Altered growth and protein turnover in rats fed sodium-deficient diets

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Abstract

The effects of feeding a sodium-deficient (NaD) diet were examined in young, growing rats. All animals were fed the same diet and drank distilled water. In the control group the water contained 37 mM sodium chloride. After 2-3 wk body composition measurements were performed and epitrochlearis muscle protein synthesis and degradation rates determined. The experimental group gained only 45% of the wt and 70% of the length seen in the control group. The difference in wt gain could not be accounted for by differences in extracellular volume which averaged only 4% of body wt. Although total food intake was equivalent in both groups, urinary ammonia plus urea nitrogen excretion was higher in the experimental animals. Protein synthesis, measured as the incorporation of, 4C-phenylalanine into muscle protein was significantly lower in NaD rats (56.58 versus 68.79) and (65.26 versus 83.88 nmoi phenylalanine/h/g wet wt (both p < 0.01) when incubated with or without the addition of insulin (1 mU/ mL). Net protein degradation rates were unchanged. Gastrocnemius muscle RNA concentrations were also lower in NaD rats (1.09 versus 1.52 mg/g wet wt, p < 0.001). There were no changes noted in the concentration of protein within either gastrocnemius or epitrochlearis muscles. These results suggest that in rats, the growth failure seen in sodium deficiency: 1) affects both length and wt gain; 2) is not associated with decreased nutrient intake; 3) is due to decreased rates of muscle protein synthesis without affecting net protein degradation rates; and 4) is associated with diminished muscle tissue RNA concentrations.

Original languageEnglish (US)
Pages (from-to)608-613
Number of pages6
JournalPediatric Research
Volume26
Issue number6
StatePublished - 1989

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Muscle Proteins
Sodium
Proteolysis
Diet
Growth
Phenylalanine
Proteins
RNA
Muscles
Control Groups
Water
Body Composition
Ammonia
Sodium Chloride
Urea
Skeletal Muscle
Nitrogen
Eating
Insulin
Food

All Science Journal Classification (ASJC) codes

  • Pediatrics, Perinatology, and Child Health

Cite this

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title = "Altered growth and protein turnover in rats fed sodium-deficient diets",
abstract = "The effects of feeding a sodium-deficient (NaD) diet were examined in young, growing rats. All animals were fed the same diet and drank distilled water. In the control group the water contained 37 mM sodium chloride. After 2-3 wk body composition measurements were performed and epitrochlearis muscle protein synthesis and degradation rates determined. The experimental group gained only 45{\%} of the wt and 70{\%} of the length seen in the control group. The difference in wt gain could not be accounted for by differences in extracellular volume which averaged only 4{\%} of body wt. Although total food intake was equivalent in both groups, urinary ammonia plus urea nitrogen excretion was higher in the experimental animals. Protein synthesis, measured as the incorporation of, 4C-phenylalanine into muscle protein was significantly lower in NaD rats (56.58 versus 68.79) and (65.26 versus 83.88 nmoi phenylalanine/h/g wet wt (both p < 0.01) when incubated with or without the addition of insulin (1 mU/ mL). Net protein degradation rates were unchanged. Gastrocnemius muscle RNA concentrations were also lower in NaD rats (1.09 versus 1.52 mg/g wet wt, p < 0.001). There were no changes noted in the concentration of protein within either gastrocnemius or epitrochlearis muscles. These results suggest that in rats, the growth failure seen in sodium deficiency: 1) affects both length and wt gain; 2) is not associated with decreased nutrient intake; 3) is due to decreased rates of muscle protein synthesis without affecting net protein degradation rates; and 4) is associated with diminished muscle tissue RNA concentrations.",
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Altered growth and protein turnover in rats fed sodium-deficient diets. / Wassner, Steven.

In: Pediatric Research, Vol. 26, No. 6, 1989, p. 608-613.

Research output: Contribution to journalArticle

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AU - Wassner, Steven

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