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ABSTRACT Many songbirds begin active incubation after laying their penultimate egg, resulting in synchronous hatching of the clutch except for a last‐hatched individual (“runt”) that hatches with a size deficit and competitive disadvantage to siblings when begging for food. However, climate change may elevate temperatures and cause environmental incubation as eggs are laid, resulting in asynchronous hatching and larger size hierarchies among siblings. Although previous work demonstrated that asynchronous hatching reduces nestling growth and survival relative to synchrony, the physiological mechanisms underlying these effects are unclear. To test the effects of asynchronous hatching on runt growth, survival, physiology, and compensatory growth‐related tradeoffs, we manipulated incubation temperature in nest boxes of European starlings (Sturnus vulgaris) to increase asynchronous hatching and collected nestling morphological measurements and blood samples to assess physiology and development. Independent of heating treatment, runts from asynchronously hatched nests had lower survival than runts from more synchronous nests. Surviving runts from asynchronous nests were smaller and had reduced stress‐induced corticosterone concentrations and reduced circulating glucose compared with runts from synchronous nests. Despite persistent size and energy deficits, runts from asynchronous nests did not have significant deficits in immunity or telomere length when compared with runts from synchronous nests, suggesting no trade‐off between investment in immune development or telomere maintenance with growth. Overall, these results suggest that increased asynchrony due to climate change could reduce clutch survival for altricial songbirds, especially for the smallest chicks in a clutch, and that the negative effects of asynchrony may be driven by persistent energetic deficits. 

In many organisms, rapidly changing environmental conditions are inducing dramatic shifts in diverse phenotypic traits with consequences for fitness and population viability. However, the mechanisms that underlie these responses remain poorly understood. Endocrine signalling systems often influence suites of traits and are sensitive to changes in environmental conditions; they are thus ideal candidates for uncovering both plastic and evolved consequences of climate change. Here, we use body size and shape, a set of integrated traits predicted to shift in response to rising temperatures with effects on fitness, and insulin-like growth factor-1 as a case study to explore these ideas. We review what is known about changes in body size and shape in response to rising temperatures and then illustrate why endocrine signalling systems are likely to be critical in mediating these effects. Lastly, we discuss research approaches that will advance understanding of the processes that underlie rapid responses to climate change and the role endocrine systems will have. Knowledge of the mechanisms involved in phenotypic responses to climate change will be essential for predicting both the ecological and the long-term evolutionary consequences of a warming climate. This article is part of the theme issue ‘Endocrine responses to environmental variation: conceptual approaches and recent developments’. 

The insulin and insulin-like signalling (IIS) network plays an important role in mediating several life-history traits, including growth, reproduction and senescence. Although insulin-like growth factors (IGFs) 1 and 2 are both key hormones in the vertebrate IIS network, research on IGF2 in juveniles and adults has been largely neglected because early biomedical research on rodents found negligible IGF2 postnatal expression. Here, we challenge this assumption and ask to what degree IGF2 is expressed during postnatal life across amniotes by quantifying the relative gene expression of IGF1 and IGF2 using publicly available RNAseq data for 82 amniote species and quantitative polymerase chain reaction on liver cDNA at embryonic, juvenile and adult stages for two lizard, bird and mouse species. We found that (i) IGF2 is expressed postnatally across amniote species and life stages—often at a higher relative expression than IGF1 , contradicting rodent models; (ii) the lack of rodent postnatal IGF2 expression is due to phylogenetic placement, not inbreeding or artificial selection; and (iii) adult IGF2 expression is sex-biased in some species. Our results demonstrate that IGF2 expression is typical for amniotes throughout life, suggesting that a comprehensive understanding of the mechanisms mediating variation in life-history traits will require studies that measure both IGFs.