Alpha-amino Nitrogen Concentrations Research Articles

Effect of Zinc applied together with compound fertilizer on yield and quality of sugar beet (Beta vulgaris L.)

ABSTRACTThis research was conducted to evaluate the effect of zinc, added into compound fertilizer in the production process, and zinc applied together with compound fertilizer on yield and quality component of sugar beet in 2009–2010.The treatments consisted of nitrogen, phosphorus and potassium (NPK) (12-30-12) compound fertilizer; 2. NPK (12-30-12) compound fertilizer + zinc sulfate and NPK (10-20-20) + 1% Zn compound fertilizer. Root yield, sugar percentage, white sugar percentage (WSP), white sugar yield (WSY), alpha-amino nitrogen, sodium and potassium concentration were investigated in this study. A total of 5 kg ha−1 zinc application on sugar beet significantly increased the yield and quality of sugar beet; the rate of increase was in the range of 4.62–6.97% in root yield, 2.09–5.75% in sugar percentage, 2.60–8.03% in WSP and 7.84–13.06% in WSY. NPK (10-20-20) + 1% Zn compound fertilizer and NPK (12-30-12) compound fertilizer + zinc applications increased the sugar beet yield and quality values in both years.

Changes of activity and mRNA expression of urea cycle enzymes in the liver of developing Holstein calves1

Urea is an important reutilizable nitrogen source for the ruminant and is mainly synthesized through the urea cycle in the liver. The cycle is undertaken by 5 enzymes: carbamoyl phosphate synthetase (CPS), ornithine transcarbamoylase (OTC), arginino-succinate synthetase (AS), argininosuccinate lyase (AL), and arginase. The purpose of this study was to investigate changes in the activity of the enzymes and mRNA expression, given that previous observations have indicated an increase in plasma urea concentrations with age in Holstein calves. First, plasma concentrations of metabolites and hormones were determined in calves at 1, 3, 8, 13, and 19 wk of age (n = 4, weaned at 6 wk of age). The plasma concentration of urea drastically increased after weaning (P < 0.001). The plasma concentration of glucose was lowest at 8 wk. The plasma concentration of IGF-I gradually increased with age, although those of NEFA, glucagon, and cortisol decreased (P < 0.001). Concentrations of triglyceride, alpha-amino nitrogen, growth hormone, and insulin did not change significantly with age of the calf. Next, using the liver tissues taken from calves at 2, 13, and 19 wk of age (n = 4 to 6 at each time point, weaned at 6 wk of age), we measured the activity and mRNA expression of the enzymes by biochemical methods and quantitative reverse transcription-PCR, respectively. The activities of CPS (P < 0.001), OTC (P = 0.001), and AS (P = 0.015) increased with age, whereas AL (P = 0.003) decreased. Although mRNA expression was decreased with age for AL (P = 0.002) and arginase (P = 0.007), no significant change was observed for CPS, OTC, or AS mRNA expression. We conclude that the increased urea production in the liver may be explained not only by an increase in the activities of the urea cycle enzymes, but also by increased ammonia production by rumen fermentation and gluconeogenesis from amino acids around weaning time.

Restriction of placental growth in sheep impairs insulin secretion but not sensitivity before birth

Restricted growth before birth is associated with impaired insulin secretion but with initially enhanced insulin sensitivity in early postnatal life, which then progresses to insulin resistance and impaired glucose homeostasis by adulthood. This suggests that prenatal restraint impairs insulin secretion, but increases insulin sensitivity, before birth. Poor placental growth and function are major causes of restricted fetal growth in humans. We have therefore investigated the effects of restricted placental growth and function on plasma glucose, alpha-amino nitrogen and insulin concentrations and glucose- and arginine-stimulated insulin secretion in the fetal sheep at 120 and 140 days gestational age, and on insulin sensitivity, measured by hyperinsulinaemic euglycaemic clamp, at 130 days gestational age. Placental restriction decreased fetal blood pH and oxygen content, and weight in late gestation by approximately 20%. Reduced fetal and placental weights and indices of poor placental function, in particular fetal hypoxia and hypoglycaemia, were associated with impaired glucose- and arginine-stimulated insulin secretion, but not with changes in insulin sensitivity in the fetal sheep. We conclude that the impaired insulin secretion capacity reported in children and adults after intrauterine growth restriction, and in the neonatal and young adult sheep which is small at birth, is present in utero and persists. Whether this reflects the actions of the adverse intrauterine environment or changes to intrinsic capacity is unclear, but in utero interventions may be necessary to improve postnatal insulin secretion in the infant who is growth-restricted before birth.

