Lowell B B, Gold R M, Adamchuk C A
Pharmacol Biochem Behav. 1980 Jun;12(6):837-41. doi: 10.1016/0091-3057(80)90440-2.
Recent evidence indicates that the paraventricular nucleus of the hypothalamus (PVN) contains both neurons that produce thyrotropic releasing hormone (TRH) and neurons that are destroyed or disconnected by the knife cuts that produce hypothalamic hyperphagia and obesity. This, and other evidence, suggested linkage between thyroid regulation and appetite control. As predicted, hyperthyroidism potentiated and hypothyroidism tempered the weight gains of knife cut rats. However, these effects were due entirely to increased and decreased, respectively, linear growth, not to differences in the degree of obesity. Enhanced linear growth and elevated growth hormone levels are a minor component of the enhanced weight gain of hypothalamically knife cut rats. Most of the weight gain is due to fat deposition. Only the enhanced linear growth and growth hormone aspect appear to possibly be mediated via the thyroid. In addition, obesifying knife cuts did not reduce goiterogenesis in PTU treated rats, as would be expected if the elaboration of TRH were blocked by obesifying knife cuts. Thus, neither TRH nor thyroxine is involved in the etiology of hypothalamic obesity.
最近的证据表明,下丘脑室旁核(PVN)既包含产生促甲状腺激素释放激素(TRH)的神经元,也包含因造成下丘脑性多食和肥胖的刀切损伤而被破坏或切断联系的神经元。这一证据以及其他证据表明甲状腺调节与食欲控制之间存在联系。正如所预测的那样,甲状腺功能亢进增强了刀切大鼠的体重增加,而甲状腺功能减退则抑制了这种体重增加。然而,这些影响完全分别归因于线性生长的增加和减少,而非肥胖程度的差异。线性生长增强和生长激素水平升高是下丘脑刀切大鼠体重增加增强的一个次要因素。大部分体重增加是由于脂肪沉积。似乎只有增强的线性生长和生长激素方面可能是通过甲状腺介导的。此外,致肥胖的刀切损伤并没有像预期的那样,如果TRH的产生被致肥胖的刀切损伤所阻断,就会减少丙硫氧嘧啶(PTU)处理大鼠的甲状腺肿形成。因此,TRH和甲状腺素均不参与下丘脑性肥胖的病因。