Truncating homozygous mutation of Carboxypeptidase E (CPE) in a morbidly obese female with type 2 diabetes mellitus, intellectual disability and hypogonadotrophic hypogonadism

Alexandra I. F. Blakemore, Anthony P. Goldstone, Suzanne I. M. Alsters, Jessica L. Buxton, Anna Zekavati, Alona Sosinsky, Andrianos M. Yiorkas, Susan Holder, Robert E. Klaber, Nicola Bridges, Mieke M. van Haelst, Carel W. le Roux, Andrew J. Walley, Robin G. Walters, Michael Mueller

    Research output: Contribution to journalArticlepeer-review

    Abstract

    Carboxypeptidase E is a peptide processing enzyme, involved in cleaving numerous peptide precursors, including neuropeptides and hormones involved in appetite control and glucose metabolism. Exome sequencing of a morbidly obese female from a consanguineous family revealed homozygosity for a truncating mutation of the CPE gene (c.76_98del; p.E26RfsX68). Analysis detected no CPE expression in whole blood-derived RNA from the proband, consistent with nonsense-mediated decay. The morbid obesity, intellectual disability, abnormal glucose homeostasis and hypogonadotrophic hypogonadism seen in this individual recapitulates phenotypes in the previously described fat/fat and Cpe knockout mouse models, evidencing the importance of this peptide/hormone-processing enzyme in regulating body weight, metabolism, and brain and reproductive function in humans.
    Original languageEnglish
    Article numbere0131417
    JournalPLoS ONE
    Volume10
    Issue number6
    DOIs
    Publication statusPublished - 29 Jun 2015

    Bibliographical note

    Note: This work was supported by Diabetes UK, Biomedical Research Centre, Medical Research Council and the Wellcome Trust.

    Keywords

    • Biological sciences

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