Food restriction in young Japanese quails: effects on growth, metabolism, plasma thyroid hormones and mRNA species in the thyroid hormone signalling pathway.
Young birds, in their post-natal growth period, may reduce their growth and metabolism when facing a food shortage. To examine how such responses can be mediated by endocrine-related factors, we exposed Japanese quail chicks to food restriction for either 2 days (age 6-8 days) or 5 days (age 6-11 days). We then measured growth and resting metabolic rate (RMR), and circulating 3,3',5-triiodo-l-thyronine (T3) and 3,5,3',5'-tetraiodothyronine (T4) levels as well as expression patterns of genes involved in growth (insulin-like growth factor-I: IGF-I) and thyroid hormone signalling (thyroid-stimulating hormone-beta: TSHbeta, type II iodothyronine deiodinase: D2, thyroid hormone receptors isoforms: TRalpha and TRbeta). The food-restricted chicks receiving a weight-maintenance diet showed reductions in structural growth and RMR. Plasma levels of both T3 and T4 were reduced in the food-restricted birds, and within the 5 days food-restricted group there was a positive correlation between RMR and T3. IGF-I mRNA showed significantly higher abundance in the liver of ad libitum fed birds at day 8 compared with food-restricted birds. In the brain, TSHbeta mRNA level tended to be lower in food-restricted quails on day 8 compared with controls. Furthermore, TRalpha expression was lower in the brain of food-restricted birds at day 8 compared with birds fed ad libitum. Interestingly, brain D2 mRNA was negatively correlated with plasma T3 levels, tending to increase with the length of food restriction. Overall, our results show that food restriction produced significant effects on circulating thyroid hormones and differentially affected mRNA species in the thyroid hormone signalling pathway. Thus, we conclude that the effects of food restriction observed on growth and metabolism were partly mediated by changes in the endocrine-related factors investigated.
Rønning
Bernt
B
Department of Biology, Norwegian University of Science and Technology, NO-7491 Trondheim, Norway. bernt.ronning@bio.ntnu.no
Mortensen
Anne S
AS
Moe
Børge
B
Chastel
Olivier
O
Arukwe
Augustine
A
Bech
Claus
C
D000818:Animals; D001481:Basal Metabolism; D049628:Body Size; D001921:Brain / Q000378:metabolism; D003370:Coturnix / Q000235:genetics / Q000254:growth & development* / Q000378:metabolism; D004435:Eating; D007334:Insulin-Like Growth Factor I / Q000235:genetics / Q000378:metabolism; D007453:Iodide Peroxidase / Q000235:genetics / Q000378:metabolism; D007668:Kidney / Q000033:anatomy & histology / Q000254:growth & development; D008099:Liver / Q000033:anatomy & histology / Q000254:growth & development; D009929:Organ Size; D012333:RNA, Messenger / Q000378:metabolism; D015398:Signal Transduction; D013961:Thyroid Gland / Q000378:metabolism; D037021:Thyroid Hormone Receptors alpha / Q000378:metabolism; D037042:Thyroid Hormone Receptors beta / Q000378:metabolism; D037322:Thyrotropin, beta Subunit / Q000235:genetics / Q000378:metabolism; D013974:Thyroxine / Q000097:blood / Q000378:metabolism; D014285:Triiodothyronine, Reverse / Q000097:blood / Q000378:metabolism; D000097564:Iodothyronine Deiodinase Type II
D007334:Insulin-Like Growth Factor I; D007453:Iodide Peroxidase; D012333:RNA, Messenger; D037021:Thyroid Hormone Receptors alpha; D037042:Thyroid Hormone Receptors beta; D037322:Thyrotropin, beta Subunit; D013974:Thyroxine; D014285:Triiodothyronine, Reverse; D000097564:Iodothyronine Deiodinase Type II