Influence of dietary calcium and phosphorus supply on epithelial phosphate transport in preruminant goats

P homeostasis affected by high or low Ca and/or P supply in preruminant goats was characterized by balance studies in vivo. The main excretion pathway was the renal P_i excretion whose extent was modulated by variations in dietary P and/or Ca supply. Faecal P excretion remained low irrespective of dietary regimen. The balance data were combined with respective in vitro data on P_i transport properties and their adaptation in response to changes in dietary Ca and/or P intake. Therefore, P_i transport capacities were determined by P_i uptake into brush border membrane vesicles of jejunum and kidney. Epithelial P_i transporters were determined semiquantitatively by northern and western blot analyses in jejunum, kidney and salivary gland. Renal P_i transport was downregulated by doubling dietary P supply while doubling both, Ca and P as well as restrictive Ca at unchanged P led to slight, but not significant reductions in renal P_i transport. Jejunal P_i transport was reduced by P excess (doubling P and doubling both, Ca and P), but only NaPi IIb protein expression was significantly diminished. In conclusion, the significance of epithelial adaptation to dietary Ca and P supply for P homeostasis is discussed in preruminant goats.     

High phosphorus feeding decreases the expression of renal PTH/PTHRP-receptor mRNA in rats

Dietary intake of high phosphorus (P) is well-described to increase serum levels of PTH, however, how this increased serum PTH affects the PTH actions in major target tissues, particularly in kidney, remains uncovered. We therefore undertook to clarify this point in intact animals fed the high-P diet by examining various parameters of the PTH actions. Twelve weanling Wistar male rats were assigned randomly into the groups; a control group Ca: P = 1: 1 and a high-P group (Ca: P = 1: 3) fed the standard AIN 76 diet supplemented with P (0.5 and 1.5 g/100 g diet). After 3 week feeding, in the high-P diet group, we observed that serum Ca is lowered without difference in serum P when compared to those in the control group. Excretion of urine cAMP, an index of the renal PTH action, was also decreased with higher excretion of urine P by feeding the high P diet. In agreement with the decreased cAMP excretion, a clear reduction in the PTH/PTHrP receptor gene expression estimated by Northern blotting was observed in the kidney irrespective of increased levels of serum PTH. Thus, the present study indicated that high P dietary intake rather reduces the PTH actions in kidney though the serum PTH is increased.     

Water and electrolyte excretion during the oestrous cycle in sheep.

Electrolyte excretion was observed during 24 oestrous cycles in housed sheep, together with mixed salivary Na/K ratio during 10 additional cycles. 1. The sharp fall in food and fluid intake at oestrus accompanied a peak of sodium excretion which changed to peak retention 3 days later, both in faeces and urine. 2. Potassium excretion declined with food intake at oestrus but subsequently failed to recover to pre-oestrous levels dispite full recovery of dietary intake. 3. Curiously, water intake also recovered completely whereas urinary and faecal water retention continued; faecal loss actually exceeded renal excretion on these liberal water intakes. 4. Changes in salivary, urinary and faecal Na/K indicated an aldosterone peak neither during the luteal phase nor at oestrus but three days later. The data raise questions concerning the regulation of water and electrolyte balance within the normal cycle. They also provide a baseline for the investigation of renal effects of gonadal steroids. Possible roles for aldosterone, ADH and progesterone in maintaining fluid and electrolyte balance are discussed, emphasising problems confronting species which have evolved with heavy obligatory potassium excretion but undependable supplies of sodium and water.     

