A High-Protein Meal Exceeds Anabolic and Catabolic Capacities in Rats Adapted to a Normal Protein Diet

Abstract

The postprandial fixation of dietary nitrogen in splanchnic and peripheral tissues as well as its dynamic transfer to the nitrogen pools of the body were quantified in rats subjected to an acute augmentation of dietary protein. For this purpose, we traced the dietary protein and studied the immediate fate of exogenous nitrogen in many tissues and biological fluids. Rats were adapted to a diet providing an adequate protein level (14 g/100 g), and then fed a meal containing either 0.42 g (Group A) or 1.50 g (Group H) of [(15)N]-labeled milk protein. The amounts of exogenous nitrogen transferred to urea (0.32 +/- 0.04 vs. 2.46 +/- 0.25 mmol, respectively), incorporated in splanchnic (0.41 +/- 0.02 vs. 0.87 +/- 0.10 mmol) and peripheral (1.65 +/- 0.84 vs. 2.36 +/- 0.49 mmol) tissue protein were higher in group H than in group A. Individual plasma amino acids (AA) [(15)N]-enrichments showed that AA respond differentially to an acute augmentation of dietary intake. This work provides new descriptive and quantitative information on the metabolic fate of dietary nitrogen in the postprandial state. It highlights the higher integration of a surplus of dietary nitrogen in the tissues even if it is rapidly limited by saturation of the protein synthesis capacities. The main metabolic response remains the stimulation of AA degradation, leading to a large rise in urea production. However, both anabolic and catabolic systems are exceeded, resulting in an elevation of peripheral AA and negative feedback on the gastric emptying rate.

Postprandial oxidative losses of dietary leucine depend on the time interval between consecutive meals: a model study with rats

“…Our observations support the idea of the important role of gastric empting rate on the regulation of amino acid utilization in the rat. The deceleration of gastric empting in response to the saturation of catabolic capacities by a meal high in protein was previously reported by Morens et al (2000). Türker and Yildirim (2011) showed that because of slower digestion, a six-meal feeding strategy was more efficient in terms of weight gain compared with 2, 3, or 4 meals.…”

IDH1 deficiency attenuates gluconeogenesis in mouse liver by impairing amino acid utilization

“…During prolonged fasting, the breakdown of skeletal muscle generates limited carbon resources in the form of AAs such as alanine. Hence, both fasting and feeding of a high-protein diet (HPD) can stimulate AA deamination and urea production in the liver (13), where AA carbon skeletons are converted into glucose or lipids. For most AAs, the amino group is transferred to α-KG to generate glutamate and other α-keto acids.…”

Metabolic Differences in the Steatosis Induced by a High-Fat Diet and High-Protein-Fat Diet in Rats

“…Even with the higher protein supply in the high-protein-fat diet, no significant differences were observed in the serum and hepatic total protein, because all excess of protein which the body does not use for the synthesis of hormone, enzymes and plasma proteins or in gluconeogenesis or in maintaining muscle mass, is excreted by the body as urea [44], or is oxidized to provide energy, because there is no place in the body for permanent storage of protein [45]. Probably, the excess of protein from high-protein-fat diet were oxidized because there was an increase in protein carbonyl concentration in the liver of HPF group.…”