The effect of sodium repletion on growth and protein turnover in sodium-depleted rats

Research output: Contribution to journalArticle

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Abstract

This study examines the consequences of sodium chloride supplementation to young rats previously made salt deficient by feeding them a sodium-deficient, chloride-replete diet. Salt-deficient rats received the test diet and distilled water for 10 days. As in our previous studies, rats cared for in this manner grew more slowly than rats fed the identical diet but allowed to drink 37 mM sodium chloride. On day 11, half of the salt-depleted animals received 37 mM sodium chloride in their drinking water. Sodium-deficient and supplemented rats were studied 1, 2, 5-6 and 11-12 days later. Urinary sodium rapidly rose from undetectable to 46 mEq/l urine within 1 day of supplementation and there was no further increase the next day, suggesting that extracellular fluid volumes were rapidly repleted. Food intake increased in the supplemented rats compared with the deficient animals but the difference in food intake equalled only 2.25 g/day for the first 2 days of supplementation. Over the last 12 days of the first 2 days of supplementation. Over the last 12 days of the study, the slopes of both weight and length gains were equal in both the supplemented and the control group and significantly higher than those in the deficient rats. Over the course of the study, full catchup was not obtained in either length or weight. In addition to total weight and length gains, liver and kidney weights increased proportionately and by 5-6 days of supplementation were equivalent to the weights seen in the control group. After 2 days of supplementation, the incorporation of14C-phenylalanine into epitrochlearis muscle preparations increased 21% (P=0.02) and by 5-12 days after supplementation, muscle protein synthesis rates increased 30%-40% (P=0.01). Net degradation, was not significantly altered by sodium repletion. Whether measured as total gastrocnemius (or liver) RNA or as the ratio of RNA/DNA, RNA levels rapidly increased after sodium chloride supplementation (P<0.01). Thus, sodium supplementation rapidly restores weight gain and linear growth, muscle and liver RNA levels and muscle protein synthesis rates in young, salt-depleted rats. Since salt depletion may exist in a variety of clinical conditions often associated with poor growth, its presence must be considered in attempts to maximize growth in infants and children with chronic illness.

Original languageEnglish (US)
Pages (from-to)501-504
Number of pages4
JournalPediatric Nephrology
Volume5
Issue number4
DOIs
StatePublished - Jul 1 1991

Fingerprint

Sodium
Sodium Chloride
Growth
Salts
Proteins
RNA
Weight Gain
Muscle Proteins
Diet
Weights and Measures
Liver
Eating
Muscles
Control Groups
Extracellular Fluid
Phenylalanine
Drinking Water
Chronic Disease
Urine
Kidney

All Science Journal Classification (ASJC) codes

  • Pediatrics, Perinatology, and Child Health
  • Nephrology

Cite this

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title = "The effect of sodium repletion on growth and protein turnover in sodium-depleted rats",
abstract = "This study examines the consequences of sodium chloride supplementation to young rats previously made salt deficient by feeding them a sodium-deficient, chloride-replete diet. Salt-deficient rats received the test diet and distilled water for 10 days. As in our previous studies, rats cared for in this manner grew more slowly than rats fed the identical diet but allowed to drink 37 mM sodium chloride. On day 11, half of the salt-depleted animals received 37 mM sodium chloride in their drinking water. Sodium-deficient and supplemented rats were studied 1, 2, 5-6 and 11-12 days later. Urinary sodium rapidly rose from undetectable to 46 mEq/l urine within 1 day of supplementation and there was no further increase the next day, suggesting that extracellular fluid volumes were rapidly repleted. Food intake increased in the supplemented rats compared with the deficient animals but the difference in food intake equalled only 2.25 g/day for the first 2 days of supplementation. Over the last 12 days of the first 2 days of supplementation. Over the last 12 days of the study, the slopes of both weight and length gains were equal in both the supplemented and the control group and significantly higher than those in the deficient rats. Over the course of the study, full catchup was not obtained in either length or weight. In addition to total weight and length gains, liver and kidney weights increased proportionately and by 5-6 days of supplementation were equivalent to the weights seen in the control group. After 2 days of supplementation, the incorporation of14C-phenylalanine into epitrochlearis muscle preparations increased 21{\%} (P=0.02) and by 5-12 days after supplementation, muscle protein synthesis rates increased 30{\%}-40{\%} (P=0.01). Net degradation, was not significantly altered by sodium repletion. Whether measured as total gastrocnemius (or liver) RNA or as the ratio of RNA/DNA, RNA levels rapidly increased after sodium chloride supplementation (P<0.01). Thus, sodium supplementation rapidly restores weight gain and linear growth, muscle and liver RNA levels and muscle protein synthesis rates in young, salt-depleted rats. Since salt depletion may exist in a variety of clinical conditions often associated with poor growth, its presence must be considered in attempts to maximize growth in infants and children with chronic illness.",
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The effect of sodium repletion on growth and protein turnover in sodium-depleted rats. / Wassner, Steven.

In: Pediatric Nephrology, Vol. 5, No. 4, 01.07.1991, p. 501-504.

Research output: Contribution to journalArticle

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AB - This study examines the consequences of sodium chloride supplementation to young rats previously made salt deficient by feeding them a sodium-deficient, chloride-replete diet. Salt-deficient rats received the test diet and distilled water for 10 days. As in our previous studies, rats cared for in this manner grew more slowly than rats fed the identical diet but allowed to drink 37 mM sodium chloride. On day 11, half of the salt-depleted animals received 37 mM sodium chloride in their drinking water. Sodium-deficient and supplemented rats were studied 1, 2, 5-6 and 11-12 days later. Urinary sodium rapidly rose from undetectable to 46 mEq/l urine within 1 day of supplementation and there was no further increase the next day, suggesting that extracellular fluid volumes were rapidly repleted. Food intake increased in the supplemented rats compared with the deficient animals but the difference in food intake equalled only 2.25 g/day for the first 2 days of supplementation. Over the last 12 days of the first 2 days of supplementation. Over the last 12 days of the study, the slopes of both weight and length gains were equal in both the supplemented and the control group and significantly higher than those in the deficient rats. Over the course of the study, full catchup was not obtained in either length or weight. In addition to total weight and length gains, liver and kidney weights increased proportionately and by 5-6 days of supplementation were equivalent to the weights seen in the control group. After 2 days of supplementation, the incorporation of14C-phenylalanine into epitrochlearis muscle preparations increased 21% (P=0.02) and by 5-12 days after supplementation, muscle protein synthesis rates increased 30%-40% (P=0.01). Net degradation, was not significantly altered by sodium repletion. Whether measured as total gastrocnemius (or liver) RNA or as the ratio of RNA/DNA, RNA levels rapidly increased after sodium chloride supplementation (P<0.01). Thus, sodium supplementation rapidly restores weight gain and linear growth, muscle and liver RNA levels and muscle protein synthesis rates in young, salt-depleted rats. Since salt depletion may exist in a variety of clinical conditions often associated with poor growth, its presence must be considered in attempts to maximize growth in infants and children with chronic illness.

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