【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 5 μg后 ,4± 1℃暴露3h ,对照组注射等体积生理盐水并置于 2 4± 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UCP1mRNA含量趋于减少 ;血清NE含量上升 ,BAT中T45′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 2 5 μg的CRH受体阻断剂α -helicalCRH 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UCP1mRNA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。更多还原

【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 8 μg of CRH or 2.5 μg of CRH receptor blocker α-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 T 45′-DⅡ activity of BAT, uncoupling protein 1 (UCP1) mRNA content in BAT, thyrotropin-releasing hormone (TRH) content in hypothylamus, levels of T 3, T 4, 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 group. TRH content in hypothalamus was decreased while levels of T 3, T 4and NE in serum, and T 45′-DⅡ of BAT were 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 BAT were decreased while content of TRH in hypothalamus, and T 3,T 4and T 3/T 4 in serum were decreased, however, NE in serum and T 45′-D Ⅱactivity of BAT were in-creased 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 T 45′-DⅡ of 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 2.5 μg of CRH receptor blocker α-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.更多还原