Effect of exogenous growth‐hormone‐releasing factor on blood metabolites and minerals in late maturing buffalo heifers (Bubalus bubalis)

Previous studies have suggested that growth-hormone-releasing factor (GRF) enhanced growth and advanced puberty onset along with hormonal changes in buffalo heifers (Bubalus bubalis). However, it is not known to what extent exogenous GRF could influence blood metabolites and minerals to bring about puberty in buffalo heifers. Therefore, we planned to investigate the effect of exogenous bovine GRF (bGRF) on blood metabolites and minerals in buffalo heifers during a 3-month pre-treatment period, 9-month treatment period and 1-month post-treatment period. Six buffalo heifers were treated intravenously with bGRF (10 mug per 100 kg body weight) at 15-day interval for 9 months. Another six buffalo heifers of weight- and age-matched received requisite amount of vehicle (0.9% NaCl solution) during the same period. Exogenous bGRF enhanced (p < 0.01) plasma non-esterified fatty acids (NEFA) concentrations in treatment group when compared with control group during the treatment and post-treatment period, while plasma alpha-amino nitrogen (AAN) concentrations showed a decreasing trend (p < 0.05) in the treatment group when compared with the control group during the treatment and post-treatment periods. The plasma inorganic phosphorus (Pi) was found to be higher (p < 0.05) in the treatment group animals in comparison with the levels recorded in the control group animals during the treatment as well as post-treatment periods. However, there was no change (p > 0.05) in plasma glucose and calcium concentrations between the two groups. Plasma NEFA was found to be positively correlated with plasma growth hormone (GH); however, it was only significant for the treatment group (r = + 0.76; p < 0.05). Plasma AAN in the treatment group exhibited negative correlation with plasma GH (r = 0.72; p < 0.05), while plasma AAN and GH were recorded to be positively correlated in the control group (r = 0.47; p < 0.05). The present findings suggest that exogenous bGRF induces GH release that increases plasma NEFA and Pi and decreases AAN concentrations, which probably help to reach a certain physiological state that initiates events necessary for bringing about puberty in buffalo heifers.

Treatment of underfed pigs with GH throughout the second quarter of pregnancy increases fetal growth.

Circulating growth hormone (GH) concentrations increase in pregnancy and administration of GH during early-mid pregnancy increases fetal growth in well-fed pigs. To determine whether increased maternal GH could promote fetal growth when feed availability is restricted, fifteen cross-bred primiparous sows (gilts) were fed at approximately 30% of ad libitum intake, from mating onwards and were injected daily i.m. with recombinant porcine GH (pGH) at doses of 0, 13.4+/-0.3 and 25.6+/-0.5 microg/kg live weight from day 25 to day 51 of pregnancy (term approximately 115 days). Treatment with pGH increased maternal backfat loss between day 25 and day 51 of pregnancy, and increased maternal plasma IGF-I concentrations measured at day 51 of pregnancy. Fetal body weight, length and skull width at day 51 of pregnancy were increased by maternal treatment with pGH. Fetal plasma glucose concentrations were increased and maternal/fetal plasma glucose concentration gradients were decreased by maternal pGH treatment at 13.4, but not 25.6 microg/kg.day. Fetal plasma concentrations of urea were decreased by both levels of pGH treatment. Overall, fetal weight was negatively correlated with fetal plasma concentrations of urea, positively correlated with maternal plasma alpha-amino nitrogen concentrations and unrelated to glucose concentrations in either maternal or fetal plasma. This suggests that the availability of amino acids, not glucose, limits fetal growth in the first half of pregnancy in underfed gilts, and that maternal GH treatment may improve amino acid delivery to the fetus.

