Homeothermy in neonatal chicks exposed to low environmental temperature with or without intracerebroventricular administration of corticotropin-releasing factor

Abstract 

To determine the mechanism of sensitivity to low-temperature exposure (20°C for 3h) and corticotropin-releasing factor (CRF) induced increased homeothermy, we investigated gene transcripts of putative thermogenic proteins and mitochondrial fatty acid (FA)-oxidation enzymes in neonatal chicks. The hypothalamic–pituitary–adrenal (HPA) axis in low-temperature-exposed neonatal chicks was activated by central administration of CRF. Neonatal chicks showed hypothermia on exposure to low-temperature, with no enhancement of HPA axis and gene transcripts of avian adenine nucleotide translocator, avian uncoupling protein, avian peroxisome-proliferator-activated receptor-γ co-activator-1α, and mitochondrial FA transport and oxidation enzymes in vital organs. However, central administration of CRF activated the HPA axis under low environmental temperature and induced increased homeothermy that was associated with the enhancement of gene transcripts and activities of mitochondrial FA-oxidation enzymes in the liver and heart.

Abbreviations: 3HADH, 3-hydroxyacyl CoA dehydrogenase, ANT, adenine nucleotide translocator, BAT, brown adipose tissue, CPT-I, carnitine-palmitoyl-transferase-I, CPT-II, carnitine-palmitoyl-transferase-II, CRF, corticotropin-releasing factor, CS, citrate synthase, EB, Evans Blue, FA, fatty acid, HPA, hypothalamic–pituitary–adrenal, ICV, intracerebroventricular, LCAD, long-chain acyl CoA dehydrogenase, NEFA, non-esterified fatty acid, PGC1, peroxisome-proliferator-activated receptor-γ co-activator-1, ROS, reactive oxygen species, SA, sympathoadrenal, UCP, uncoupling protein

Keywords: Thermoregulation, Neonatal chick, Cold stress, Fatty acid oxidation, CRF, UCP