scholarly journals A high protein diet upregulates whole‐body protein turnover during energy deficit

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Lee M. Margolis ◽  
Jay J. Cao ◽  
Edward R. Sauter ◽  
Leah D. Whigham ◽  
James P. McClung ◽  
...  
1987 ◽  
Vol 51 (1) ◽  
pp. 261-262
Author(s):  
Ryuhei FUNABUCI ◽  
Kouichi SAITO ◽  
Kazumi YAGASAKI

2018 ◽  
Vol 3 (4) ◽  
pp. 62
Author(s):  
Jose Antonio ◽  
Anya Ellerbroek ◽  
Cassandra Carson

The effects of long-term high-protein consumption (i.e., >2.2 g/kg/day) are unclear as it relates to bone mineral content. Thus, the primary endpoint of this investigation was to determine if consuming a high-protein diet for one year affected various parameters of body composition in exercise-trained women. This investigation is a follow-up to a prior 6-month study. Subjects were instructed to consume a high-protein diet (>2.2 g/kg/day) for one year. Body composition was assessed via dual-energy X-ray absorptiometry (DXA). Subjects were instructed to keep a food diary (i.e., log their food ~three days per week for a year) via the mobile app MyFitnessPal®. Furthermore, a subset of subjects had their blood analyzed (i.e., basic metabolic panel). Subjects consumed a high-protein diet for one year (mean ± SD: 2.3 ± 1.1 grams per kilogram body weight daily [g/kg/day]). There were no significant changes for any measure of body composition over the course of the year (i.e., body weight, fat mass, lean body mass, percent fat, whole body bone mineral content, whole body T-score, whole body bone mineral density, lumbar bone mineral content, lumbar bone mineral density and lumbar T-score). In addition, we found no adverse effects on kidney function. Based on this 1-year within-subjects investigation, it is evident that a diet high in protein has no adverse effects on bone mineral density or kidney function.


Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2457 ◽  
Author(s):  
Jess A. Gwin ◽  
David D. Church ◽  
Robert R. Wolfe ◽  
Arny A. Ferrando ◽  
Stefan M. Pasiakos

Protein intake recommendations to optimally stimulate muscle protein synthesis (MPS) are derived from dose-response studies examining the stimulatory effects of isolated intact proteins (e.g., whey, egg) on MPS in healthy individuals during energy balance. Those recommendations may not be adequate during periods of physiological stress, specifically the catabolic stress induced by energy deficit. Providing supplemental intact protein (20–25 g whey protein, 0.25–0.3 g protein/kg per meal) during strenuous military operations that elicit severe energy deficit does not stimulate MPS-associated anabolic signaling or attenuate lean mass loss. This occurs likely because a greater proportion of the dietary amino acids consumed are targeted for energy-yielding pathways, whole-body protein synthesis, and other whole-body essential amino acid (EAA)-requiring processes than the proportion targeted for MPS. Protein feeding formats that provide sufficient energy to offset whole-body energy and protein-requiring demands during energy deficit and leverage EAA content, digestion, and absorption kinetics may optimize MPS under these conditions. Understanding the effects of protein feeding format-driven alterations in EAA availability and subsequent changes in MPS and whole-body protein turnover is required to design feeding strategies that mitigate the catabolic effects of energy deficit. In this manuscript, we review the effects, advantages, disadvantages, and knowledge gaps pertaining to supplemental free-form EAA, intact protein, and protein-containing mixed meal ingestion on MPS. We discuss the fundamental role of whole-body protein balance and highlight the importance of comprehensively assessing whole-body and muscle protein kinetics when evaluating the anabolic potential of varying protein feeding formats during energy deficit.


2020 ◽  
Vol 112 (6) ◽  
pp. 1468-1484 ◽  
Author(s):  
Grith Højfeldt ◽  
Jacob Bülow ◽  
Jakob Agergaard ◽  
Ali Asmar ◽  
Peter Schjerling ◽  
...  

ABSTRACT Background Efficacy of protein absorption and subsequent amino acid utilization may be reduced in the elderly. Higher protein intakes have been suggested to counteract this. Objectives We aimed to elucidate how habituated amounts of protein intake affect the fasted state of, and the stimulatory effect of a protein-rich meal on, protein absorption, whole-body protein turnover, and splanchnic amino acid metabolism. Methods Twelve men (65–70 y) were included in a double-blinded crossover intervention study, consisting of a 20-d habituation period to a protein intake at the RDA or a high amount [1.1 g · kg lean body mass (LBM)−1 · d−1 or >2.1 g · kg LBM−1 · d−1, respectively], each followed by an experimental trial with a primed, constant infusion of D8-phenylalanine and D2-tyrosine. Arterial and hepatic venous blood samples were obtained after an overnight fast and repeatedly 4 h after a standardized meal including intrinsically labeled whey protein concentrate and calcium-caseinate proteins. Blood was analyzed for amino acid concentrations and phenylalanine and tyrosine tracer enrichments from which whole-body and splanchnic amino acid and protein kinetics were calculated. Results High (compared with the recommended amount of) protein intake resulted in a higher fasting whole-body protein turnover with a resultant mean ± SEM 0.03 ± 0.01 μmol · kg LBM−1 · min−1 lower net balance (P < 0.05), which was not rescued by the intake of a protein-dense meal. The mean ± SEM plasma protein fractional synthesis rate was 0.13 ± 0.06%/h lower (P < 0.05) after habituation to high protein. Furthermore, higher fasting and postprandial amino acid removal were observed after habituation to high protein, yielding higher urea excretion and increased phenylalanine oxidation rates (P < 0.01). Conclusions Three weeks of habituation to high protein intake (>2.1 g protein · kg LBM−1 · d−1) led to a significantly higher net protein loss in the fasted state. This was not compensated for in the 4-h postprandial period after intake of a meal high in protein. This trial was registered at clinicaltrials.gov as NCT02587156.


