Skip to main content
. Author manuscript; available in PMC: 2022 Mar 15.
Published in final edited form as: Sci Bull (Beijing). 2020 Oct 28;66(5):478–489. doi: 10.1016/j.scib.2020.10.015

Fig. 1.

Fig. 1.

Excessive glucocorticoid exposure during pregnancy impairs brown fat development and thermogenesis, hurdling cold adaption and survivals of neonatal offspring. (a–i) Data were collected from in neonates on postnatal day 1 (P1) born from mice administrated with dosed synthetic glucocorticoids dexamethasone (DEX) in last trimester of pregnancy at room temperature (22°C) (n = 8 in each group). (a and b) Neonatal birth weight and survival percentage in the first postnatal week (n = 8 in each group). (c and d) Thermal imaging of neonates on P1 at room temperature. After neonates were removed from nests, thermal images were recorded immediately to reduce heat loss and noise effects. Scanning distance and neonatal behaviors were also controlled to avoid artificial effects (n = 8 in each group). (e) mRNA expression of cold stress genes in dorsal skins of neonates on P1. Gene expression was normalized to 18S rRNA (n = 8 in each group). (f) BAT mass (% body mass) of neonates on P1 (n = 8 in each group). (g) Immunoblotting measurements of GR, PRDM16, UCP-1, and DIO2 protein contents in neonatal BAT. β-actin was used as a loading control (n = 8 in each group). (h) Concentration of corticosteroids in neonatal serum on P1 (n = 5 in each group). (i) Heatmap of gene expressions in brown adipogenesis and thermogenesis. mRNA expression was normalized to 18S rRNA (n = 6 in each group). (j) Neonatal survivals in the postnatal week under thermoneutrality at 30°C (n = 8 in each group). Data are mean ± SEM and each dot represents one replicate (each pregnancy); *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001; unpaired one-way ANOVA multiple test was used in analyses.