Leptin as a potential mediator of trade-offs among performance, reproduction, and immune function in green anole lizards


Meeting Abstract

P2-228  Friday, Jan. 6 15:30 – 17:30  Leptin as a potential mediator of trade-offs among performance, reproduction, and immune function in green anole lizards WANG, AZ*; HUSAK, JF; Univ. of St. Thomas; Univ. of St. Thomas andrew.wang@stthomas.edu

Life history trade-offs result from allocation of limited energetic resources to particular traits, restricting those same resources from different traits. This differential allocation of resources is dependent on the conditions the organism is living in, and promotes traits that suit the organism’s best needs between survival and reproduction. In previous studies, green anole lizards were shown to have dramatic decreases in fat stores, immune function, and reproduction when physically trained, and this was exacerbated by diet restriction. We gave supplemental leptin to green anole lizards in an attempt to mitigate the negative effects of shifting resource allocation due to a combination of exercise training and diet manipulation. We hypothesized that supplemental leptin would ‘rescue’ energy allocation to reproduction and immunity due to the artificial signal that there is more energetic resources than there actually is available. Lizards were assigned to one of six treatment combinations across three factors (diet restricted or not, trained or not, and leptin or saline control) over the course of nine weeks. To measure immune function, we measured the swelling response to phytohemagglutinin. Leptin supplementation did not override the stress of injections to ‘rescue’ reproduction, but leptin did increase immune response across both diet treatments. Endurance and growth were unaffected by leptin, though the stress of injections seemed to decrease performance enhancement. Diet restriction decreased growth in both sexes, with or without leptin supplementation. Our results highlight the complex nature of how trade-offs are mediated, and suggest differential and interactive roles for leptin, corticosterone, and pathways associated with the exercise response.

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