三碘甲状腺原氨酸对大鼠脂肪组织中瘦素释放及瘦素mRNA积累的影响。
Effect of tri-iodothyronine on leptin release and leptin mRNA accumulation in rat adipose tissue.
作者信息
Fain J N, Bahouth S W
机构信息
Department of Biochemistry, College of Medicine, University of Tennessee, Memphis, TN 38163, USA.
出版信息
Biochem J. 1998 Jun 1;332 ( Pt 2)(Pt 2):361-6. doi: 10.1042/bj3320361.
Leptin, the product of the obese gene, is produced by white adipocytes. The release of leptin, as well as leptin mRNA content, was enhanced in adipocytes isolated from hypothyroid rats. The administration of tri-iodothyronine (T3) 8 h before death inhibited leptin release by adipocytes incubated for 6 or 24 h. Direct addition of T3 to pieces of adipose tissue enhanced the loss of leptin mRNA seen over 24 h in the presence of dexamethasone plus the beta3-adrenergic agonist Cl 316,243. In contrast, if pieces of adipose tissue were incubated with dexamethasone plus insulin, enhanced the T3 accumulation of leptin mRNA. These results indicate that T3 enhances net adipocyte leptin mRNA accumulation in a condition that approximates the fed state (presence of insulin) but inhibits leptin mRNA accumulation in a condition that approximates the fasted state (absence of insulin).
瘦素是肥胖基因的产物，由白色脂肪细胞产生。从甲状腺功能减退大鼠分离出的脂肪细胞中，瘦素的释放以及瘦素mRNA含量均有所增加。在处死前8小时给予三碘甲状腺原氨酸（T3）可抑制脂肪细胞培养6小时或24小时后的瘦素释放。将T3直接添加到脂肪组织块中，可增强在存在地塞米松和β3-肾上腺素能激动剂Cl 316,243的情况下24小时内瘦素mRNA的减少。相反，如果将脂肪组织块与地塞米松和胰岛素一起孵育，则会增强瘦素mRNA的T3积累。这些结果表明，T3在接近进食状态（存在胰岛素）的条件下增强脂肪细胞瘦素mRNA的净积累，但在接近禁食状态（不存在胰岛素）的条件下抑制瘦素mRNA的积累。
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