treatment consistently decreased urinary protein excretion by an average of 82 percent at the end of a cycle (P < 0.001). In one patient proteinuria disappeared, and in another urinary protein excretion remained below 2.5 g per day with repeated cycles of protein adsorption. In all but one patient the effect of adsorption was limited in time, with a return to the preadsorption level of protein excretion within a maximum of two months. The administration to rats of material eluted from the protein A increased urinary albumin excretion 2.9- to 4.6-fold (P < 0.001 and P = 0.005, respectively). Although protein A primarily binds immunoglobulins, the active fraction of the eluted proteins had a molecular weight below 100,000, indicating that immunoglobulin was not directly involved. CONCLUSIONS: Adsorption of plasma protein decreases urinary protein excretion in patients with recurrence of the nephrotic syndrome after renal transplantation. Studies of the adsorbed proteins should provide information about the mechanism of this disease.

Adolescent↗

Renal endothelin in heart failure and its relation to sodium excretion.

BACKGROUND: Recent studies have shown that endothelin-1 (ET-1) antagonists increase sodium excretion and improve renal blood flow in experimental heart failure (HF). However, despite a number of investigations that have reported a significant increase in ET-1 plasma levels in patients with HF, it is still not known whether increased renal synthesis and urinary excretion of ET-1 occur. Our aim was to investigate renal ET-1 formation and its relation to sodium excretion in patients with HF. METHODS: One hundred forty-seven patients with HF, subdivided according to New York Heart Association (NYHA) functional classes, and 28 healthy controls were studied. ET-1 and big ET-1 were measured in plasma and in 24-hour urine by radioimmunoassay. Atrial and brain natriuretic peptide, arginine vasopressin, plasma renin activity, and hemodynamic variables were also investigated. RESULTS: Urinary ET-1 excretion was already increased in NYHA class II patients (P <.001 vs controls), whereas plasma ET-1 increased only in NYHA class III and IV patients (P <.001). In the 71 subjects who were not receiving diuretic treatment, urinary ET-1 was selected as the strongest predictor of sodium excretion by multivariate stepwise analysis. CONCLUSIONS: Urinary ET-1 excretion increases in an earlier phase of HF than plasma ET-1 and appears to be closely correlated with sodium excretion, indicating renal ET-1 is a target for ET-1 antagonists in patients with HF.

Aged↗

Methane excretion in the growing pig.

Total methane excretion (CH4 in breath + flatus) was measured in two experiments with thirty-six castrated male pigs (Danish Landrace) during the growth period from 20 to 120 kg live weight (LW). In Expt A, twenty-eight pigs were fed on a commercial diet alternately at high (HFL; metabolizable energy (ME) 1234 (SE 41) kJ/kg LW 0.75) or low (LFL; ME 784 (SE 31) kJ/kg LW 0.75) feed levels in different weight classes. In Expt B, eight pigs were constantly fed on a semi-purified diet at HFL without (-oil) or with 90 g soya-bean oil/kg diet (+oil) corresponding to daily intakes of ME of 1339 (SE 11) and 1413 (SE 8) kJ/kg LW 0.75 respectively. CH4 excretion was measured during 24 h respiration trials in open-air-circulation chambers. About 1 litre CH4 was excreted per day at 20-25 kg LW increasing to a maximum of 12 litres at 120 kg LW, which corresponded to no more than 1.2% of dietary gross energy. In Expt A, CH4 excretion increased linearly with LW, while in Expt B the increase was linear until about 70 kg LW, when it reached a plateau. On average LFL reduced CH4 excretion by 23% compared with HFL. When related to dry matter (DM) intake, however, the pigs on LFL excreted 3.1 litres CH4/kg dietary DM and those on HFL 2.5 litres CH4/kg dietary DM, the difference being significant (P less than 0.05). In Expt B the inclusion of soya-bean oil in the basal diet (+oil) reduced CH4 excretion by 26% compared with the diet without oil (-oil).(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Nutritional Physiological Phenomena↗

Endogenous purine and pyrimidine derivative excretion in pregnant sows.

The present experiment was carried out to study the endogenous losses of purine and pyrimidine derivatives from pregnant sows. Three pregnant and three non-pregnant Large White x Landrace sows were fed on a purine-free diet composed of starch, glucose, sucrose and vegetable oil, with casein as the protein source. The experiment began, for the six animals, after diagnosis of pregnancy and was divided into six 12 d periods. Urine was collected during the first 3 d of each experimental period by means of a urethral catheter for determination of allantoin, uric acid, xanthine, hypoxanthine and pseudouridine concentrations. In the absence of dietary nucleic acids (NA), allantoin and, as a consequence, excretion of total purine derivatives (PD) decreased significantly to a constant value (128.3 (SE 7.07) mumol/kg metabolic live weight (W0.75) per d), an amount assumed to represent endogenous excretion. Excretion of uric acid (38.7 (SE 2.15) mumol/kg W0.75 per d), hypoxanthine (21.0 (SE 2.58) mumol/kg W0.75 per d) and xanthine (11.2 (SE 0.83) mumol/kg W0.75 per d) were not affected by the experimental treatment, although there was a significant decrease in hypoxanthine excretion in pregnant sows (from 25.5 to 5.2 mumol/kg W0.75 per d) compared with non-pregnant sows (from 26.7 to 44.8 mumol/kg W0.75 per d). Creatinine excretion was not affected by pregnancy and was used as an internal urinary marker. Purine excretion, either expressed as mumol/kg W0.75 per d or as the ratio PD: creatinine, was not affected by experimental treatment, although an apparent increase in pseudouridine excretion, a modified unsalvageable catabolite of RNA-pyrimidine, was found in late pregnancy (3.6 v. 5.2 mol/100 mol creatinine in non-pregnant sows compared with pregnant sows at 102 d collection.

Allantoin↗