Aminoaciduria and glycosuria following severe childhood lead poisoning.

To determine the incidence of renal functional abnormalities after lead poisoning, we evaluated the parameters of renal tubular function in 134 children and young adults, 8-13 years after chelation therapy for severe lead poisoning. There was no evidence of hypertension or reduced kidney function as assessed by serum creatinine (Cr) concentrations. Urinary alpha-amino nitrogen (Uaan) concentrations were significantly increased compared with 19 healthy age-matched controls. Ninety-four children (70%) had aminoaciduria (Uaan/Cr >0.23). Urinary glucose excretion was also significantly higher than that of 2 historical controls. Thirty-two children (24%) had glycosuria (>125 mg/24 h). Fractional excretion of phosphate was normal in all children. We conclude that a partial Fanconi syndrome can persist up to 13 years after childhood lead poisoning.

Growth performance and gut function of piglets weaned at four weeks of age and fed protease-treated soya-bean meal

Abstract Two experiments were carried out to investigate the effects of the protease-treatment of soya-bean meal (SBM) on its composition and nutritive value when fed to piglets weaned at 4 weeks of age in cereal-based diets. In experiment 1, two proteases, active at either alkaline (protease P1) or acid pH (protease P2), were compared with alkali or acid treatment alone. In experiment 2, treatment with protease P2 at acid pH was compared with untreated-SBM, acid-treated SBM, a soya protein concentrate or skim milk powder+fishmeal. Protease treatment increased SBM alpha amino nitrogen concentrations and reduced in vitro SBM antigenicity. Protease P1 reduced in vitro antigenicity to a greater extent than protease P2. However, protease P1 hydrolysed SBM polypeptides non-specifically whereas protease P2 preferentially hydrolysed a high molecular weight polypeptide. In experiment 1, piglets (12 diet −1 ) fed alkali-treated SBM gained more weight than piglets fed acid-treated SBM in the first 7 days after weaning. Protease P1 did not improve live-weight gain compared with alkali-treatment whereas protease P2 did improve live-weight gain compared with acid treatment. In experiment 2, piglets (24 diet −1 ) fed protease P2-treated SBM or skim milk powder+fishmeal gained significantly more weight over the first 7 days post-weaning than piglets fed untreated SBM. In neither experiment were there significant differences between diets in piglet serum anti-SBM specific antibodies. There were no consistent changes in small intestine enzyme specific activities in response to the diets fed. Histopathological examination of the small intestine of piglets in experiment 2 revealed no evidence of enteric disease. Neither were there any differences between diets in villus height or crypt depth.

Effects of xylitol on urea synthesis in normal humans: relation to glucagon.

Xylitol exerts a nitrogen-sparing effect in stress catabolic states with hyperglucagonemia, but the mechanism(s) is unknown. We examined the effects of xylitol on urea synthesis during physiologic glucagon concentrations and during hyperglucagonemia. Urea synthesis was measured independently of blood amino acid concentration by means of functional hepatic nitrogen clearance (FHNC) (ie, the linear slope of the relation between urea synthesis rate and blood alpha-amino nitrogen concentration during infusion of alanine). FHNC was measured on four separate occasions in each of seven healthy subjects: during constant infusion of alanine alone, alanine superimposed on a constant infusion of xylitol (blood xylitol 1 mmol/L), alanine superimposed on infusion of glucagon, and alanine superimposed on infusions of xylitol and glucagon. During alanine infusion alone, plasma glucagon rose to -170 ng/L, and FHNC was (mean +/- sem) 27.9 +/- 1.3 L/h. Xylitol did not affect plasma glucagon and only moderately reduced FHNC to 24.3 +/- 1.0 L/h (p < .05). Glucagon infusion increased plasma glucagon to -450 ng/L and FHNC twofold to 50.9 +/- 6.2 L/h; this increase was totally prevented by the addition of xylitol that reduced FHNC to 27.4 +/- 2.6 L/h (p < .01). The results show that xylitol only inhibited FHNC minimally during spontaneous glucagon levels. In contrast, xylitol completely inhibits the increase in FHNC by glucagon. This suggests that the mechanism whereby xylitol reduces nitrogen loss in stress catabolic conditions with hyperglucagonemia involves an effect on liver metabolism. The mechanism is unknown but may be related to depletion of hepatocyte adenine nucleotides.

