title: The role of glucocorticoids in naturally fasting grey seal (Halichoerus grypus) pups: dexamethasone stimulates mass loss and protein utilisation, but not departure from the colony.
abstract: Seals must manage their energy reserves carefully while they fast on land to ensure that they go to sea with sufficient fuel to sustain them until they find food. Glucocorticoids (GCs) have been implicated in the control of fuel metabolism and termination of fasting in pinnipeds. Here we tested the hypothesis that dexamethasone, an artificial GC, increases fat and protein catabolism, and induces departure from the breeding colony in wild, fasting grey seal pups. A single intramuscular dose of dexamethasone completely suppressed cortisol production for 24-72 h, demonstrating activation of GC receptors. In experiment 1, we compared the effects of a single dose of dexamethasone or saline administered 10 days after weaning on fasting mass and body composition changes, cortisol, blood urea nitrogen (BUN) and glucose levels, and timing of departure from the colony. In experiment 2, we investigated the effects of dexamethasone on short-term (5 days) changes in mass loss, body composition and BUN levels. In experiment 1, dexamethasone induced a short-lived increase in mass loss, but there was no difference in timing of departure between dexamethasone- and saline-treated pups (N=10). In experiment 2, dexamethasone increased protein and water loss and prevented a decrease in BUN levels (N=11). Our data suggest changes in cortisol contribute to regulation of protein catabolism in fasting seal pups, irrespective of the sex of the animal, but do not terminate fasting. By affecting the rate of protein depletion, lasting changes in cortisol levels could influence the amount of time seal pups have to find food, and thus may have important consequences for their survival.
authors.affiliation: Marine Biology and Ecology Research Centre, School of Marine Science and Engineering, Portland Square, Drake Circus, Plymouth University, Plymouth PL4 8AA, UK.
authors.forename: K A
authors.initials: KA
authors.lastname: Bennett
authors.forename: M A
authors.initials: MA
authors.lastname: Fedak
authors.forename: S E W
authors.initials: SE
authors.lastname: Moss
authors.forename: P P
authors.initials: PP
authors.lastname: Pomeroy
authors.forename: J R
authors.initials: JR
authors.lastname: Speakman
authors.forename: A J
authors.initials: AJ
authors.lastname: Hall
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001806:Blood Urea Nitrogen; D001823:Body Composition / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D003907:Dexamethasone / Q000008:administration & dosage / Q000494:pharmacology; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology*; D005215:Fasting / Q000502:physiology*; D005260:Female; D005938:Glucocorticoids / Q000378:metabolism*; D006854:Hydrocortisone / Q000096:biosynthesis; D007273:Injections, Intramuscular; D008297:Male; D046048:Seals, Earless / Q000378:metabolism / Q000502:physiology*
chemical_list: D001786:Blood Glucose; D005938:Glucocorticoids; D003907:Dexamethasone; D006854:Hydrocortisone