Limits of adaptation to high dietary protein intakes

Abstract

Ingested protein is made available to the body following digestion and absorption as amino acids and contributes to the body's demand for amino acids for protein synthesis and other metabolic pathways. As the pattern of amino acids required for metabolism is substantially different from that ingested, extensive metabolic interchange serves to improve the match. As a matter of course oxidation of amino acids contributes to satisfying the energy needs of the body. Amino acids in excess of immediate requirements follow degradative pathways and if the capacity of these pathways is exceeded adverse consequences ensue. In pathological states, such as inborn errors of metabolism, there is an obvious constraint on metabolic¯ow with serious sequelae. Pathways may be constrained to a lesser extent due to genetic polymorphisms, metabolic programming, limitation of cofactors or lack of associated substrates. Any of these can result in metabolic derangements, which do not manifest as overt disease, but limit normal function. There is the need to determine the dose response to increases in dietary protein and amino acid availability, using critical metabolic intermediates as outcome indices in order to clarify the upper limit of intake with which the body can cope under a range of physiological and pathological states.

Adaptative increase of ornithine production and decrease of ammonia metabolism in rat colonocytes after hyperproteic diet ingestion

“…In Western Europe and in the United States for example, protein consumption averages ϳ1.5-2 times the recommended intakes (i.e., 0.75-0.83 g⅐kg Ϫ1 ⅐day Ϫ1 ) (13,33) and as much as four times these values in slimming high-protein diets. Although there are many studies on the metabolic adaptations involved in response to increased protein ingestion (23,34), the physiological consequences of high-protein diet consumption are still poorly understood, and the maximal nondeleterious level of intake is still to be defined (17,23).…”

Effects of Long Term Consumption of Animal Proteins in the High Calorie Diet

“…The consumption of high protein diet dramatically increases the amino acid delivery to the body by increasing the pathways involved in the elimination of ammonia and maintenance of the nitrogen balance (Jackson 1999 ). In rats and humans, consumption of high protein diet increases oxidation of proteins, reduces carbohydrate oxidation, and elevates lipid oxidation, (Petzke et al 2007 ;Tentolouris et al 2008 ;Leidy et al 2007 ).…”

Vernon Young and the development of current knowledge in protein and amino acid nutrition. Vernon Young 1937–2004

“…However, the suggestion that the utilisation of urea-N in this way in Papua New Guinea highlanders could improve their N balance on low-and poor-quality-protein diets (Rikimaru et al 1984) was something Young was very sceptical of. He was also sceptical of Jackson's idea that urea salvage was an important control point in the regulation of N balance (see Jackson 1998Jackson , 1999 since this was contrary to his own work on urea kinetics (El-Khoury et al 1996). Nevertheless as further evidence emerged from Malcolm Fuller's work with pigs in Aberdeen (for example, Torrallardona et al 2003) and our own work (Millward et al 2000), Young set up the appropriate experiments with Fuller and went on to show with […”

“…It was discussed in the Food & Agriculture Organization/World Health Organization/United Nations University (1985) report and has been often revisited especially by Waterlow (1999) and Jackson (1999Jackson ( , 2000.…”