The effect of barbiturates on 24-h water intake and renal excretion of sodium and water in dogs

The effects of barbiturates on 24-h intakes of water and food and urinary excretion of sodium and potassium as well as on plasma concentration of sodium and potassium and osmolality were examined in dogs placed in metabolism cages and fed with a semiliquid diet. Administration of barbiturates stimulated drinking in a Series of 8 dogs having free access to water. Twenty four-h water intake and water balance increased significantly. Food intake, urinary output and urinary excretion of solutes, sodium and water did not change in this Series. A significant decrease in urine output as well as in osmolal clearance and urinary excretion of sodium was observed in a Series of 7 dogs having water restricted for 24 h following administration of barbiturates. Water balance increased in this Series. The same restriction of water in the dogs which had not received barbiturates did not modify renal excretion of water and electrolytes. Plasma osmolality, sodium and potassium concentrations did not change in either Series of experiments. It is concluded that barbiturates induce positive water balance either by stimulation of drinking when water is freely available or by reduction in urine output when water is restricted. The results suggest that expansion of the body fluids following the increased water intake may abolish reduction in urine output and sodium excretion which otherwise occur after administration of barbiturates.     

The effect of a low-protein diet in pregnancy on offspring renal calcium handling

Low birth weight humans and rats exposed to a low-protein diet in utero have reduced bone mineral content. Renal calcium loss during the period of rapid skeletal growth is associated with bone loss. Because young rats exposed to low protein display altered renal function, we tested the hypothesis that renal calcium excretion is perturbed in this model. Pregnant Wistar rats were fed isocalorific diets containing either 18% (control) or 9% (low) protein throughout gestation. Using standard renal clearance techniques, Western blotting for renal calcium transport proteins, and assays for Na(+)-K(+)-ATPase activity and serum calcitropic hormones, we characterized calcium handling in 4-wk-old male offspring. Histomorphometric analyses of femurs revealed a reduction in trabecular bone mass in low-protein rats. Renal calcium (control vs. low protein: 10.4 +/- 2.1 vs. 27.6 +/- 4.5 nmol x min(-1) x 100 g body wt(-1); P < 0.01) and sodium excretion were increased, but glomerular filtration rate was reduced in low-protein animals. Total plasma calcium was reduced in low-protein rats (P < 0.01), but ionized calcium, serum calcitropic hormone concentrations, and total body calcium did not differ. There was no significant change in plasma membrane Ca(2+)-ATPase pump, epithelial calcium channel, or calbindin-D(28K) expression in low-protein rat kidneys. However, Na(+)-K(+)-ATPase activity was 36% lower (P < 0.05) in low-protein rats. These data suggest that the hypercalciuria of low-protein rats arises through a reduction in passive calcium reabsorption in the proximal tubule rather than active distal tubule uptake. This may contribute to the reduction in bone mass observed in this model.     

Dietary boron supplementation enhances the effects of estrogen on bone mineral balance in ovariectomized rats

The present study investigated whether boron would enhance the action of 17β-estradiol (E₂) or parathyroid hormone (PTH) on bone mineral balance in ovariectomized (OVX) rats. Forty-three days after OVX, the rats were treated for 5 wk with vehicle, boron (5 ppm as boric acid), E₂ (30 μg/kg/d, sc), PTH (60 μg/kg/d, sc), or a combination of boron and E₂ or PTH. Bone mineral balance was assessed by measuring apparent absorption, excretion, and retention of calcium (Ca), phosphorus (P), and magnesium (Mg). Serum Ca, P, Mg, and osteocalcin were also measured in this experiment. Boron alone had no effects on food consumption, weight gain, bone mineral balance, and serum levels of Ca, P, Mg, and osteocalcin. E₂ alone increased serum P and Mg and decreased serum osteocalcin, but it had no effect on bone mineral balance. The combination of boron and E₂ markedly improved apparent absorption of Ca, P, and Mg. In addition, the combination treatment increased the apparent retention of Ca and Mg (but not P) and also increased serum Ca and Mg but not serum P. On the other hand, boron cotreatment did not prevent the E₂-induced reduction in serum osteocalcin in OVX rats. PTH alone significantly increased serum Ca, P, Mg, and osteocalcin concentrations, although it had no effect on bone mineral balance. Contrary to the boron-E₂ combination treatment, the combination of boron and PTH did not enhance bone mineral balance. However, inasmuch as boron-PTH cotreatment did not enhance the stimulatory action of PTH on serum Ca, P, and osteocalcin, boron completely abolished the stimulatory effect of PTH on serum Mg. In conclusion, we have demonstrated for the first time that although boron by itself has no effect on bone mineral homeostasis, it appears to have synergistic enhancing effects on the action of E₂ on Ca and Mg homeostasis in OVX rats.     

