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Vitamin D-dependent rickets type I in pigs.

J Fox, E M Maunder, V A Randall

    Clinical Science (London, England : 1979)
    |November 1, 1985
    PubMed
    Summary

    A new pig model for vitamin D-dependent rickets type I was developed. Affected piglets show hypocalcaemia and impaired growth due to deficient vitamin D activation, treatable with vitamin D3 supplementation.

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    Area of Science:

    • Genetics
    • Biochemistry
    • Animal Models

    Background:

    • Inherited hypocalcaemic rickets is a debilitating condition.
    • Vitamin D metabolism is crucial for calcium homeostasis.
    • A genetic model is needed to study this disease.

    Purpose of the Study:

    • To characterize a novel inherited disorder in pigs resembling vitamin D-dependent rickets type I.
    • To investigate the underlying biochemical and genetic mechanisms.

    Main Methods:

    • Breeding and phenotyping of pigs with inherited hypocalcaemic rickets.
    • Biochemical analysis of plasma calcium, phosphate, and vitamin D metabolites.
    • Enzyme activity assays for vitamin D hydroxylases.
    • Assessment of calcium-binding protein levels.

    Main Results:

    • Affected piglets exhibited autosomal-recessive hypocalcaemic rickets with reduced growth rates.
    • Low plasma 1,25-dihydroxyvitamin D and 24,25-dihydroxyvitamin D3 levels were observed.
    • Absence of renal 25-hydroxyvitamin D3-1- and -24-hydroxylase activity.
    • Vitamin D3 administration corrected hypocalcaemia.

    Conclusions:

    • The developed pig strain represents a viable model for vitamin D-dependent rickets type I.
    • The condition is caused by a deficiency in vitamin D activation.
    • This model can aid in understanding rickets pathogenesis and testing therapies.

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