Wolf B, Aratan-Spire S, Czernichow P
Endocrinology. 1984 Apr;114(4):1334-7. doi: 10.1210/endo-114-4-1334.
The effect of hypothyroidism on pancreatic TRH (P-TRH) and P-TRH-degrading activity (P-TRH-DA) was studied in adult rats. Hypothyroidism was induced in three groups during 4, 6, or 9 weeks by propylthiouracil (PTU) in drinking water and a low iodine diet (LID). Another group received PTU-LID for 6 weeks, followed by 5 weeks on a normal diet to restore euthyroidism. A possible toxic effect of PTU per se was eliminated by treating one control group with PTU and T3. P-TRH and TRH-DA were measured by specific RIA. In the hypothyroid groups, P-TRH concentrations (mean +/- SEM) were increased 10-fold (6.95 +/- 2.09; 5.51 +/- 1.3; 9.79 +/- 3.3 pg/(mg X 100 g BW), respectively, with a control value of 0.55 +/- 0.39, P less than 0.01). This increase was reversible, as shown by the group on PTU-LID followed by a normal diet (0.58 +/- 0.39, NS). P-TRH-DA present in the control group was decreased after 4 weeks of PTU-LID treatment and totally abolished after 6 and 9 weeks of PTU-LID treatment. In conclusion, these results suggest that thyroid status modulates P-TRH concentrations. This effect may be due to the disappearance of the TRH-DA in response to hypothyroidism. P-TRH stores may be regulated by the enzyme(s) involved in P-TRH-DA.
在成年大鼠中研究了甲状腺功能减退对胰腺促甲状腺激素释放激素（P-TRH）和P-TRH降解活性（P-TRH-DA）的影响。通过在饮水中添加丙硫氧嘧啶（PTU）和低碘饮食（LID），在三组大鼠中分别诱导4周、6周或9周的甲状腺功能减退。另一组接受PTU-LID治疗6周，然后改为正常饮食5周以恢复甲状腺功能正常。通过用PTU和T3治疗一个对照组，消除了PTU本身可能的毒性作用。通过特异性放射免疫分析（RIA）测量P-TRH和TRH-DA。在甲状腺功能减退组中，P-TRH浓度（平均值±标准误）分别增加了10倍（分别为6.95±2.09；5.51±1.3；9.79±3.3 pg/（mg×100 g体重）），而对照组值为0.55±0.39，P＜0.01）。如接受PTU-LID后改为正常饮食的组所示（0.58±0.39，无显著性差异），这种增加是可逆的。PTU-LID治疗4周后，对照组中的P-TRH-DA降低，PTU-LID治疗6周和9周后则完全消失。总之，这些结果表明甲状腺状态调节P-TRH浓度。这种作用可能是由于甲状腺功能减退导致TRH-DA消失所致。P-TRH储备可能受参与P-TRH-DA的酶调节。
