Prenatal programming of renal salt wasting resets postnatal salt appetite, which drives food intake in the rat

Saleh H. Alwasel, David J P Barker, Nick Ashton

    Research output: Contribution to journalArticlepeer-review

    Abstract

    Sodium retention has been proposed as the cause of hypertension in the LP rat (offspring exposed to a maternal low-protein diet in utero) model of developmental programming because of increased renal NKCC2 (Na + /K + /2Cl - co-transporter 2) expression. However, we have shown that LP rats excrete more rather than less sodium than controls, leading us to hypothesize that LP rats ingest more salt in order to maintain sodium balance. Rats were fed on either a 9% (low) or 18% (control) protein diet during pregnancy; male and female offspring were studied at 4 weeks of age. LP rats of both sexes held in metabolism cages excreted more sodium and urine than controls. When given water to drink, LP rats drank more and ate more food than controls, hence sodium intake matched excretion. However, when given a choice between saline and water to drink, the total volume of fluid ingested by LP rats fell to control levels, but the volume of saline taken was significantly larger [3.8± 0.1 compared with 8.8± 1.3 ml/24 h per 100 g of body weight in control and LP rats respectively; P
    Original languageEnglish
    Pages (from-to)281-288
    Number of pages7
    JournalClinical Science
    Volume122
    Issue number6
    DOIs
    Publication statusPublished - Mar 2012

    Keywords

    • Developmental programming
    • Extracellular fluid
    • Hyperphagia
    • Kidney
    • Salt appetite

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