Effect of dietary calcium on renal prostaglandins.

The present study was designed to clarify the possible role of renal prostaglandins (PGs) on blood pressure (BP) regulation during calcium (Ca) restriction or supplementation. Twelve normotensive women with a mean age of 21.2 years participated in the study. After 1 week of normal Ca intake (mean +/- SE, 536 +/- 2 mg/day), a low-Ca diet (163 +/- 1 mg/day) was given for a further 1 week. Additional asparagine Ca (3 g as Ca/day) was also given to half of the subjects. BP, heart rate, and serum total and ionized Ca concentrations were measured at the end of each period. Levels of Ca, sodium, PGE2, 6-keto-PGF1 alpha and thromboxane (TX) B2 excreted into urine were also determined. The plasma level of ionized Ca was significantly increased without any change in total Ca in both groups. Low and high Ca intake decreased and increased urinary Ca excretion by 28% and 56%, respectively. BP was not altered after Ca deprivation or loading. However, urinary PGE2 excretion was significantly augmented from 668.9 +/- 68.1 to 959.7 +/- 183.1 ng/day by Ca loading, whereas Ca deprivation decreased PGE2 excretion (695.4 +/- 108.1 to 513.2 +/- 55.2 ng/day). No changes were observed in 6-keto-PGF1 alpha or TXB2 urinary excretion. These results suggest that renal PGE2 synthesis is stimulated or decreased by 1-week Ca loading or deprivation, indicating a possible antihypertensive role of renal PGE2 during high-Ca intake in hypertensives.     

Effects of a Mild and Prolonged Restriction in Sodium or Food Intake on the Circadian Rhythm of Aldosterone and Related Variables

The effect of a mild reduction in dietary sodium intake (-30 mEq/24 hr) and body weight (-2 kg/2 months) on circadian rhythms of urinary aldosterone (UA), sodium (UNa), potassium (UK), creatinine (UC) and volume (UV) have been investigated in nine clinically healthy subjects. The mild reduction in dietary sodium is associated with: (1) a decrease in the 24-hr excretion rate of UNa, UK and UV, and an increased mesor of UA and UC; (2) a lowered extent of the circadian variation for UNa, UK, UV and a greater amplitude for UA and UC (3) a later crest in the temporal phase for UK, UA, UC, an earlier phasic wave for UNa. The mild reduction in calorie intake resulting in a body weight loss is associated with a more pronounced decrease in the 24-hr excretion rate of UNa and UK, and in the extent of circadian fluctuation for UNa. Peculiar events are: (1) the decreased 24-hr excretion rate for UA, and the increased mesor for UV; (2) the extent variability increased for UV, decreased for UC. Such effect may have a practical resonance for heuristic physiology since the role of dietary sodium and food intake has been better clarified. Dietary sodium and food can be regarded as 'chronomodulatory agents' for the adrenal cortex since their adrenotropic influence is extended to the tonic as well as phasic secretion of aldosterone.     

Effects of weak amplitude-modulated microwave fields on calcium efflux from awake cat cerebral cortex

Calcium (45Ca2+) efflux was studied from preloaded cortex in cats immobilized under local anesthesia, and exposed to a 3.0-mW/cm2 450-MHz field, sinusoidally amplitude modulated at 16 Hz modulation depth 85%). Tissue dosimetry showed a field of 33 V/m in the interhemispheric fissure (rate of energy deposition 0.29 W/kg). Field exposure lasted 60 min. By comparison with controls, efflux curves from field exposed brains were disrupted by waves of increased 45Ca2+ efflux. These waves were irregular in amplitude and duration, but many exhibited periods of 20-30 min. They continued into the postexposure period. Binomial probability analysis indicates that the field-exposed efflux curves constitute a different population from controls at a confidence level of 0.96. In about 70% of cases, initiation of field exposure was followed by increased end-tidal CO2 excretion for about 5 min. However, hypercapnea induced by hypoventilation did not elicit increased 45Ca2+ efflux. Thus this increase with exposure does not appear to arise as a secondary effect of raised cerebral CO2 levels. Radioactivity measurements in cortical samples after superfusion showed 45Ca2+ penetration at about 1.7 mm/hr, consistent with diffusion of the ion in free solution.     

