Excess energy intake promotes the development of hypoalbuminaemia in rats fed on low-protein diets

Abstract

1. A group of rats were given ad lib. a diet with a protein-energy: total energy (P: E) value of 0.03. Other animals received the same protein intake (g/kg body-weight per d) as this group, but had their energy consumption reduced lo either 90, 80. 70, 60 or SO% of the ad lib. value.2. The restricted growth rate of rats fed on the P:E -0.03 diet ad lib. has been shown to be due entirely to their insufficient protein consumption. In contrast, energy intake was far in excess of that required for maintenance and the limited amount of growth.3. Carcass analysis demonstrated that some of the excess energy intake was stored as fat, but a greater part had been dissipated, presumably by diet-induced thennogenesis.4. The plasma concentration of triiodothyronine (T,) was elevated in all animals consuming excess energy and was significantly related to both the total surplus and the amount of energy dissipated.5. In the group of animals restricted to SO% of the ad lib. intake, energy rather than protein appeared to be the factor limiting growth. Energy intake was below estimated requirements for maintenance and was associated with values for plasma T, that were lower than those found in well-fed control rats.6. Although all the animals had similar protein intakes, plasma albumin concentration differed between the groups and was found to be inversely proportional to the energy intake. Thus it was lowest in animals receiving food ad lib. and rose to near normal values in the most-severely-restricted rats.7. It is suggested that hypoalbuminaemia, and perhaps other features of protein deficiency, seen in animals fed on low-P: E diets may occur as an undesirable consequence of the metabolic response required to deal with excess energy consumption.It has become generally accepted that rats offered diets of low-protein content voluntarily reduce their food intake and thus suffer from a shortage of energy as well as protein. It has been argued, therefore, that it is difficult to know whether the metabolic abnormalities seen in such animals are a result of the low protein-energy: total energy (P:E) value of the diet, or occur as a response to the voluntary food restriction. However, the findings of Coward et al. (1977) showed that food consumption, when expressed as a function of body-weight, was not reduced in rats maintained on diets of low P: E despite severely-restricted growth rates. Moreover, a theoretical estimation of energy requirements for maintenance and growth (using the values of Evans & Miller, 1968) suggests that far from being short of energy, the animals may be facing the problem of how to deal with a surplus.The present paper describes a practical investigation into the relative deficiencies and excesses of protein and energy consumed by rats offered ad lib. a low-P:E diet. The relationship between these dietary constituents and plasma albumin concentration, an accepted index of protein deficiency, is also examined. E X P E R I M E N T A LMales from a specific-pathogen-free colony of hooded rats kept at the Dunn N...

Serum Insulin-Like Growth Factors I and II Concentrations and Growth Hormone and Insulin Responses to Arginine Infusion in Children with Protein-Energy Malnutrition before and after Nutritional Rehabilitation

“…Such diets have been shown in experimental animals to cause hypoalbuminemia, whereas the energy-and protein-deficient diets, similar to those consumed by the marasmic children, did not lead to hypoalbuminemia (53).…”

Differences in Nitrogen Metabolism between Protein-Deficient and Energy-Deficient Rats with Similarly Restricted Growth Rates

“…It therefore seems un likely that these particular hormones could be responsible for the observed differences in nitrogen metabolism seen in the present ex periment. Recently, data showing that plasma triiodothyronine (T3) concentration differed markedly between protein-and ener gy-deficient animals, has been reported [Tulp et al, 1979], and a possible effect of this hor mone on the direction of nitrogen metabo lism is at present under investigation [Lunn and Austin, 1983], Whatever the mechanism however, the current results do suggest that the presence and severity of the dysadaptation might be indicated by the existence of hypoalbuminaemia or the raised non-essential to essen tial plasma amino acid ratio. Both of these abnormalities were present in the animals fed the least severe protein-deficient diet, and became more marked as the inappropriate protein distribution increased.…”

Increase in skeletal muscle protein content by the ß-2 selective adrenergic agonist clenbuterol exacerbates hypoalbuminemia in rats fed a low-protein diet

“…Data from balance studies have shown that for hypoalbuminemia to occur, not only has dietary protein to be inadequate, but it is also necessary for energy consumption to be in excess of requirements for the protein-limited growth rate (1,2). However, the mechanisms by which an energy surplus interferes with protein metabolism remain unknown.…”

“…This could be reasonable evidence that hypoalbuminemia is also promoted by increased ß-2 selective agonist activity during consumption of low-protein diets. In addition, to have a better picture of the metabolic changes produced by the present drug treatment, two hormones, T 3 and insulin, known to be associated with plasma albumin levels in rats fed a low-protein diet, were measured (1,4,6,15).…”