Effects of insulin and glucose on urea synthesis in normal man, independent of pancreatic hormone secretion

We investigated the inhibitory effect of insulin and glucose on hepatic amino- to urea-nitrogen conversion independent of endogenous insulin and glucagon secretion. Alanine-stimulated urea synthesis kinetics, as quantified by functional hepatic nitrogen clearance, i.e. the slope of the linear relation between blood alpha-amino nitrogen concentration and urea synthesis rate, were measured four times in each of six healthy volunteers, namely during spontaneous hormone responses, and during hormonal control by somatostatin and maintenance of basal hormone levels and euglycaemia, hyperinsulinaemia (85 +/- 8 mU/l), or hyperglycaemia (8.4 +/- 0.5 mmol/l). Hormonal control and euglycaemia reduced functional hepatic nitrogen clearance (mean +/- SD) by two-thirds (from 32.9 +/- 5.2 l/h to 12.2 +/- 3.4 l/h, p < 0.01). Hyperinsulinaemia did not change this (13.2 +/- 2.8 l/h), whereas hyperglycaemia further reduced functional hepatic nitrogen clearance by 40% to 7.4 +/- 1.3 l/h (p < 0.01). The reduction by hormonal control and euglycaemia is attributable to the abolition of the glucagon response to alanine infusion, as glucagon is known to up-regulate functional hepatic nitrogen clearance. Insulin did not regulate hepatic amino- to urea-nitrogen conversion, implying that the effect of insulin on urea production is due to its effect on blood amino acid supply to the liver. In contrast, glucose in itself reduced hepatic amino nitrogen conversion, independent of the hormonal responses to glucose. This means that the hepatic component of the amino-N-sparing effect of glucose depends on hyperglycaemia but not on hyperinsulinaemia.

Effects of glucose on hepatic conversion of aminonitrogen to urea in patients with cirrhosis: Relationship to glucagon

