Kolesnick R N, Musacchio I, Thaw C, Gershengorn M C
Endocrinology. 1984 Feb;114(2):671-6. doi: 10.1210/endo-114-2-671.
TRH stimulated the metabolism of lipids of the phosphatidylinositol (PI)-phosphatidic acid (PA) cycle and caused an increase in the level of free or unesterified arachidonic acid in mouse pituitary thyrotropic tumor (TtT) cells. In cells labeled with [32P]orthophosphate for 45 min, TRH caused a rapid specific increase in [32P]PA to 190 +/- 8% (+/- SE) of the control value at 15 sec (P less than 0.005) and in [32P]PI to 158 +/- 8% at 2 min (P less than 0.005). In cells labeled to isotopic steady state with [3H]inositol, TRH caused a decrease in [3H]PI to 92 +/- 1.8% of the control value at 1 min (P less than 0.01) and increased the level of [3H]inositolmonophosphate. In cells labeled to isotopic steady state with [14C]stearic acid, TRH caused a transient rise in [14C]diacylglycerol and a more prolonged increase in [14C]PA. In cells labeled to isotopic steady state with [3H]arachidonic acid, TRH stimulated a rise in free [3H]arachidonic acid to 210 +/- 8% of the control value at 15 sec (P less than 0.001), with a return to a level of 125 +/- 2% of the control value by 5 min. Arachidonic acid added exogenously caused efflux of 45Ca2+ from prelabeled cells and stimulated TSH secretion. Hence, in TtT cells, TRH 1) rapidly stimulated a decrease in the level of PI and increased inositolmonophosphate, diacylglycerol, and PA; and 2) caused a rapid increase in the level of free arachidonic acid. These effects may be important in stimulation of TSH secretion by TRH. Because arachidonic acid, when added exogenously, mobilized cellular Ca2+ and stimulated TSH secretion, arachidonic acid may mediate, at least in part, TRH-stimulated TSH secretion. The action of TRH on lipid metabolism in TtT cells is different from that in mammotropic pituitary cells, since TRH does not cause an increase in the level of free arachidonic acid in GH3 cells.
促甲状腺激素释放激素（TRH）刺激了磷脂酰肌醇（PI）-磷脂酸（PA）循环中的脂质代谢，并导致小鼠垂体促甲状腺肿瘤（TtT）细胞中游离或未酯化花生四烯酸水平升高。在用[32P]正磷酸盐标记45分钟的细胞中，TRH使[32P]PA在15秒时迅速特异性增加至对照值的190±8%（±标准误）（P<0.005），使[32P]PI在2分钟时增加至158±8%（P<0.005）。在用[3H]肌醇标记至同位素稳态的细胞中，TRH使[3H]PI在1分钟时降至对照值的92±1.8%（P<0.01），并增加了[3H]肌醇单磷酸的水平。在用[14C]硬脂酸标记至同位素稳态的细胞中，TRH使[14C]二酰基甘油短暂升高，使[14C]PA升高更为持久。在用[3H]花生四烯酸标记至同位素稳态的细胞中，TRH在15秒时刺激游离[3H]花生四烯酸升高至对照值的210±8%（P<0.001），到5分钟时恢复至对照值的125±2%。外源性添加的花生四烯酸导致预标记细胞中45Ca2+外流，并刺激促甲状腺激素（TSH）分泌。因此，在TtT细胞中，TRH 1）迅速刺激PI水平降低，增加肌醇单磷酸、二酰基甘油和PA；2）使游离花生四烯酸水平迅速升高。这些作用可能在TRH刺激TSH分泌中起重要作用。因为外源性添加花生四烯酸可动员细胞内Ca2+并刺激TSH分泌，所以花生四烯酸可能至少部分介导TRH刺激的TSH分泌。TRH对TtT细胞脂质代谢的作用不同于对垂体催乳素细胞的作用，因为TRH不会使GH3细胞中游离花生四烯酸水平升高。
