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The common hamster Cricetus cricetus was long considered to be a pest species for crops, but its populations are now dramatically declining. The conservation of this species can only be achieved via an up‐to‐date knowledge of its ecology. However, its diet composition has never been exhaustively reviewed and the last peer‐reviewed publication on its feeding ecology in farmlands dates back to 1974.This review of the literature aims to establish a list of plant and animal taxa consumed by common hamsters, providing knowledge to be applied to the conservation of hamsters and to identify the main avenues of future research.Hamsters consume four main categories of food: crops, weeds, trees/shrubs and animals, including mammals, birds, herptiles and invertebrates. Vegetable foods are more diverse (114 taxa) than animal foods (11 taxa). Hamsters mainly consume animals and green parts of plants (flowers and leaves) in spring and summer, and store energy‐rich and non‐perishable foods for winter.Weeds are the most diverse food category (61 taxa), followed by crops (31 taxa). However, diet shifts from crop products towards tree products in urban habitats, probably in response to a marked difference in availability.We conclude that hamsters have an opportunist diet that shows a high degree of plasticity, and that weeds make up an important part of their food supply. However, the studies published to date have considered diet composition without taking food availability into account, and therefore lack information on whether the hamsters select the foods consumed or simply consume them because other foods are not readily available. Research on food availability and selection is therefore needed. Moreover, we argue that there is a need for recent data on the feeding ecology of the hamster in relation to fitness. This would provide a crucial tool for the implementation of adapted conservation measures for this declining species of rodent. [ABSTRACT FROM AUTHOR]

Maternal effects provide a mechanism to adapt offspring phenotype and optimize the mother’s fitness to current environmental conditions. Transferring steroids to the yolk is one way mothers can translate environmental information into potential adaptive signals for offspring. However, maternally-derived hormones might also have adverse effects for offspring. For example, recent data in zebra finch chicks suggested that ageing related-processes (i.e. oxidative stress and telomere loss) were increased after egg-injection of corticosterone (CORT). Still, we have few experimental data describing the effect of maternal effects on the growth-ageing trade-off in offspring. Here, we chronically treated pre-laying zebra finch females (Taeniopygia guttata) with 17-β-estradiol (E2) or CORT, and followed offspring growth and cellular ageing rates (oxidative stress and telomere loss). CORT treatment decreased growth rate in male chicks and increased rate of telomere loss in mothers and female offspring. E2 increased body mass gain in male offspring, while reducing oxidative stress in both sexes but without affecting telomere loss. Since shorter telomeres were previously found to be a proxy of individual lifespan in zebra finches, maternal effects may, through pleiotropic effects, be important determinants of offspring life-expectancy by modulating ageing rate during embryo and post-natal growth. [ABSTRACT FROM AUTHOR]

Maternal effects provide a mechanism to adapt offspring phenotype and optimize the mother’s fitness to current environmental conditions. Transferring steroids to the yolk is one way mothers can translate environmental information into potential adaptive signals for offspring. However, maternally-derived hormones might also have adverse effects for offspring. For example, recent data in zebra finch chicks suggested that ageing related-processes (i.e. oxidative stress and telomere loss) were increased after egg-injection of corticosterone (CORT). Still, we have few experimental data describing the effect of maternal effects on the growth-ageing trade-off in offspring. Here, we chronically treated pre-laying zebra finch females (Taeniopygia guttata) with 17-β-estradiol (E2) or CORT, and followed offspring growth and cellular ageing rates (oxidative stress and telomere loss). CORT treatment decreased growth rate in male chicks and increased rate of telomere loss in mothers and female offspring. E2 increased body mass gain in male offspring, while reducing oxidative stress in both sexes but without affecting telomere loss. Since shorter telomeres were previously found to be a proxy of individual lifespan in zebra finches, maternal effects may, through pleiotropic effects, be important determinants of offspring life-expectancy by modulating ageing rate during embryo and post-natal growth. [ABSTRACT FROM AUTHOR]