Effect of protein intake on weight gain and plasma amino acid levels in uremic rats

Wang, M; Vyhmeister, Irma B.; Jd, Kopple; Swendseid, Marian E.

doi:10.1152/ajplegacy.1976.230.5.1455

Cited by 44 publications

(15 citation statements)

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“…Adult stature is usually far below that expected for a child's genetic potential, even with adequate dialysis, treatment of acidosis, administration of phosphate binders, nutritional counseling, and supplemental vitamin D ( 1 , 2). Similar findings have been noted in other animal models of chronic renal insufficiency (3)(4)(5). Disturbances in the growth hormone/somatomedin system have been implicated in the etiology of the reduced growth rates of children with renal insuffi-ciency (6,7 ) ; however, the mechanisms remain unclear.…”

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confidence: 77%

The Effects of Exogenous Rat Growth Hormone Therapy on Growth of Uremic Rats Fed an 8% Protein Diet

et al. 1989

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ABSTRACT. Although the mechanisms underlying the inhibitory effects of chronic renal insufficiency on growth are poorly understood, large doses of growth hormone (GH) have been used to improve growth. The present study examines the effects of rat G H and a reduced (8%) protein diet on 75% nephrectomized weanling rats by measuring changes in growth parameters, food utilization, serum albumin concentration, and muscle water content. Significantly greater improvement in growth was found in the GH-treated uremic rats compared with the uremic controls. The mean percent change in wt, length (nose to tail tip), and cranial biparietal diameter was significantly increased in the GH-treated uremic rats, compared with the uremic controls, but foot length and femur length showed only moderate improvement. Food utilization efficiency and serum albumin concentration were significantly higher in GH-treated uremic rats compared with uremic controls, achieving levels that were not different from sham-operated rats. Muscle water content was not significantly different between GH-treated uremic rats, uremic controls, and sham-operated rats. Thus, rat G H treatment administered a t an early age in mild renal insufficiency significantly improved overall growth, food efficiency, and serum albumin concentrations, despite a low protein diet, suggesting that further evaluation of this form of therapy for growth failure of uremia is warranted. (Pediatr Res 26:204-207, 1989) Abbreviations GH, growth hormone U, uremic control group U + GH, uremic rats treated with growth hormone Growth failure is a major complication of chronic renal insufficiency in children. Adult stature is usually far below that expected for a child's genetic potential, even with adequate dialysis, treatment of acidosis, administration of phosphate binders, nutritional counseling, and supplemental vitamin D ( 1 , 2). Similar findings have been noted in other animal models of chronic renal insufficiency (3)(4)(5). Disturbances in the growth hormone/somatomedin system have been implicated in the etiology of the reduced growth rates of children with renal insuffi- Received February 6, 1989; accepted May 8, 1989. Correspondence Dr. James C. M. Chan, Medical College of Virginia, 1101 E. Marshall St., Richmond, VA 23219.ciency (6, 7 ) ; however, the mechanisms remain unclear. The recent availability of large quantities of recombinant human growth hormone (8) may open new avenues for the treatment of growth retardation in uremic children. Preliminary data suggest that large doses of recombinant growth hormone can improve growth in uremic children (9).Large doses of heterologous growth hormone have been used to overcome the inhibitory effect of uremia on growth in fivesixths nephrectomized rats fed 22-24% protein diets (10, 1 1 ) . With respect to the current concerns regarding the role of high protein intake in the progression of renal damage, the present study was designed to examine the effects of parenteral rat G H in rapidly growing weanling rats with mild chronic ren...

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confidence: 77%

The Effects of Exogenous Rat Growth Hormone Therapy on Growth of Uremic Rats Fed an 8% Protein Diet

et al. 1989

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“…Increased creatinine is a commonly used marker of decreased renal function. Decreased body weight in patients with end-stage renal disease can be explained by malnutrition and increased catabolism attributable to uremia or chronic hemodialysis (42)(43)(44). We showed that serum cLDL was significantly higher in uremic patients than in controls.…”

