Cettour-Rose Philippe, Burger Albert G, Meier Christoph A, Visser Theo J, Rohner-Jeanrenaud Françoise
Division of Endocrinology and Diabetology, Department of Medicine, Faculty of Medicine, University of Geneva, 1211 Geneva 14, Switzerland.
Am J Physiol Endocrinol Metab. 2002 Nov;283(5):E980-7. doi: 10.1152/ajpendo.00196.2002.
To assess whether intracerebroventricular leptin administration affects monodeiodinase type II (D2) activity in the tissues where it is expressed [cerebral cortex, hypothalamus, pituitary, and brown adipose tissue (BAT)], hepatic monodeiodinase type I (D1) activity was inhibited with propylthiouracil (PTU), and small doses of thyroxine (T4; 0.6 nmol. 100 g body wt(-1). day(-1)) were supplemented to compensate for the PTU-induced hypothyroidism. Two groups of rats were infused with leptin for 6 days, one of them being additionally treated with reverse triiodothyronine (rT3), an inhibitor of D2. Control rats were infused with vehicle and pair-fed the amount of food consumed by leptin-infused animals. Central leptin administration produced marked increases in D2 mRNA expression and activity in BAT, changes that were likely responsible for increased plasma T3 and decreased plasma T4 levels. Indeed, plasma T3 and T4 concentrations were unaltered by central leptin administration in the presence of rT3. The additional observation of a leptin-induced increased mRNA expression of BAT uncoupling protein-1 suggested that the effect on BAT D2 may be mediated by the sympathetic nervous system.
为评估脑室内注射瘦素是否会影响其表达组织（大脑皮层、下丘脑、垂体和棕色脂肪组织）中的II型单碘甲状腺原氨酸脱碘酶（D2）活性，用丙硫氧嘧啶（PTU）抑制肝脏I型单碘甲状腺原氨酸脱碘酶（D1）活性，并补充小剂量甲状腺素（T4；0.6 nmol·100 g体重⁻¹·天⁻¹）以补偿PTU诱导的甲状腺功能减退。两组大鼠连续6天注射瘦素，其中一组额外用D2抑制剂反式三碘甲状腺原氨酸（rT3）处理。对照大鼠注射溶媒，并按瘦素注射组动物的食量进行配对喂养。脑室内注射瘦素使棕色脂肪组织中D2 mRNA表达和活性显著增加，这些变化可能是导致血浆T3升高和血浆T4降低的原因。事实上，在存在rT3的情况下，脑室内注射瘦素并未改变血浆T3和T4浓度。另外观察到瘦素诱导棕色脂肪组织解偶联蛋白-1 mRNA表达增加，提示对棕色脂肪组织D2的影响可能由交感神经系统介导。