Glucose reduces the hepatic conversion of aminonitrogen to urea, quantified by the functional hepatic nitrogen clearance (i.e., the slope of the linear relation between urea synthesis rate and blood alpha-aminonitrogen concentration). This is due to a direct effect of glucose and to inhibition of glucagon. In this study, the effect of glucose on functional hepatic nitrogen clearance was examined during spontaneous hormone responses and during hormonal control by somatostatin. In 7 control subjects (study 1) and 9 patients with cirrhosis (study 2), functional hepatic nitrogen clearance was assessed twice in each subject: during infusion of alanine and during alanine administration superimposed on a continuous glucose infusion (blood glucose, on average = 8.4 mmol/L). In study 3, 6 patients with cirrhosis had functional hepatic nitrogen clearance determined on three occasions: during infusions of alanine and of alanine superimposed on infusion of somatostatin with either euglycemia or hyperglycemia (blood glucose = 8.4 mmol/L). In the control subjects (study 1), functional hepatic nitrogen clearance was 32.5 +/- 1.9 L/hr, and glucose reduced it to 18.4 +/- 0.9 L/hr (p < 0.01). In the cirrhotic patients, functional hepatic nitrogen clearance was only 9.8 +/- 1.3 L/hr (p < 0.01 vs. controls), and glucose did not change it. In the control subjects, glucose reduced the glucagon response to alanine from 204 +/- 36 ng/L to 106 +/- 8 ng/L (p < 0.05). In the cirrhotic patients the mean fasting glucagon level was increased twofold (180 +/- 21 ng/L). The response to alanine increased to 968 +/- 265 ng/L; it was not reduced by glucose. In study 3, somatostatin and hyperglycemia reduced functional hepatic nitrogen clearance from 13.2 +/- 1.5 L/hr to 6.4 +/- 0.7 L/hr (p < 0.01). Somatostatin and euglycemia reduced functional hepatic nitrogen clearance to 9.2 +/- 1.2 L/hr (p < 0.01 vs. alanine and hyperglycemia). The results show that the reduction by glucose of hepatic aminonitrogen conversion is lost in cirrhotic patients. The markedly increased glucagon response to alanine was not suppressed by glucose. Inhibition of the glucagon response by somatostatin reestablished the glucose effect, which was in part due to inhibition of glucagon in itself. Thus hepatic aminonitrogen conversion in cirrhosis depends on increased glucagon levels. The hormone-independent effect of glucose is preserved if the hyperglucagonemia is abolished, but the spontaneous high glucagon level overrules the glucose effect. The results indicate reduced hepatic contribution to the nitrogen-sparing effect of glucose in cirrhotic patients.

Metabolic response to glucose ingested with various amounts of protein

Seven healthy, normal-weight subjects were fed breakfasts of 50 g protein, 50 g glucose, and 10, 30, or 50 g protein plus 50 g glucose in random sequence. Plasma glucose, insulin, C peptide, glucagon, nonesterified fatty acids, and alpha-amino nitrogen were then measured from samples obtained over 4 h. The postmeal net area of each response curve was calculated. Ingestion of 50 g protein alone did not change the serum glucose concentration. The various amounts of protein ingested with 50 g glucose also did not alter the serum glucose response compared with that observed with 50 g glucose alone. Ingestion of the various amounts of protein also did not result in a further increase in insulin concentration when ingested with glucose, except with the 50-g-protein dose. This increase was modest. Ingestion of glucose resulted in a decrease in alpha-amino nitrogen and glucagon concentrations whereas ingestion of protein increased them as expected. Additions of progressively larger amounts of protein to the glucose meal resulted in a progressive increase in the alpha-amino-nitrogen- and glucagon-area responses. The relationship was curvilinear for both the alpha-amino-nitrogen response and the glucagon response. The null point, that is, the protein dose ingested with 50 g glucose at which there would be no change in area response, was estimated to be 9 g protein for alpha-amino nitrogen and 5 g protein for glucagon.

Effects of dietary carbohydrate composition on rumen fermentation, plasma hormones and metabolites in growing-fattening bulls

ABSTRACTTwo groups of six bulls were offered a fattening diet based on barley or sugar-beet pulp in the proportions of either 500: 200 g/kg or 200: 500 g/kg to compare the effects of starch and degradable fibre on rumen fermentations, plasma hormones and metabolites. The bulls were fed twice daily at 08.00 and 16.00 h.The large proportion of sugar-beet pulp in the diet induced higher levels of acetic and butyric acids and less propionic acid than the high proportion of barley. The diurnal patterns over a 24-h period of rumen pH, volatile fatty acids, glucose and ammonia were characterized by two cycles. Sugar-beet pulp in large proportions induced more even fermentations as indicated by flatter curves with less extreme values than those produced by a large inclusion of barley in the diet. Ammonia concentration was high before feeding and decreased subsequently during 4 to 6 h after the meal.No typical patterns were observed in plasma concentrations of glucose and alpha-amino nitrogen. Plasma urea concentration rose 2h after feeding and dropped during the following 6 to 8 h. There were no effects of dietary carbohydrate composition on growth hormone concentration but plasma insulin was significantly reduced with the diet high in sugar-beet pulp. Furthermore, the insulin profile showed peaks after each meal with the barley diet but only after the afternoon feeding with the diet high in sugar-beet pulp.

