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    Proc Natl Acad Sci U S A. 2009 Nov 17;106(46):19617-22. Epub 2009 Nov 3.

    Deletion of Drosophila insulin-like peptides causes growth defects and metabolic abnormalities.

    Zhang H, Liu J, Li CR, Momen B, Kohanski RA, Pick L.

    Source

    Department of Entomology, University of Maryland, College Park, MD 20742, USA.

    Abstract

    Insulin/Insulin-like growth factor signaling regulates homeostasis and growth in mammals, and is implicated in diseases from diabetes to cancer. In Drosophila melanogaster, as in other invertebrates, multiple Insulin-Like Peptides (DILPs) are encoded by a family of related genes. To assess DILPs' physiological roles, we generated small deficiencies that uncover single or multiple dilps, generating genetic loss-of-function mutations. Deletion of dilps1-5 generated homozygotes that are small, severely growth-delayed, and poorly viable and fertile. These animals display reduced metabolic activity, decreased triglyceride levels and prematurely activate autophagy, indicative of "starvation in the midst of plenty," a hallmark of Type I diabetes. Furthermore, circulating sugar levels are elevated in Df [dilp1-5] homozygotes during eating and fasting. In contrast, Df[dilp6] or Df[dilp7] animals showed no major metabolic defects. We discuss physiological differences between mammals and insects that may explain the unexpected survival of lean, 'diabetic' flies.

    PMID:
    19887630
    [PubMed - indexed for MEDLINE]
    PMCID:
    PMC2780814
    Free PMC Article

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