Section: Discussionmentioning

confidence: 74%

Quantification of Carbamylated LDL in Human Sera by a New Sandwich ELISA

Apostolov

Shah

et al. 2005

Clinical Chemistry

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Background:We previously suggested that increased carbamylated LDL (cLDL), a product of nonenzymatic modification of LDL in human serum by urea-derived cyanate, may cause cardiovascular complications in patients with chronic renal insufficiency. An assay for precise measurement of cLDL in serum was not previously available. Methods: Polyclonal antibodies against human cLDL and nonmodified, native LDL (nLDL) were raised in rabbits and extensively purified by affinity chromatography. New sandwich ELISAs to measure cLDL and nLDL with use of these antibodies were developed. Serum concentrations of cLDL and nLDL were measured by the sandwich ELISAs in 41 patients with end-stage renal disease (ESRD) and 40 healthy controls. Results: Both assays showed satisfactory reproducibility, linearity, and recovery. The assays could detect 2.7 mg/L cLDL with a linear detection range of 5-1000 mg/L and 5 mg/L nLDL with a linear detection range of 50 -1000 mg/L. These measurements showed that patients with ESRD have significantly increased serum cLDL [281.5 (46.9) mg/L compared with 86.1 (29.7) mg/L in a control group; P <0.001]. There was no significant difference in nLDL concentrations between the groups. Conclusions: These assays are a potentially valuable tool for cardiovascular research in renal patients and healthy individuals. The cLDL concentration appears to be the highest among all previously described modified LDL isoforms in both controls and ESRD patients.

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“…At each level of dietary protein, net protein degradation was higher in CRF rats; the difference was greatest when 10% protein was fed even though the degree of azotemia was least in this group of rats. It is possible that the adverse effect of the 10% protein diet was the result of an inadequate protein intake, since at most 10 g of food was allowed each day and the average weight of both CRF and control rats decreased (2,9). When CRF rats were given more protein, which lead to more severe azotemia, it is possible that these rats were acidotic, and that this contributed to the significant increase in net protein degradation compared with that in muscles of control rats.…”

Section: Discussionmentioning

confidence: 99%

“…The calculated bicarbonate was used to estimate each rat's acid-base status to eliminate the influence of varying degrees of Co2 retention during anesthesia and preparation for perfusion. The perfusate consisted of Krebs-Henseleit bicarbonate buffer, 3.5 g/dl bovine serum albumin (fraction V; Miles Laboratories, Elkhart, IN) that had been dialyzed for 48 h at 4VC against Krebs-Henseleit bicarbonate buffer, aged, washed human erythrocytes (hematocrit 25%), 10 mM glucose, and amino acids in concentrations found in rat plasma (9). In some experiments in studies 1 and 3, 1 mU/ml of regular pork insulin (Eli Lilly & Co., Indianapolis, IN) was added and the glucose concentration in the perfusate was increased to 20 mM because preliminary studies showed that glucose fell to very low levels if the initial glucose concentration was 10 mM.…”

Section: Methodsmentioning

confidence: 99%

Mechanisms for defects in muscle protein metabolism in rats with chronic uremia. Influence of metabolic acidosis.

May¹,

Kelly²,

Mitch³

1987

J. Clin. Invest.

313

193

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Chronic renal failure (CRF) is associated with metabolic acidosis and abnormal muscle protein metabolism. As we have shown that acidosis by itself stimulates muscle protein degradation by a glucocorticoid-dependent mechanism, we assessed the contribution of acidosis to changes in muscle protein turnover in CRF. A stable model of uremia was achieved in partially nephrectomized rats (plasma urea nitrogen, 100-120 mg/dl, blood bicarbonate < 21 meq/liter). CRF rats excreted 22% more nitrogen than pair-fed controls (P < 0.005), so muscle protein synthesis and degradation were measured in perfused hindquarters. CRF rats had a 90% increase in net protein degradation (P < 0.001); this was corrected by dietary bicarbonate. Correction of acidosis did not reduce the elevated corticosterone excretion rate of CRF rats, nor did it improve a second defect in muscle protein turnover, a 34% lower rate of insulin-stimulated protein synthesis. Thus, abnormal nitrogen production in CRF is due to accelerated muscle proteolysis caused by acidosis and an acidosis-independent inhibition of insulin-stimulated muscle protein synthesis.

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Effect of protein intake on weight gain and plasma amino acid levels in uremic rats

Cited by 44 publications

References 0 publications

The Effects of Exogenous Rat Growth Hormone Therapy on Growth of Uremic Rats Fed an 8% Protein Diet

The Effects of Exogenous Rat Growth Hormone Therapy on Growth of Uremic Rats Fed an 8% Protein Diet

Quantification of Carbamylated LDL in Human Sera by a New Sandwich ELISA

Mechanisms for defects in muscle protein metabolism in rats with chronic uremia. Influence of metabolic acidosis.

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