Abstract
Nitrogen balance studies have shown that a portion of the N ingested but not excreted is not accounted for. We compared several diets (standard, high-fat, high-protein, and self-selected cafeteria) to determine how diet-dependent energy sources affect nitrogen handling, i.e., the liver urea cycle. Diet components and rat homogenates were used for nitrogen, lipid, and energy analyses. Plasma urea and individual amino acids, as well as liver urea cycle enzyme activities, were determined. Despite ample differences in N intake, circulating amino acids remained practically unchanged in contrast to marked changes in plasma urea. The finding of significant correlations between circulating urea and arginine-succinate synthase and lyase activities supported their regulatory role of urea synthesis, the main N excretion pathway. The cycle operation also correlated with the food protein/energy ratio, in contraposition to total nitrogen losses and estimated balance essentially independent of dietary energy load. The different regulation mechanisms observed have potentially important nutritional consequences, hinting at nitrogen disposal mechanisms able to eliminate excess nitrogen under conditions of high availability of both energy and proteins. Their operation reduces urea synthesis to allow for a safe (albeit unknown) mechanism of N/energy excess accommodation.
Highlights
Dietary excess of amino acid N, an obvious consequence of high-protein diets, necessarily induces its oxidation for energy, increasing urea synthesis [1]
Cafeteria diet-fed rats showed a higher percentage of body fat
We were able to show the importance of the food protein/energy ratio in the control of urea cycle operation, in contraposition to total nitrogen losses and nitrogen balance, which were essentially independent of the diet energy content
Summary
Dietary excess of amino acid N, an obvious consequence of high-protein diets, necessarily induces its oxidation for energy, increasing urea synthesis [1] This function is mainly carried out by the liver, which plays an active role in the adaptation of whole-body nitrogen homoeostasis to dietary protein, possibly via glucagon [2]. Liver urea production is both a tight control system to prevent the loss of valuable amino acid N and the best-controlled outlet for excretion of excess N. This way, daily dietary variations in amino acid availability are counteracted in significant part through adjustments in liver metabolic function. This mechanism, used to maintain N homeostasis, is complemented by other tissues and pathways, which are in part practically unknown
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