Observations on the mechanism of adaptation to low protein intakes.
Observations on the mechanism of adaptation to low protein intakes.
复制标题
低蛋白质摄入适应机制的观察。
DOI:
10.1016/s0140-6736(68)91576-6
复制
发表时间:
1968
期刊:
影响因子:
168.9
通讯作者:
J. Waterlow
中科院分区:
文献类型:
--
作者:
J. Waterlow
In this, the Charles West lecture, given at the Royal College of Physicians, London, on Oct. 3, 1968, the author outlined much of the work done, under his direction, at the Medical Research Council Tropical Metabolism Research Unit, Jamaica.The question of adaptation is crucial to the understanding of nutritional problems. Although some nutritional conditions lead to breakdown, there must be a wide range of adaptation to different conditions compatible with health. To distinguish between the end of the normal and the beginning of the abnormal, we must identify those characteristics which the body tries to maintain constant at the expense of others.A simplified model assumes that there is a single pool of constant size containing metabolic nitrogen; this will receive amino acids by two routes-from the food and from catabolism of body protein-and will lose amino nitrogen by two routes-synthesis into body protein and urinary excretion. between intake of nitrogen and excretion there is a continual flux between the metabolic pool and body protein. Two alternative hypotheses can explain the reduction of urinary nitrogen to match intake. In the first, the catabolic rate may fall with intake so that the total nitrogen entering the pool is greatly reduced, the turnover rate being closely related to protein intake. In the second, the catabolic rate may remain unchanged so that the amount of nitrogen entering the pool does not change much; this implies a redistribution of the flow of amino nitrogen; the synthesis of protein remains open, while the excretion of urea is almost closed.These hypotheses were tested by measuring the total lysine flux in rats given continuous infusions of14C-lysine. Short periods of low protein intake did not cause any decrease in the turnover rate, although urinary excretion of nitrogen was reduced to between a quarter and a third of that in control rats. A similar study with the use of glycine labelled with15N was made with 6 infants on a high protein diet (5.2 g protein/kg/day) and 5 infants on low protein (1.2 g/kg/day). There was no reduction of the overall rates of protein synthesis and catabolism with low protein intakes; both groups of children had a total turnover of 5-6 g protein/kg/day-about a quarter of that found in rats and 2 or 3 times the estimated turnover in adults. These values bear a similar relationship to each other, as do rates of basal oxygen consumption in rat, infant and adult.Though the total turnover was unchanged, post-mortem analysis of rats following continuous infusion withuC-lysine indicated a change in the pattern of protein synthesis with low protein diets; in the liver, the rate remained normal or increased, but in muscle it was markedly reduced. It appeared that muscle reduced its demands, leaving more available amino acid for other tissues.Studies of serum-albumin in malnourished and recovering children on high and low protein diets showed that, when protein intake was reduced, there was an immediate fall in the rate of albumin synthesis, followed, after a lag of several days, by a fall in the rate of catabolism, with a transfer of albumin from the extravascular to the intravascular pool.With the use of labelled arginine, it has been shown that in rats on a normal diet about 50%, and in those on a low protein diet about 70%, of amino acid liberated in the liver is re-utilized for protein synthesis.Studies of adaptive enzyme changes in rats have shown that on low protein diets there is an increase in the activity of the amino acid activating enzymes in the liver and a decrease in the activity of urea cycle enzymes,i.e. an amino acid entering the liver would have a greater chance of being incorporated into protein and a smaller chance …