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Insulin signaling during immune challenges: Friend or foe?
Author(s) -
Cambron Lizzette D,
Greenlee Kendra J
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.lb711
Subject(s) - wortmannin , insulin , insulin receptor , biology , immune system , signal transduction , microbiology and biotechnology , endocrinology , medicine , immunology , pi3k/akt/mtor pathway , insulin resistance
One commonality between humans, dogs, and even insects, is that when faced with an illness all three will cease eating. This response across varying taxa is called sickness‐induced anorexia (SIA). SIA is hypothesized to be an energy reallocation toward immune function. However, the mechanism mediating the response, and the signal telling the body to stop eating is still unknown. Along with this response, insulin signaling is conserved between vertebrate and invertebrates. Because insulin signaling plays a role in regulating many physiology processes such as metabolism, development, and reproduction, this experiment aimed to investigate the role of insulin signaling in immune responses, specifically that of SIA, using the tobacco hornworm, Manduca sexta. In the beginning of the last larval stage, caterpillars were injected with either vehicle (PBS) or Escherichia coli to initiate an immune challenge. Then, insulin signaling was either inhibited by wortmannin, a covalent inhibitor of phosphoinositide 3‐kinases, or increased with exogenous bovine insulin. Growth, feeding, development, and fecal pellet measurements were taken daily until prepupation, indicated by the appearance of the dorsal vessel. Caterpillars that were injected with E. coli exhibited SIA, as previously shown. We predicted that caterpillars lacking insulin signaling would still exhibit SIA in response to E. coli , however, in this and previous studies, wortmannin showed contradictory results, suggesting that wortmannin may be activating other pathways or incompletely inhibiting insulin signaling. Interestingly, SIA was completely blocked in caterpillars that received extra insulin, supporting the hypothesis that insulin signaling mediates feeding. Further studies are needed to discover the mechanism tying insulin signaling to immunity. Elucidating the mechanism behind SIA will lead to a better understanding of how insulin signaling and the immune system intertwine, improving how we treat diabetics which are more susceptible to contracting infections. Support or Funding Information This research was funded in part, by grants from the National Science Foundation (NSF IOS‐0953297 to KJG) and the NSF Graduate Research Fellowships Program.