Effect of high protein diet on stone-forming propensity and bone loss in rats

Amanzadeh, Jamshid; Gitomer, William L.; Zerwekh, Joseph E.; Preisig, Patricia A.; Moe, Orson W.; Pak, Charles Y.C.; Levi, Moshe

doi:10.1046/j.1523-1755.2003.00309.x

Cited by 88 publications

(80 citation statements)

References 29 publications

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“…These increases were likely due to greater contents of sulfur amino acids and organic phosphorus, respectively, in the HP diets (20). Hypocitraturia, also associated with high-protein intakes (12), was observed in the HP groups, as well, as a consequence of a decrease in proximal tubule reabsorption of citrate and an impairment of citrate transport in the kidney (20).…”

Section: Discussionmentioning

confidence: 90%

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Dietary Protein Supplementation Increases Peak Bone Mass Acquisition in Energy-Restricted Growing Rats

et al. 2009

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Peak bone mass is a major determinant of osteoporosis pathogenesis during aging. Respective influences of energy and protein supplies on skeletal growth remains unclear. We investigated the effect of a 5-mo dietary restriction on bone status in young rats randomized into six groups (n ϭ 10 per group). Control animals were fed a diet containing a normal (13%) (C-NP) or a high-protein content (26%) (C-HP). The other groups received a 40% protein energy-restricted diet (PER-NP and PER-HP) or a 40% energyrestricted diet (ER-NP and ER-HP). High-protein intake did not modulate bone acquisition, although a metabolic acidosis was induced and calcium retention impaired. PER and ER diets were associated with a decrease in femoral bone mineral density. The compensation for protein intake in energy-restricted conditions induced a bone sparing effect. Plasma osteocalcin (OC) and urinary deoxypyridinoline (DPD) assays revealed a decreased OC/DPD ratio in restricted rats compared with C animals, which was far more reduced in PER than in ER groups. Circulating IGF-1 levels were lowered by dietary restrictions. In conclusion, both energy and protein deficiencies may contribute to impairment in peak bone mass acquisition, which may affect skeleton strength and potentially render individuals more susceptible to osteoporosis. In particular, alterations in energy intake have been demonstrated to impair bone quality and strength in rodent models (1-5). Lamothe et al. (1) and Mardon et al. (2) reported that energy restriction adversely affected bone mineral content (BMC), bone mineral density (BMD), and mechanical properties in old rats, despite a micronutrient compensation. Nevertheless, the impact of energy restriction on bone was suggested to be modulated by the age at onset of restriction (5,6). To date, no clear consensus regarding the effects of energy restriction on peak bone mass acquisition has been established.Protein intake is widely linked to bone growth, hence to bone strength (7). Indeed, collagen is the major constituent of bone organic matrix, and noncollagenic proteins are involved in the regulation of the mineralization process. Dietary proteins provide the essential amino acids necessary for new matrix synthesis and may modulate circulating IGF-1 levels as well, an osteotrophic growth factor (8). In growing animals, protein deficiency was demonstrated to lead to decreased bone status (9). Ammann et al. (10) also reported that a 2.5% casein diet during 16 wk in 5-mo-old rats was associated with bone loss.Consequently, one would expect high-protein intake to promote bone health. However, other reports suggest that such a diet may alter calcium homeostasis in ways that could lead to bone loss (11,12). The metabolic acidosis, derived from sulfur amino acids catabolism, would also exert a direct stimulatory effect on bone resorption and an inhibitory action on matrix mineralization (13,14). Actually, the role of dietary protein on bone remains controversial.In the current context of rising incidence of obesity...

