Adaptation to a high-protein diet progressively increases the postprandial accumulation of carbon skeletons from dietary amino acids in rats
Résumé
Adaptation to a high-protein diet progressively increases the postprandial accumulation of carbon skeletons from dietary amino acids in rats..—We aimed to determine whether oxidative pathways adapt to the overproduction of carbon skeletons resulting from the progressive activation of amino acid (AA) deamination and ureagenesis under a high-protein (HP) diet. Ninety-four male Wistar rats, of which 54 were implanted with a permanent jugular catheter, were fed a normal protein diet for 1 wk and were then switched to an HP diet for 1, 3, 6, or 14 days. On the experimental day, they were given their meal containing a mixture of 20 U-[ 15 N]-[ 13 C] AA, whose metabolic fate was followed for 4 h. Gastric emptying tended to be slower during the first 3 days of adaptation. 15 N excretion in urine increased progressively during the first 6 days, reaching 29% of ingested protein. 13 CO2 excretion was maximal, as early as the first day, and represented only 16% of the ingested proteins. Consequently, the amount of carbon skeletons remaining in the metabolic pools 4 h after the meal ingestion progressively increased to 42% of the deaminated dietary AA after 6 days of HP diet. In contrast, 13 C enrichment of plasma glucose tended to increase from 1 to 14 days of the HP diet. We conclude that there is no oxidative adaptation in the early postprandial period to an excess of carbon skeletons resulting from AA deamination in HP diets. This leads to an increase in the postprandial accumulation of carbon skeletons throughout the adaptation to an HP diet, which can contribute to the sustainable satiating effect of this diet. dietary amino acids; oxidation; deamination; glycogen; stable isotopes THE EFFECT OF HIGH-PROTEIN (HP) diets on energy metabolism has been often questioned (15, 29, 43). In rats fed ad libitum, an HP diet has been shown to lower adiposity, an effect that is not only due to a reduction in the spontaneous energy intake, as revealed by pair-fed studies (4, 30), but also due to metabolic adaptations. When dietary proteins are given in excess, the metabolic pathways adapt in a few days to cope with the excess nitrogen originating from amino acids through an activation of various liver enzymes involved in their catabolism. This has been well documented for the urea cycle (25, 33). In contrast, less is known about the remaining carbon skeletons. It seems that the carbon skeletons produced from the increased deami-nation are poorly catabolized during the postprandial window (14). Indeed, using 15 N and 13 C amino acids administered as oral tracers in an HP meal given to rats, we found that 4 h after ingestion almost half of the carbon skeletons produced from dietary amino acids were still not oxidized (14). Minimal data exist on the adaptation of energy pathways to a large increase in dietary protein intake. In a previous study, we examined the time course adaptation of energy metabolism components to a high-protein diet in rats (38). Together with the adaptation of key enzymes involved in energy pathways (39), we reported a progressive adaptation of glucose metabolism over 2 wk, characterized by an increase in carbohydrate (CHO) oxidation above CHO intake. In contrast, we found no significant changes in energy expenditure. A better understanding of the channeling of carbon skeletons from dietary amino acids toward metabolic pathways is of importance to better understand how amino acids contribute to energy metabolism in situations of protein excess. To compare the time course adaptation of dietary nitrogen and carbon skeleton metabolism to an HP diet, we used a double stable isotope method (15 N and 13 C) to trace dietary proteins and determine the metabolic fate of the nitrogen and carbon compounds .
Domaines
Alimentation et Nutrition
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