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

Published online by Cambridge University Press:  09 March 2007

P. G. Lunn
Affiliation:
Medical Research Council, Dunn Nutrition Unit, Milton Road, Cambridge CB4 1XJ
S. Austin
Affiliation:
Medical Research Council, Dunn Nutrition Unit, Milton Road, Cambridge CB4 1XJ
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Abstract

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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 to either 90, 80. 70, 60 or 50% 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 thermogenesis.

4. The plasma concentration of triiodothyronine (T3) 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 50% 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 T3 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.

Type
Papers of direct relevance to Clinical and Human Nutrition
Copyright
Copyright © The Nutrition Society 1983

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