Effects of a Mild and Prolonged Restriction in Sodium or Food Intake on the Circadian Rhythm of Aldosterone and Related Variables

The effect of a mild reduction in dietary sodium intake (?30 mEq/24 hr) and body weight (?2 kg/2 months) on circadian rhythms of urinary aldosterone (UA), sodium (UNa), potassium (UK), creatinine (UC) and volume (UV) have been investigated in nine clinically healthy subjects. The mild reduction in dietary sodium is associated with: (1) a decrease in the 24-hr excretion rate of UNa, UK and UV, and an increased mesor of UA and UC; (2) a lowered extent of the circadian variation for UNa, UK, UV and a greater amplitude for UA and UC (3) a later crest in the temporal phase for UK, UA, UC, an earlier phasic wave for UNa. The mild reduction in calorie intake resulting in a body weight loss is associated with a more pronounced decrease in the 24-hr excretion rate of UNa and UK, and in the extent of circadian fluctuation for UNa. Peculiar events are: (1) the decreased 24-hr excretion rate for UA, and the increased mesor for UV; (2) the extent variability increased for UV, decreased for UC. Such effect may have a practical resonance for heuristic physiology since the role of dietary sodium and food intake has been better clarified. Dietary sodium and food can be regarded as ‘chronomodulatory agents’ for the adrenal cortex since their adrenotropic influence is extended to the tonic as well as phasic secretion of aldosterone.     

Ca-P interaction at the nutritional and bone levels in male quail (Coturnix coturnix japonica)

Five experiments were conducted in which various levels of calcium (Ca) and phosphorus (P) were fed to adult male quail (diets D-1: Ca = 1.54%, p = 0.80%; D-2: Ca = 3.20%, P = 0.81%; D-3: Ca = 1.57%, P = 1.66%; D-4: Ca = 3.40%, P = 1.71%; D-5: Ca - 2.20%, P = 0.81%). The interaction between Ca and P, and the effect on some nutritive hematic and osseous parameters were investigated for each diet. Feeding high P caused a body weight decrease in D-4 adult quail (P less than 0.05) and diminished food intake in the birds of trial D-3 (P less than 0.05). The results indicated that the excretion of Ca or P is a lineal function of its own intake. Neither the pattern of relationship between the intake and excretion of Ca was altered by the levels of phosphorus in the diets, nor the levels of calcium altered the pattern of P. With these levels of Ca and P interaction between both nutrients were not demonstrated. Plasma Ca levels and dry weight of femur as well as the ash content in them, were not significantly decreased, although the levels of the latter components were inferior in the groups fed non-adjusted diets in the Ca:P ratio (diets D-1, D-2, D-3 and D-4).     

Species-specific responses of N homeostasis and electrolyte handling to low N intake: a comparative physiological approach in a monogastric and a ruminant species