1948 ◽  
Vol 87 (6) ◽  
pp. 457-471 ◽  
Author(s):  
Frank W. McKee ◽  
Paul R. Schloerb ◽  
John A. Schilling ◽  
Garson H. Tishkoff ◽  
George H. Whipple

Constriction of inferior vena cava above the diaphragm is used to produce experimental ascites in the dog. This type of experimental ascites drains the body protein reserves, reduces the level of circulating plasma proteins, and in effect is an internal plasmapheresis. As the ascitic fluid is withdrawn and the proteins measured, we observe a production of ascitic protein (80–90 gm. per week) comparable to that removed by plasmapheresis (bleeding and replacement of red cells in saline). High protein diet tends to decrease the ascites but the protein content of the ascitic fluid may increase. Sodium chloride increases notably the volume of the ascites which accumulates and the total ascitic protein output increases. Sodium-free salt mixtures have a negative influence. High protein diet low in sodium salts gives minimal ascitic accumulation under these conditions. The question of circulation of the ascitic fluid is raised—how rapid is the absorption and the related accumulation?


2006 ◽  
Vol 38 (Supplement) ◽  
pp. S225
Author(s):  
Tracey J. Smith ◽  
Harris R. Lieberman ◽  
J. Phillip Karl ◽  
Susan McGraw ◽  
Matthew A. Pikosky ◽  
...  

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Tracey J Smith ◽  
Matthew A Pikosky ◽  
Jean‐Marc Schwartz ◽  
Jennifer Rood ◽  
Carmen Castaneda‐Sceppa ◽  
...  

2019 ◽  
Vol 317 (6) ◽  
pp. E1015-E1021 ◽  
Author(s):  
Tristan Chalvon-Demersay ◽  
Joanna Moro ◽  
Patrick C. Even ◽  
Catherine Chaumontet ◽  
Daniel Tomé ◽  
...  

General control nonderepressible 2 (GCN2) is a kinase that detects amino acid deficiency and is involved in the control of protein synthesis and energy metabolism. However, the role of hepatic GCN2 in the metabolic adaptations in response to the modulation of dietary protein has been seldom studied. Wild-type (WT) and liver GCN2-deficient (KO) mice were fed either a normo-protein diet, a low-protein diet, or a high-protein diet for 3 wk. During this period, body weight, food intake, and metabolic parameters were followed. In mice fed normo- and high-protein diets, GCN2 pathway in the liver is not activated in WT mice, leading to a similar metabolic profile with the one of KO mice. On the contrary, a low-protein diet activates GCN2 in WT mice, inducing FGF21 secretion. In turn, FGF21 maintains a high level of lipid oxidation, leading to a different postprandial oxidation profile compared with KO mice. Hepatic GCN2 controls FGF21 secretion under a low-protein diet and modulates a whole body postprandial oxidation profile.


Author(s):  
Maha Alsaif ◽  
Lucila Triador ◽  
Eloisa Colin-Ramirez ◽  
Sarah Elliott ◽  
Michelle L Mackenzie ◽  
...  

Abstract The aim of this study was to explore the feasibility of measuring a postprandial increase in energy expenditure (ΔEE) using a state-of-the-art whole-body calorimetry unit (WBCU), in children and youth with Prader-Willi syndrome (PWS). Five participants (aged 10–25 years) received both a standard and a high protein diet in a random order (crossover design). Resting energy expenditure (REE), postprandial ΔEE 6 hours post-intake of a standard (15% of total energy [TE]) and a high protein (30% TE) meal, and respiratory exchange ratio (RER) were measured in a WBCU. No differences were observed in ΔEE comparing the two meals. Mean RER was lower following the high protein meal (0.80 ± 0.01) compared to the standard meal (0.87 ± 0.02),  p = 0.009. Despite the high participant burden, it was feasible to conduct this metabolic test in children and youth with PWS. This study paves the way for further studies targeting EE in this patient population.


2007 ◽  
Vol 39 (Supplement) ◽  
pp. S83
Author(s):  
Matthew A. Pikosky ◽  
Tracey J. Smith ◽  
Lauri Byerley ◽  
Ann Grediagin ◽  
Carmen Castaneda-Sceppa ◽  
...  

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