Abstract

Lack of nutrient intake results in a loss of body fat and lean tissue [1] and hitherto the effects of nutritional depletion and repletion with refeeding have been judged by changes in body composition, especially of lean tissue. Lean tissue is composed of water, minerals, nitrogen and glycogen [2, 3], and feeding wasted individuals results in a gain of the multiple elements in lean tissue [4] as well as body fat. One of the elements responding to nutrient intake is body potassium, which has been used as an index of body cell mass [5], the metabolically active component of the lean tissue. We [6, 7] and others [8–10] have shown that in contrast to body nitrogen, body potassium responds rapidly to feeding by both oral [7] and intravenous routes [6, 8–10]. These changes have been interpreted as being due to changes in lean mass. However, the early restitution of body potassium without a rise in body nitrogen indicates that cell ion uptake occurs earlier than protein synthesis with nutritional support [9]. In support of this conclusion it has been shown, using ion selective electrodes, that hypocaloric feeding results in a fall in muscle membrane potential and in the concentration of intracellular ionic K+ [11, 12]. The changes were specifically related to nutrient deprivation as they could not be reversed by potassium supplementation per se [12].

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