(1/2033) Sodium requirement of adult cats for maintenance based on plasma aldosterone concentration.
The sodium requirement of adult cats for maintenance was determined using a randomized block design of eight dietary sodium treatments (0.1, 0.4, 0.5, 0.66, 0.8, 1.2, 1.6 or 2.0 g Na/kg in a casein-lactalbumin-based purified diet) administered for periods of 4 wk. A total of 35 adult specific-pathogen-free domestic shorthaired cats (26 males and 9 females, 1.5-3 y of age) was given an equilibration diet (2 g Na/kg) for 14 d before assignment (or reassignment) to the treatments. A total of 12 cats (8 males, 4 females) was randomly assigned to the lowest six levels of sodium, and four cats to the highest two sodium levels. Cats consuming the diet containing 0.1 g Na/kg had significantly elevated aldosterone concentration in plasma, and packed cell volume. In addition, these cats exhibited anorexia, body weight loss, reduced urinary specific gravity and sodium excretion, and had a negative sodium balance. However, adult cats did not develop polydypsia and polyuria reported in sodium-deficient kittens. Cats given the diet containing 0.66 g Na/kg did not have an increased packed cell volume, but aldosterone concentration in the plasma was significantly elevated. However, cats given diets containing >/=0.8 g Na/kg had plasma aldosterone concentrations =0.7 nmol/L (reference value for sodium-replete cats) and normal packed-cell volumes. A minimal sodium requirement of adult cats for maintenance of 0.8 g Na/kg diet (energy density = 22 kJ/g diet) or 0.4 mmol Na. kg body weight-1. d-1 is proposed. (+info)
(2/2033) Lysine deficiency alters diet selection without depressing food intake in rats.
Under states of protein deficiency, the dietary limiting amino acid, rather than protein content, can act as the dietary stimulus to control diet selection. If fact, threonine-deficient rats will alter their diet selection patterns solely on the basis of very small changes (0.009 g/100 g) in the dietary threonine concentration. In these studies, we assessed whether lysine-deficient rats will also alter their diet selection patterns on the basis of small changes in dietary Lys concentration. In all experiments, growing rats were adapted to diets in which the protein fraction (purified amino acids or wheat gluten) was limiting in Lys. They were then given a choice between the adaptation diet (AD) diet and a slightly more deficient diet. Rats that were adapted to a Lys-deficient diet (0.25 g Lys/100 g) selected their AD over diets containing as little as 0.01% less Lys (P < 0.01) within 5 d. To determine how deficient rats must be before they alter their selection patterns, rats were adapted to diets containing various levels of Lys, i.e., 2 levels below the requirement for growth and 2 levels above the requirement for growth, but below the requirement for maximal nitrogen retention. Only rats adapted to diets containing Lys below their requirement for growth selected their AD over a diet containing 0.05% less Lys (P < 0.005). Finally, to determine whether rats will alter their selection to whole protein-based diets, rats were adapted to 25% wheat gluten diets supplemented with 0.03-0.21% Lys. Rats selected the AD over a diet containing as little as 0.09% less supplemental Lys by d 4 of the trial (P < 0.05). We conclude that rats are sensitive to changes as small as 0.01% in dietary Lys concentration, but that sensitivity requires prior adaptation to Lys-deficient diets. (+info)
(3/2033) An estimation of the requirement for folic acid in gestating sows: the metabolic utilization of folates as a criterion of measurement.
Sows at their second parity were randomly distributed in five groups of seven animals each to determine the dietary concentration of folic acid that optimizes the metabolic utilization of the vitamin during gestation. The groups differed by dietary supplement of folic acid: 0, 5, 10, 15, or 20 ppm. Sows were fed 2.5 kg of diet each day. The response of serum folates and folate binding capacity to treatments and the excretion of urinary folates after an i.v. injection of folic acid were measured. The total daily excretion of urinary folates was corrected according to the response to one i.v. injection of saline on the day preceding the i.v. injection of folic acid. The decrease of total serum folates throughout gestation was less pronounced in the groups fed 15 and 20 ppm of dietary folic acid (supplement x period interaction, P<.06) than it was in the other three treatments. The proportion of i.v. folic acid not recovered in sow urine (injected - excreted) decreased as the amount of dietary folic acid increased to reach a minimum, which differed according to the period (supplement x period interaction, P<.02); it was 15 ppm during wk 1 of gestation and 10 ppm for the other periods studied. The unrecovered folates increased over a dietary concentration of 15 ppm. These minimum values correspond to the most appropriate feed concentration that covered the whole body utilization (tissue and cell metabolism, catabolism, and storage) of folates by the sows and could be interpreted as a reliable index of the requirement. (+info)
(4/2033) Comparison of indirect calorimetry, the Fick method, and prediction equations in estimating the energy requirements of critically ill patients.
BACKGROUND: Accurate measurement of resting energy expenditure (REE) is helpful in determining the energy needs of critically ill patients requiring nutritional support. Currently, the most accurate clinical tool used to measure REE is indirect calorimetry, which is expensive, requires trained personnel, and has significant error at higher inspired oxygen concentrations. OBJECTIVE: The purpose of this study was to compare REE measured by indirect calorimetry with REE calculated by using the Fick method and prediction equations by Harris-Benedict, Ireton-Jones, Fusco, and Frankenfield. DESIGN: REEs of 36 patients [12 men and 24 women, mean age 58+/-22 y and mean Acute Physiology and Chronic Health Evaluation II score 22+/-8] in a hospital intensive care unit and receiving mechanical ventilation and total parenteral nutrition (TPN) were measured for > or = 15 min by using indirect calorimetry and compared with REEs calculated from a mean of 2 sets of hemodynamic measurements taken during the metabolic testing period with an oximetric pulmonary artery catheter. RESULTS: Mean REE by indirect calorimetry was 8381+/-1940 kJ/d and correlated poorly with the other methods tested (r = 0.057-0.154). This correlation did not improve after adjusting for changes in respiratory quotient (r2 = 0.28). CONCLUSIONS: These data do not support previous findings showing a strong correlation between REE determined by the Fick method and other prediction equations and indirect calorimetry. In critically ill patients receiving TPN, indirect calorimetry, if available, remains the most appropriate clinical tool for accurate measurement of REE. (+info)
(5/2033) Dietary pantothenic acid requirement of juvenile grass shrimp, Penaeus monodon.