In our former studies low crude protein (LCP) intake influenced N homeostasis and electrolyte handling in goats. We hypothesised that due to rumino-hepatic nitrogen (N) recycling adaptation of N homeostasis and adjustment of electrolyte handling to LCP intake differs between goats and monogastric animals. Therefore, an experiment similar to that with goats was conducted with rats. Two feeding groups received a diet either containing 20 or 8 % crude protein (as fed basis) for 5 weeks and intake and excretion of N, calcium (Ca) and phosphorus (P) were determined. To detect systemic and endocrine adaptation to LCP intake plasma concentrations of urea, Ca, phosphate (Pi), insulin-like growth factor 1 (IGF-1), 1,25-dihydroxyvitamin D₃ (calcitriol), parathyroid hormone (PTH) and cross-linked telopeptide of type I collagen (CTX) were measured. Adjustment of renal electrolyte transport was assessed by detecting protein expression of key proteins of renal Pi transport. All data were compared with the data of the goat experiment. LCP intake decreased plasma urea concentration stronger in goats than in rats. In both species urinary N excretion declined, but faecal N excretion decreased in goats only. Furthermore, in goats urinary Ca excretion decreased, but in rats urinary Ca concentration increased. Decreased plasma IGF-1 and calcitriol concentrations were found in goats only. Thus, renal Ca excretion appears to be a common target in adaptation of electrolyte homeostasis in both species, but is regulated differently.     

Weight loss induced by chronic dapagliflozin treatment is attenuated by compensatory hyperphagia in diet-induced obese (DIO) rats

Dapagliflozin is a potent and selective sodium glucose cotransporter-2 (SGLT2) inhibitor which promotes urinary glucose excretion and induces weight loss. Since metabolic compensation can offset a negative energy balance, we explored the potential for a compensatory physiological response to the weight loss induced by dapagliflozin. Dapagliflozin was administered (0.5-5 mpk; p.o.) to diet-induced obese (DIO) rats with or without ad libitum access to food for 38 days. Along with inducing urinary glucose excretion, chronic administration of dapagliflozin dose-dependently increased food and water intake relative to vehicle-treated controls. Despite this, it reduced body weight by 4% (relative to controls) at the highest dose. The degree of weight loss was increased by an additional 9% if hyperphagia was prevented by restricting food intake to that of vehicle controls. Neither oxygen consumption (vO2) or the respiratory exchange ratio (RER) were altered by dapagliflozin treatment alone. Animals treated with dapagliflozin and pair-fed to vehicle controls (5 mpk PF-V) showed a reduction in RER and an elevation in nonfasting β-hydroxybutyrate (BHBA) relative to ad libitum-fed 5 mpk counterparts. Fasting BHBA was elevated in the 1 mpk, 5 mpk, and 5 mpk PF-V groups. Serum glucose was reduced in the fasted, but not the unfasted state. Insulin was reduced in the non-fasted state. These data suggest that in rodents, the persistent urinary glucose excretion induced by dapagliflozin was accompanied by compensatory hyperphagia, which attenuated the weight loss induced by SGLT2 inhibition. Therefore, it is possible that dapagliflozin-induced weight loss could be enhanced with dietary intervention.     

Comparative Study on the Effect of Variable Phosphorus Intake at two Different Calcium Levels on P Excretion and P Flow at the Terminal Ileum of Laying Hens

A 3 ‐ 2-factorial balance trial was conducted with dietary concentrations of P below the requirement (3.6, 4.3 and 5.0g/kg DM) and Ca below or at the requirement (28 and 37g/kg DM) adjusted by monobasic calcium phosphate (MCP, Ca(H₂PO₄)₂) and calcium carbonate (CaCO₃). The diets were mainly based on maize and soybean meal. Six 18-week old laying hens were allocated to each of the diets, and excreta were quantitatively collected for 21 days from week 22 of age onwards. Feed allowance was 95 g/d according to pre-treatment ad libitum intake of the hens receiving the lowest P concentration. After the balance trial was terminated, ileal digesta was obtained from each hen, and the flow at the terminal ileum was calculated using TiO₂ as indigestible marker. Linear regression analysis was applied to determine the effect of supplementary P. Hens were in a negative energy balance, indicated by a loss in BW across all treatments. Intake and excretion of both N and energy were not significantly affected by the P or Ca content of the diet. P from supplemented MCP was almost completely recovered in excreta, irrespective of dietary Ca concentration. At the terminal ileum, however, the P flow was not significantly affected by the MCP supplementation. Net absorption of P from MCP was almost complete until the terminal ileum, but P was re-directed into the excreta, likewise via the urine. The supplementation of Ca reduced praecaecal net absorption and utilisation of P from the basal diet, likewise due to a reduced phytate hydrolysis. It is suggested by the data, that comparative measurements of P availability for laying hens should be conducted on the basis of praecaecal net absorption rather than on total excretion measurements.     