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Section: Discussionmentioning

confidence: 90%

“…However, other reports suggest that such a diet may alter calcium homeostasis in ways that could lead to bone loss (11,12). The metabolic acidosis, derived from sulfur amino acids catabolism, would also exert a direct stimulatory effect on bone resorption and an inhibitory action on matrix mineralization (13,14).…”

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confidence: 99%

Dietary Protein Supplementation Increases Peak Bone Mass Acquisition in Energy-Restricted Growing Rats

et al. 2009

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“…However, we cannot completely rule out a role in this regard for a separate urinary factor(s), cosegregating with, but independent from, urinary urea concentration. For example, although high protein diets increase urinary urea excretion, they also decrease urinary pH while increasing urinary ammonium, net acid, phosphorous, and calcium excretion (2). Because Hlad and coworkers (15) showed that low urinary pH increases transport of urinary sodium and chloride (they did not study urea) across dog bladder in vivo and because recent work in sheep rumen epithelium has demonstrated a lumenal pH modification of urea transport, likely by affecting UT-B (1), we cannot rule out an effect of urine pH on urothelial permeability.…”

Section: Discussionmentioning

confidence: 99%

Dietary protein affects urea transport across rat urothelia

Spector

Deng

Stewart

2012

American Journal of Physiology-Renal Physiology

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Spector DA, Deng J, Stewart KJ. Dietary protein affects urea transport across rat urothelia. Am J Physiol Renal Physiol 303: F944-F953, 2012. First published July 25, 2012 doi:10.1152/ajprenal.00238.2012.-Recent evidence suggests that regulated solute transport occurs across mammalian lower urinary tract epithelia (urothelia). To study the effects of dietary protein on net urothelial transport of urea, creatinine, and water, we used an in vivo rat bladder model designed to mimic physiological conditions. We placed groups of rats on 3-wk diets differing only by protein content (40,18,6, and 2%) and instilled 0.3 ml of collected urine in the isolated bladder of anesthetized rats. After 1 h dwell, retrieved urine volumes were unchanged, but mean urea nitrogen (UN) and creatinine concentrations fell 17 and 4%, respectively, indicating transurothelial urea and creatinine reabsorption. The fall in UN (but not creatinine) concentration was greatest in high protein (40%) rats, 584 mg/dl, and progressively less in rats receiving lower protein content: 18% diet, 224 mg/dl; 6% diet, 135 mg/dl; and 2% diet, 87 mg/dl. The quantity of urea reabsorbed was directly related to a urine factor, likely the concentration of urea in the instilled urine. In contrast, the percentage of instilled urea reabsorbed was greater in the two dietary groups receiving the lowest protein (26 and 23%) than in those receiving higher protein (11 and 9%), suggesting the possibility that a bladder/urothelial factor, also affected by dietary protein, may have altered bladder permeability. These findings demonstrate significant regulated urea transport across the urothelium, resulting in alteration of urine excreted by the kidneys, and add to the growing evidence that the lower urinary tract may play an unappreciated role in mammalian solute homeostasis.solute transport across bladder epithelia; urothelial creatinine transport; regulation of urothelial urea transport ALTHOUGH MAMMALIAN LOWER URINARY tract functions primarily as a short-term transit and storage vehicle for urine made by the kidneys (13), recent data demonstrate that mammalian urothelia (the epithelial cell lining of the urinary tract from renal pelvis to proximal urethra) is a surprisingly dynamic and complex tissue that may play an unappreciated role in water and solute homeostasis (35)(36)(37)(38)(39) reviewed in Ref. 22). While the urothelial permeability barriers, thought to reside in the apical membrane of the large "umbrella" cells lining the urinary tract lumens, the tight junction (TJ) between those cells, and the adherent overlying urinary glycosaminoglycans (GAG) layer (18,19,22,24,48), have been shown in vitro to have low permeability to water, urea, and ions (9,25,28), there are a number of physiological factors that might be expected to promote (even) passive diffusion of water and solutes across these barriers, including the large urinary tract lumenal surface area, long storage time of urine, enormous and changing concentration gradients for water, solutes, and ions, and ...

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“…Animal protein intake represents an acid load and increases urinary calcium, (35)(36)(37) whereas alkali administration decreases it (9,10). Thus, the positive association between urinary sulfate, a marker for animal protein intake, and urinary calcium was expected.…”

Section: Discussionmentioning

confidence: 99%