A feeding trial was conducted to estimate the minimal dietary pantothenic acid (PA) requirement for juvenile grass shrimp, Penaeus monodon. Purified diets with seven levels (0, 20, 40, 60, 120, 240, and 480 mg/kg) of supplemental PA were fed to P. monodon (mean weight 0.88 +/- 0.01 g) for 8 wk. The level of PA detected in the unsupplemented diet was 0.02 mg/kg. Each diet was fed to three replicate groups of shrimp. Feed efficiencies (FE) and protein efficiency ratios were highest in shrimp fed the diets supplemented with 120, 240, and 480 mg PA/kg diet, followed by the groups fed 60 mg/kg, then 40 mg/kg, and finally the unsupplemented control group (P < 0.05). Shrimp fed diets supplemented with PA had significantly higher survival percentages and lower hepatopancreatic lipid concentration than those fed the unsupplemented, control diets. Broken-line regression analyses of weight gain percentage and hepatopancreatic CoA and PA concentrations of the shrimp indicated that the adequate dietary PA concentration in growing P. monodon is 101-139 mg/kg. (+info)
(6/2033) Criteria for choosing amino acid therapy in acute renal failure.
Metabolic studies were performed on 19 patients with acute renal failure. Therapy included intravenous hyperalimentation using 15 to 20 g of essential amino acids or 20 to 40 g of essential plus nonessential amino acids and hypertonic glucose (37 to 50%). The effect of this parenteral feeding appears to be primarily pharmacological. Hypertonic glucose promotes the hyperinsulinemia important to be membrane function, the operation of the sodium pump, and cell metabolism. Administration of high biological value crystalline amino acdis potentiates the effect of insulin by inhibiting protein breakdown and promoting protein synthesis, particularly in muscle. This reduces tissue catabolism and urea formation, and promotes potassium, magnesium, and phosphate homeostasis. The branched-chain ketogenic amino acids valine, leucine, and isoleucine may be of particular importance. When indicated, administration of renal failure hyperalimentation and peritoneal or hemodialysis can be expected to complement each other and accelerate recovery. This intravenous fluid therapy, in turn, must be coordinated with proper hemodynamics, usually requiring a colloidal solution to maintain intravascular volume, and cardiotrophic agents such as digitalis and dopamine. Early use of renal failure can be expected to demonstrate the most striking response in terms of survival, early recovery from acute renal failure, and the preservation of physiological homeostasis. (+info)
(7/2033) Folate metabolism and requirements.
Folate functions in multiple coenzyme forms in acceptance, redox processing and transfer of one-carbon units, including nucleotides and certain amino acids. Folate-requiring metabolic processes are influenced by folate intake, intake of other essential nutrients, including vitamins B-12 and B-6, and at least one common genetic polymorphism. Estimates of folate requirements have been based on intakes associated with maintenance of normal plasma and erythrocyte folate concentrations and functional tests that reflect abnormalities in folate-dependent reactions. Dietary Reference Intakes for folate that have been developed recently are based primarily on metabolic studies in which erythrocyte folate concentration was considered the major indicator of adequacy. For adults >/=19 y, the Recommended Dietary Allowance (RDA) is 400 microg/d of dietary folate equivalents (DFE); for lactating and pregnant women, the RDAs include an additional 100 and 200 microg of DFE/d, respectively. (+info)
(8/2033) Postnatal profiles of glycogenolysis and gluconeogenesis are modified in rat pups by maternal dietary glucose restriction.
Because glucose is an important metabolic fuel during perinatal development, the effect of restriction of maternal dietary glucose on the developmental profile of neonatal glucoregulatory pathways was investigated. Pregnant rats were fed isoenergetic diets (0, 12, 24 or 60% glucose) and offspring were killed at seven postpartum time periods: 0-2, 4-6, 12-16 and 24 h, and 3, 6 and 15 d. Failure of the most restricted pups (0%) to survive 24 h was explained by persistent hypoglycemia resulting from the following: 1) insufficient tissue glycogen reserves at birth; 2) lower liver glycogen mobilization; 3) delayed phosphorylase a induction; and 4) low phosphoenolpyruvate carboxykinase (PEPCK) gene expression, all of which occurred despite the lower insulin:glucagon ratio. Differences in liver glycogen stores, which had been exhausted in all dietary groups by 16 h, could not account for the high d 1 pup mortality in the moderately restricted (12 and 24% glucose) groups. However, a certain metabolic distress was suggested because these moderately restricted neonates had significantly higher liver PEPCK gene expression at 12-16 h but significantly lower plasma glucose at 24 h. The high d 3 mortality, confirmed by analysis of deviance, was not supported by significant differences in any of the measured glucoregulatory indices. We conclude that dietary glucose during pregnancy is required for neonatal survival; its restriction not only lowers tissue glycogen reserves, but can disrupt the normal gene expression of liver PEPCK and the neonatal profile of phosphorylase a activity. Importantly, these observations show that the development of neonatal glucoregulatory mechanisms is modified by the availability of maternal dietary glucose. (+info)