Hypoxic induction of Ca2+-dependent action potentials in small pulmonary arteries of the cat

Small pulmonary arteries (less than 300 micron) from cats were mounted in myographs to record mechanical and electrical responses to hypoxia. When these preparations were exposed to a PO2 of 30-50 Torr after equilibration at 300 Torr they consistently developed active force, which increased or decreased in amplitude as [Ca2+] was raised or lowered, respectively, and was blocked on addition of verapamil. Intracellular electrical recording with glass microelectrodes demonstrated membrane depolarization and action potential generation when PO2 was lowered. Steady-state voltage vs. applied current curves obtained before and during hypoxia showed a significant reduction in input resistance. The relationship between membrane potential and extracellular K+ was not different during hypoxia compared with control, suggesting that there were not marked changes in K+ permeability under this condition. In the presence of verapamil to block Ca2+ inward current the hypoxia-induced action potentials were abolished concomitant with partial membrane repolarization. The results of these studies suggest that in certain isolated pulmonary arteries hypoxia induces contraction by a mechanism involving an increased Ca2+ conductance. These data suggest that the sensor involved in hypoxic pulmonary vasoconstriction may lie within the vessel wall and somehow mediates changes in smooth muscle ionic conductances.     

Effect of water restriction on feeding and metabolism in dairy cows

We investigated how lactating cows are able to cope with a sustained water restriction. In experiment 1, body weight and meal patterns were recorded with ad libitum access to water (baseline) and during 8 days of 25 and 50% restriction of drinking water relative to ad libitum intake. In experiment 2, indirect calorimetry was combined with nitrogen and energy balance and plasma hormone and metabolite measurements to assess the effects of 50% water restriction on digestion and metabolism. In experiment 1, food intake and body weight declined during the first 3 days of water restriction depending on the restriction level and stabilized thereafter at a lower level. The daily food intake reduction with 50% water restriction was entirely due to a reduction of meal size. The size of the first meal on every day was markedly (>50%) reduced with 25 and 50% water restriction. In experiment 2, urea concentrations in milk and blood as well as plasma sodium and hematocrit were increased by 50% water restriction. Energy balance was not affected by 50% water restriction, but nitrogen balance became negative, because, relative to intake, nitrogen excretion via urine and milk was higher. The lower energy intake during 50% water restriction was compensated by a lower milk production, a higher digestibility of organic matter and energy, and, apparently, a more efficient energy use. Through these changes and a preserved water balance, the cows reached a new equilibrium at a lower water turnover level, which enabled them to cope with a sustained drinking water restriction of 50%.     

Oxytocin, water intake, and food sodium availability in male rats

This study examined the effect of subcutaneous administration of the neurohormone oxytocin on water intake of ad lib-fed (with or without sodium availability in the diet) and food-deprived animals. Results of the first experiment showed that oxytocin increased water intake and urine excretion in food-deprived but not in ad lib-fed animals. However, oxytocin treatment did not modify the reduced water "balance" (fluid intake minus urine volume) resulting from food deprivation or the daily food intake (Experiment 1). The dose-dependent polydipsic effect of oxytocin on food-deprived rats was always preceded by an increase in sodium and fluid urine excretion (Experiment 2). Oxytocin also increased the water intake of animals fed ad lib with a low sodium diet (Experiment 3). These results suggest that the effect of oxytocin on water intake is dependent on the presence or absence of sodium in the diet and that the excretion of sodium is the main mechanism of oxytocinergic polydipsia in food-deprived male rats.     

