Albumin Metabolism in Children With Protein Malnutrition1

Depressions of the serum albumin level are seen in clinical and in experimentally produced hyperglobulinemia (1-3); dextran infusions are also associated with hypoalbuminemia (4). However, the mechanisms for the production of these changes in albumin levels are not clearly defined. A colloid osmotic regulatory system has been postulated which effects control through either changes in plasma volume (1) or alterations in albumin metabolism (4). Previous studies employing dextran infusions supported the existence of a colloid osmotic regulatory mechanism in the control of serum albumin metabolism (4). The purpose of the studies reported here was to reexamine this hypothesis by measuring the rates of albumin synthesis and degradation during the development of induced hyperglobulinemia and after the attainment of this state. METHODSFemale rabbits were used in all studies. The rabbits were kept in metabolism cages, and complete urine and stool collections were made daily. All rabbits were fed a standard rabbit diet. Two to three drops of Lugol's solution was administered daily in the rabbits' drinking water to inhibit thyroid uptake of P"31.The distribution and metabolism of albumin were measured by means of rabbit serum albumin labeled with P131. The procedures used to separate, purify, and iodinate

“…Starvation and malnutrition in children have resulted in a depressed albumin concentration (14). Also, depressed albumin levels have been seen in patients with carcinoma (15).…”

Section: Discussionmentioning

confidence: 99%

“…Also, depressed albumin levels have been seen in patients with carcinoma (15). Lowered albumin synthesis has been considered the cause in both conditions (14,15). In addition, there are reports that increased nitrogen intake results in an increased rate of protein turnover (16,17).…”

Section: Discussionmentioning

confidence: 99%

The Effect of Hypergammaglobulinemia on Albumin Metabolism in Hyperimmunized Rabbits Studied With Albumin-I131*

Rothschild¹,

Oratz²,

Franklin³

et al. 1962

“…Experiments in which plasma proteins are depleted by means of a low protein diet (19)(20)(21) may not be directly comparable with plasmapheresis experiments, since the depletion is produced in a different way.…”

Section: Discussionmentioning

confidence: 99%

Effects of Plasmapheresis on Albumin Pools in Rabbits

Matthews¹

1961

The normal regulation of intravascular plasma protein mass has not been fully investigated. It has long been known that plasma proteins rapidly return to normal concentrations after plasmapheresis, but the means by which this takes place has not been clearly demonstrated. In pathological states, such as nephrosis and hypercatabolic hypoproteinemia, where there may be a steady loss of plasma protein, some compensatory mechanism (see next paragraph) must be involved in cases in which the intravascular plasma proteins are in a steady state. Frequently the protein concentration alone is determined, so that it is not known whether changes are due to variations in plasma volume or in total intravascular protein mass. A steady state can only be said to exist when the plasma protein synthesized is equal to that catabolized, so that the total mass of protein, but not necessarily the concentration, is constant.Disturbances of intravascular protein mass could be compensated for by a) change in synthesis rate, b) change in catabolic rate, c) net transfer of protein between extravascular and intravascular protein pools or d) a combination of several of these. There is also the possibility that the proportion of the different protein fractions is altered and that loss of one fraction is replaced by an increase of another fraction.The purpose of this investigation was to obtain further evidence on this problem by removing protein by plasmapheresis and observing the effect on the catabolic rate, intravascular pool mass, concentration and volume, and on the sum of synthesis rate plus net transfer rate from extravascular to intravascular pool. Rabbits on a normal diet were used, and a single protein fraction, albumin, was considered.I131-rabbit albumin was injected intravenously into rabbits, and plasma albumin specific activity (microcuries per gram), total body radioactivity * Present address: Radiotherapeutic Research Unit, Hammersmith Hospital, London, England. and urinary radioactivity were measured. It is assumed throughout that I131-albumin behaves as normal rabbit albumin (1, 2), that after catabolism the I131 is rapidly excreted, and that there is rapid mixing in each separate protein pool so that within any one pool the specific activity is uniform.A control period of ten days from the injection was allowed before starting plasmapheresis. The normal catabolic rate and pool masses were thus determined for each animal. Daily determinations of intravascular protein mass, concentration and volume were also made throughout each experiment in a control animal not subject to plasmapheresis.Intravascular protein mass and plasma volume were determined by isotope dilution. Since the proportion of albumin to total plasma protein was found to be constant throughout the experiment, albumin masses could be calculated from total protein masses. METHODS TheoreticalExtravascular pool. During the control period, the extravascular protein mass was determined by the equilibrium time method (3-5). In this method the ratio of extravascular t...

“…Animal and human studies of albumin metabolism in protein depletion have been concerned largely with the assessment of the catabolic rate of albumin and the extent to which it changes in the depleted subject or animal (1)(2)(3)(4)(5).…”

Section: Introductionmentioning

confidence: 99%

Albumin metabolism: effect of the nutritional state and the dietary protein intake

James¹,

Hay²

1968

176

A B S T R A C T Nine malnourished and nine children who had recovered from malnutrition were given a single injection of albumin-131I and were studied during consecutive periods in which the dietary protein was changed.Malnourished children had significantly lower catabolic rates of albumin than had recovered children on the same protein intake. Both nutritional groups, however, showed a progressive fall in catabolic rate after 3-5 days on a low protein diet (0.7-1.0 g/kg per day), and the maximum effect was seen in the 2nd wk of low protein feeding. The catabolic rate could return to normal within 3 wk in a malnourished child fed 4 g of protein/kg per day.The albumin synthetic rate was measured by a computer technique suitable for nonsteady-state conditions. The synthetic rate in the malnourished groups (101 mg/kg per day) fed on a low protein diet was significantly lower than the rate in the recovered groups (148 mg/kg per day). The synthetic rate responded rapidly to a change in diet; when the rate fell, the intravascular albumin mass was maintained by two compensating mechanisms: (1) a net transfer of extravascular albumin into the intravascular pool; and (2) by a delayed fall in the catabolic rate. The net transfer of albumin into the intravascular compartment diminished as the catabolic rate fell.Adaptation to a low protein diet was associated with: (a) low synthetic and catabolic rates of albumin; (b) a reduced extravascular albumin mass;