The insulin and glucose responses to meals of glucose plus various proteins in type II diabetic subjects

We previously have shown that ingested beef protein is just as potent as glucose in stimulating a rise in insulin concentration in type II diabetic patients. A synergistic effect was seen when given with glucose. Therefore, we considered it important to determine if other common dietary proteins also strongly stimulate an increase in insulin concentration when given with glucose. Seventeen type II (non-insulin-dependent) untreated diabetic subjects were given single breakfast meals consisting of 50 g glucose, or 50 g glucose plus 25 g protein in the form of lean beef, turkey, gelatin, egg white, cottage cheese, fish, or soy. The peripheral plasma concentrations of glucose, insulin, glucagon, alpha amino nitrogen, urea nitrogen, free fatty acids, and triglycerides were measured. Following ingestion of the meals containing protein, the plasma insulin concentration was increased further and remained elevated longer compared with the meal containing glucose alone. The relative area under the insulin response curve was greatest following ingestion of the meal containing cottage cheese (360%) and was least with egg white (190%) compared with that following glucose alone (100%). The glucose response was diminished following ingestion of the meals containing protein with the exception of the egg white meals. The peripheral glucagon concentration was decreased following ingestion of glucose alone and increased following all the meals containing protein. The alpha amino nitrogen concentration varied considerably. It was decreased after glucose alone, was unchanged after egg white ingestion, and was greatest after ingestion of gelatin. The free fatty acid concentration decrease was 4- to 8-fold greater after the ingestion of protein with glucose compared with ingestion of glucose alone.

Substrate utilization by the fetal sheep lung during the last trimester.

In vivo substrate utilization has not been described for the maturing fetal lung. We, therefore, studied pulmonary delivery and use of major fetal substrates in six chronically catheterized fetal lambs over 119-141 days gestation. Oxygen, glucose, lactate, and alpha-amino nitrogen concentrations were measured in the pulmonary artery and pulmonary vein whereas lung blood flow was determined using labeled microspheres. We found that lung oxygen availability and use increased near term. Oxygen delivery averaged 4960 +/- 480 (SEM) microliters/min and rose with fetal age (p less than 0.05); uptake averaged 708 +/- 111 microliters/min and increased 93% near term (p less than 0.05). In contrast, glucose availability and use fell with gestation. Pulmonary artery glucose decreased with time (p less than 0.001), with a mean drop of 5.05 +/- 1.71 mg/dl in individual animals (p less than 0.05). Average glucose uptake was 844 +/- 225 micrograms/min and fell near term (p less than 0.05). Lactate was produced by the lung at a mean rate of 534 +/- 176 micrograms/min; this did not change with gestation. Lung amino nitrogen availability increased with fetal age. Pulmonary artery amino nitrogen rose by 1.35 mg/dl, or 43% (p less than 0.001) and lung delivery of amino nitrogen increased (p less than 0.05). The mean pulmonary glucose/O2 ratio was 1.48 +/- 0.26 and decreased with gestation (p less than 0.05), being less than 1.0 near term. The glucose-lactate/O2 ratio was 0.67 +/- 0.26, implying that 30% of lung oxidative metabolism is still unaccounted for. The alterations in delivery of substrates to the lung which were identified may serve as signals for pulmonary maturation, inducing the changes in lung metabolism that were found near term.

Metabolic actions of cortisol in a macropodid marsupial Thylogale billardierii.