Glycomacropeptide, a low-phenylalanine protein isolated from cheese whey, supports growth and attenuates metabolic stress in the murine model of phenylketonuria

Phenylketonuria (PKU) is caused by a mutation in the phenylalanine (phe) hydroxylase gene and requires a low-phe diet plus amino acid (AA) formula to prevent cognitive impairment. Glycomacropeptide (GMP) contains minimal phe and provides a palatable alternative to AA formula. Our objective was to compare growth, body composition, and energy balance in Pah(enu2) (PKU) and wild-type mice fed low-phe GMP, low-phe AA, or high-phe casein diets from 3-23 wk of age. The 2 × 2 × 3 design included main effects of genotype, sex, and diet. Fat and lean mass were assessed by dual-energy X-ray absorptiometry, and acute energy balance was assessed by indirect calorimetry. PKU mice showed growth and lean mass similar to wild-type littermates fed the GMP or AA diets; however, they exhibited a 3-15% increase in energy expenditure, as reflected in oxygen consumption, and a 3-30% increase in food intake. The GMP diet significantly reduced energy expenditure, food intake, and plasma phe concentration in PKU mice compared with the casein diet. The high-phe casein diet or the low-phe AA diet induced metabolic stress in PKU mice, as reflected in increased energy expenditure and intake of food and water, increased renal and spleen mass, and elevated plasma cytokine concentrations consistent with systemic inflammation. The low-phe GMP diet significantly attenuated these adverse effects. Moreover, total fat mass, %body fat, and the respiratory exchange ratio (CO(2) produced/O(2) consumed) were significantly lower in PKU mice fed GMP compared with AA diets. In summary, GMP provides a physiological source of low-phe dietary protein that promotes growth and attenuates the metabolic stress induced by a high-phe casein or low-phe AA diet in PKU mice.     

Effect of dietary energy intake on tubular reabsorption of urea in sheep

The aim of the experiment was to determine the effect of dietary energy intake on renal urea excretion in sheep with different nitrogen intakes. The control sheep, with a high nitrogen and energy intake, were given a daily feed dose of 21.18 g N and 15.2 MJ digestible energy (DE). The two experimental groups, with an equal, low nitrogen intake, were given diets with a different energy content. The high energy diet contained 3.63 g N and 14.18 MJ DE, the low energy diet 3.4 g N and 6.44 MJ DE. After nine weeks' adaptation to the diets, renal functions were measured by a standard clearance technique. It was found that, under stable urine flow conditions, both groups given the low nitrogen diet had a significantly lower glomerular filtration rate, fractional urea excretion and total urea excretion. A reciprocal comparison of these two groups showed that fractional urea excretion by the sheep with a high energy intake was significantly lower than in the group with a low energy intake. There were no differences in the glomerular filtration rate. A raised dietary energy intake in the presence of a low nitrogen intake caused marked natriuresis and kaliuresis. The results indicate that a raised dietary energy intake can be a significant factor in potentiating the renal effect of urea retention in sheep with a low nitrogen intake.     

Effect of dietary protein intake on plasma leucine flux, protein synthesis, and degradation in sheep

Combined experiments of an isotope dilution method of [1-(13)C]leucine with open circuit calorimetry and a nitrogen (N) balance test were applied to determine the effect of dietary crude protein (CP) intake on plasma leucine flux and protein synthesis and degradation in four sheep. The experiment was conducted in a 3 x 4 Latin rectangle design of three 3-week periods. Dietary CP intake was 5.6, 7.7, and 10.8 g/(kg(0.75) x d). Metabolizable energy intake was 120% of requirement for all dietary treatments. [1-(13)C]Leucine was intravenously infused for 8 h and blood and breath samples were collected during the latter 2-h period of infusion. Isotopic enrichments of plasma [1-(13)C]leucine, alpha-[1-(13)C]ketoisocaproic acid, and exhaled (13)CO(2) were determined. For the N balance test, N digestibility, N excretion in urine, and protein balance (N x 6.25) increased with increasing dietary CP intake. Rates of plasma leucine turnover, protein synthesis, and degradation changed toward reduction with increased dietary CP intake. It is likely that in sheep, high CP intake enhances protein deposition with reduced protein degradation rather than increased protein synthesis.