Abstract: This study investigated effects of corticotropin-releasing hormone (CRH) on thermogenesis of brown adipose tissue (BAT) and its regulatory mechanism in groups of male Mongolian gerbils ( Meriones unguiculatus) . Gerbils were introventricularly injected with 8μg of CRH or 2.5μg of CRH receptor blockerα-helical CRH 9 - 41 and then exposed to 4 ±1 ℃for 3 hours. Two other groups of gerbils were injected with the same volume of physiological saline as the former groups and kept in regular temperature (RT, 24 ±2 ℃) or exposed to 4 ±1 ℃as controls. Weight , protein content and T₄5′- D Ⅱactivity of BAT, uncoupling protein. (UCP1) mRNA content in BAT, thyrotropin-releasing hormone (TRH) content in hypothylamus , levels of T₃ , T₄ , norepinephrine (NE) and corticosterone content in serum were measured. As compared with RT - control , the weight of BAT decreased and UCP1 mRNA content was promoted in cold control group1 TRH content in hypothalamus was decreased while levels of T₃ , T ₄ and NE in serum , and T₄5′- D Ⅱof BATwere increased in cold group. It was suggested that cold exposure activated hypothalamus- pituit ary-thyroid (HPT) axis and sympathetic nervous system , and increased thermogenesis of BAT in Mongolian gerbils. In the CRH injected animals , weight and protein content of BAT and UCP1 mRNA content in BATwere decreased while content of TRH in hypothalamus , and T₃ , T₄ and T₃/T₄ in serum were decreased , however , NE in serum and T₄5′- D Ⅱactivity of BAT were increased markedly as compared with gerbils with cold control. It was speculated that CRH may restrain HPT axis and therefore , suppress the gene expression of UCP1 by decreasing content of UCP1 mRNA. CRH may also activate central sympathetic nervous system resulting in higher level of serum NE and then increase activity of T₄5′- D Ⅱof BAT in CRH injected group than that in cold control group. The activated sympathetic nervous system may increase thermogenesis of BAT which consume fat as source of energy. The 2.5μg of CRH receptor blockerα-helical CRH 9 - 41 injected introventricularly did not cause marked change in the
parameters measured. This may be due to the insufficient dosage used in the experiment.

Key words: Cold exposure, Brown adipose tissue (BAT), Hypothalamus-pituitary-thyroid gerbils (Meriones unguiculatus)(HPT), UCP1 mRNA, Mongolian gerbils (Meriones unguiculatus)

摘要： 长爪沙鼠侧脑室注射促肾上腺皮质激素释放激素(CRH) 8μg 或CRH受体阻断剂2.5μg 后, 4 ±1 ℃暴露3 h ,对照组注射等体积生理盐水并置于24 ±2 ℃或4 ±1 ℃下。与常温对照组相比, 低温对照组褐色脂肪组织(BAT) 重量下降, BAT中解偶联蛋白(UCP1) mRNA 上调; 下丘脑促甲状腺激素释放激素(TRH) 含量降低, 血清T₃ 、T₄ 、T₃/T₄水平及BAT中T₄5′脱碘酶活性均增加, 血清去甲肾上腺素(NE) 含量上升。与低温对照组相比, 侧脑室注射CRH后再冷暴露, BAT重量、蛋白总含量和UCP1 mRNA 含量趋于减少; 血清NE 含量上升, BAT 中T₄ 5′脱碘酶活性增加, 但下丘脑TRH 含量、血清T₃ 、T₄ 及T₃/T₄ 水平均降低。侧脑室注射215μg 的CRH 受体阻断剂α- helical CRH 9 - 41 , 对冷暴露长爪沙鼠甲状腺轴的分泌、BAT重量、血清中NE 水平及UCP1 mRNA 含量没有明显影响。结果表明, 急性冷暴露激活了长爪沙鼠下丘脑- 垂体- 甲状腺(HPT) 轴和交感神经系统, 刺激BAT产热和UCP1 合成; 而CRH作用于中枢, 可能一方面抑制HPT轴的分泌, 进而抑制UCP1 的基因表达, 另一方面又刺激交感神经,增加产热。

关键词: 急性冷暴露, 褐色脂肪组织, 下丘脑- 垂体- 甲状腺轴, UCP1 mRNA, 长爪沙鼠