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Proc Natl Acad Sci U S A. 2009 Nov 17;106(46):19617-22. doi: 10.1073/pnas.0905083106. Epub 2009 Nov 3.

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

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  • 1Department 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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