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Zhang, H, Liu, J, Li, CR, Momen, B, Kohanski, RA and Pick, L (2009) Deletion of Drosophila insulin-like peptides causes growth defects and metabolic abnormalities. Proc. Natl. Acad. Sci. U.S.A. 106:19617-22
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.
Animals; Autophagy; Diabetes Mellitus, Type 1/genetics; Diabetes Mellitus, Type 1/metabolism; Disease Models, Animal; Drosophila Proteins/genetics; Drosophila melanogaster/genetics; Drosophila melanogaster/growth & development; Drosophila melanogaster/metabolism; Gene Deletion; Glucose/metabolism; Homozygote; Insulin/genetics; Triglycerides/metabolism