In undisturbed pademelon wallabies (Thylogale billardierii) with indwelling jugular venous catheters, an increase in the plasma cortisol concentration from 0.25 +/- 0.05 to 1.35 +/- 0.15 (S.E.M.) mumol/l in 2 h, during i.v. infusion of cortisol at 1.0 mg/kg per h, caused no significant change in the plasma glucose concentration from the control value of 4.26 +/- 0.25 mmol/l. The rates of appearance (Ra) and metabolic clearance (MCR) of glucose, measured by steady-state isotope dilution, also did not change significantly from the control values of 14.9 +/- 0.7 mumol/kg per min and 3.52 +/- 0.19 ml/kg per min respectively. Twice-daily i.m. injections of 7 mg cortisol/kg for 7 days caused increases in plasma concentrations of cortisol, from 0.26 +/- 0.02 to 0.66 +/- 0.04 mumol/l on day 7, and glucose, from 5.1 +/- 0.1 to 7.2 +/- 0.6 mmol/l by day 5. The concentration of glycogen in the liver of wallabies fasted for 24 h increased from the control level of 1.17 +/- 0.56 to 5.92 +/- 1.14 g/100 g on day 7 (P less than 0.01), but mean glucose Ra and MCR did not change significantly. Plasma concentrations of alpha-amino nitrogen rose from 2.73 +/- 0.13 to 3.22 +/- 0.12 mmol/l on day 1 and remained at this level. Plasma concentrations of urea rose from 8.59 +/- 0.62 to 9.70 +/- 0.32 mmol/l on day 1, but then declined below the control level. Food intake and urinary excretion of nitrogen did not change in undisturbed animals. However, fasting followed by liver biopsy was accompanied by urinary excretion of nitrogen in excess of food intake, persisting until day 2 of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

An Oxalate-Sodium Hydroxide Buffer to Study the Role of Milk Replacer Coagulation in Preruminant Calves

An oxalate-NaOH buffer, which prevents coagulation in the abomasum of young calves, was added to a nonclotting milk replacer based on high heat skim milk powder, to investigate effects of this buffer on digestibility and metabolism of dietary components. Twelve Holstein male calves were allotted at random in two groups of six animals each and fed the experimental milk replacers from 3 to 17 d of age. Digestibility of dry matter, protein, and fat was similar for both control and buffered milk replacers. Concentrations of plasma glucose, triglycerides, alpha-amino nitrogen, and urea were the same in animals receiving buffer treated milk replacer and control diets. The data suggests that this oxalate-NaOH buffer would be suitable to prevent milk clotting in studies dealing with the importance of coagulation in digestion and metabolism in preruminant calves.

Evidence for amino acid induced cholestasis in very-low-birth-weight infants with increasing enteral protein intake.

In the present investigation 32 very-low-birth-weight (VLBW) infants fed at three different levels of protein intake (2.92 g/kg/d from human milk, 3.22 and 4.06 g/kg/d from formula) were studied at the mean age of 21 days. Serum total alpha-amino nitrogen concentration correlated directly to total bile acid concentration. The serum and urine alpha-amino nitrogen and the serum bile acid concentration correlated with protein intake. The increase in protein intake was accompanied by a concomitant decrease in the intraluminal bile acid concentration in the AGA infants. The results offer indirect evidence of decreased bile flow in VLBW-infants on excessive oral protein intake. The cholestatic effect could be mediated by an increase in the plasma amino acid concentration.

A method for determination of the capacity of urea synthesis in the rat.

The relationship between total blood alpha-amino nitrogen concentration and urea synthesis rate was investigated with alanine as nitrogen source in 24 rats. Alanine was given as prime-continuous doses for 70 min so that constant amino acid concentration was attained between 5.5 and 34 mmol/l. Urea synthesis rate was assessed as accumulation in body water, corrected for intestinal hydrolysis. There was a positive correlation between nitrogen balance and alpha-amino nitrogen concentration. Urea synthesis rate in relation to amino acid concentration suggested barrier-limited substrate inhibition kinetics and data were examined accordingly by non-linear regression analysis. The estimated kinetic constants (mean +/- standard deviation) were: Vmax: 19.2 +/- 3.3 mumol (min X 100 g BW)-1, Km: 1.74 +/- 0.5 mmol/l, Ki: 6.84 +/- 1.9 mmol/l, and the barrier: 5.4 +/- 0.13 mmol/l. Because of the substrate inhibition, saturation cannot be attained, but the maximum synthesis rate, i.e. the capacity of urea nitrogen synthesis (CUNS), can be measured within 95% of the theoretical maximum in the concentration interval 7.3-11.6 mmol/l. CUNS was 9.16 +/- 0.81 mumol (min X 100 g BW)-1 (mean +/- standard deviation). Substrate-independent regulation of urea synthesis, e.g. by changes in liver mass or hormonal concentration, can be studied by this measure.

