Thyroid hormone actions are temperature-specific and regulate thermal acclimation in Zebrafish (Danio rerio)
- Authors
- Little, A.G., Kunisue, T., Kannan, K., and Seebacher, F.
- ID
- ZDB-PUB-130410-12
- Date
- 2013
- Source
- BMC Biology 11(1): 26 (Journal)
- Registered Authors
- Keywords
- Thyroid hormone; Zebrafish; Temperature; Cold acclimation; Hypothyroid; Ectotherm; Metabolism; Thermal plasticity; Thermal response
- MeSH Terms
-
- Acclimatization/drug effects*
- Animals
- Body Temperature Regulation/drug effects*
- Dietary Supplements
- Diiodothyronines/pharmacology
- Hypothyroidism/physiopathology
- Multivariate Analysis
- Muscles/drug effects
- Muscles/metabolism
- Organ Specificity/drug effects
- RNA, Messenger/genetics
- RNA, Messenger/metabolism
- Temperature*
- Thyroid Hormones/pharmacology*
- Triiodothyronine/pharmacology
- Zebrafish/physiology*
- PubMed
- 23531055 Full text @ BMC Biol.
Background
Thyroid hormone (TH) is best known for its role in development in animals, and for its control of metabolic heat production (thermogenesis) during cold-acclimation in mammals. It is unknown whether its regulatory role of thermogenesis is derived in mammals, or whether TH also mediates thermal responses in earlier vertebrates. Ectothermic vertebrates show complex responses to temperature variation, but the mechanisms mediating these are poorly known. The molecular mechanisms underpinning TH action are very similar across vertebrates, which suggests that TH may also regulate thermal responses in ectotherms. We therefore aimed to determine whether TH regulates thermal acclimation in zebrafish (Danio rerio). We induced hypothyroidism, followed by supplementation with 3,5-diiodothyronine (T2) or 3,5,3'-triiodothyronine (T3) in zebrafish exposed to different chronic temperatures. We measured whole animal responses (swimming performance and metabolic rates), tissue-specific regulatory enzyme activities, gene expression, and free levels of T2 and T3.
Results
We are the first to show that T3, as well as the lesser-known T2, regulate thermal acclimation in an ectotherm. Hypothyroid treatment impaired performance measures in cold-acclimated but not warm-acclimated individuals, while supplementation with both TH metabolites restored it. We also show that TH can either induce or repress responses depending on the actual temperature and thermal history of the animal.
Conclusions
The low sensitivity to TH at warm temperatures could mean that increasing temperatures (i.e. global warming) will reduce the capacity of animals to regulate their physiologies to match demands. We suggest that the properties that underlie TH's role in thermal acclimation (temperature-sensitivity and metabolic control) may have predisposed it for a regulatory role in the evolution of endothermy.