The effects of pancreatectomy on the sheep fetus in utero.

The effects of the removal of the fetal pancreas on the fetal metabolite concentrations and body weight have been investigated in chronically catheterized sheep fetuses during the last third of gestation. Between 390 and 1175 mg of pancreatic tissue was removed under halothane anaesthesia from sixteen fetuses between 113 and 121 d of gestation (term = 147 +/- 2d). In six fetuses from which 928 +/- 58 mg of pancreas had been removed the insulin level (3.4 +/- 0.3 micro micron/ml, n = 6) was below or equal to the limit of sensitivity of the assay. As only very small pieces of pancreas, if any, could be found in these fetuses at delivery, removal of the pancreas was regarded as complete in these animals. Pancreatectomy was incomplete in five fetuses from which 659 +/- 62 mg of pancreas had been removed. Insulin was detected in the plasma of these fetuses although the mean concentration (9.1 +/- 0.7 micro micron./ml, n = 5) significantly less than that in sham-operated animals (P less than 0.01). Small fragments of pancreas (0-26 mg) containing endocrine cells were found in these fetuses at delivery. Fetuses from which less than 50% of the pancreas had been removed had plasma insulin and metabolite concentrations similar to those of the sham-operated fetuses. Significant amounts of histologically normal pancreas were found in these fetuses at delivery. The plasma concentrations of glucose, fructose and alpha-amino nitrogen were significantly greater in the incompletely and completely pancreatectomized fetuses than in the sham-operated animals (P less than 0.01). In addition, the completely pancreatectomized animals also had higher plasma levels of lactate and free fatty acids than the sham-operated fetuses (P less than 0.01). There were no significant differences in the urea concentrations between sham-operated and pancreatectomized fetuses, but the fetal to maternal concentration difference in arterial plasma urea was greatest in the completely pancreatectomized fetuses (P less than 0.05). The hypoinsulinaemic fetuses were significantly smaller in birth weight than the sham-operated animals (P less than 0.02). The results show that removal of about 70% of the fetal pancreas will produce hypoinsulinaemia in the fetus and confirm that the pancreas is essential for normal growth and development in utero.

Oedema fluid composition in childhood disorders.

Oedema fluid was collected from the leg through a sterile 21 gauge needle inserted into the subcutaneous space in 12 patients with protein energy malnutrition, 12 with nephrosis, 5 with Indian childhood cirrhosis, 4 with acute nephritis, 4 with epidemic dropsy and 3 with congestive heart failure. The concentrations of protein, free amino acids and electrolytes were measured in plasma and oedema fluid. The plasma/oedema fluid ratios were 36:1, 49:1, 32:1 and 52:1 in protein energy malnutrition, nephrosis, Indian childhood cirrhosis and congestive heart failure. These ratios were significantly smaller in epidemic dropsy (4:1) and acute nephritis (21:1). The free alpha amino nitrogen concentrations in these two compartments were almost in equilibrium. This was also found for essential and non-essential amino acid distributions in protein energy malnutrition and nephrosis, whereas differences in amino acid patterns were found in nephritis and epidemic dropsy. Sodium and potassium concentrations varied substantially between diseases where the underlying cause was gross hypoproteinemia compared to non-hypoproteinemic conditions.