Brain mechanism mediating fasting-induced suppression of reproductive function

禁食应激以雌激素依赖的方式显著抑制大鼠促黄体生成激素（LH）的分泌。已经证明，这种抑制是由投射到下丘脑室旁核（PVN）的去甲肾上腺素能神经元介导的。禁食48h后，大鼠下丘脑室旁核（PVN）和孤束核（NTS）A2区雌激素受体阳性细胞数显著增加，而下丘脑室旁核（PVN）和孤束核（NTS）A2区雌激素受体阳性细胞数显著增加，且与禁食抑制LH释放有关。急性注入雌激素到PVN引起的脉冲LH释放的抑制，只有在48小时禁食卵巢切除（OVX）大鼠，但不是在自由进食OVX大鼠。另一方面，雌激素注入NTS不影响LH分泌。结果表明，禁食诱导室旁核雌激素受体表达，雌激素抑制LH分泌，但不影响去甲肾上腺素的释放，静脉注射葡萄糖拮抗剂2-脱氧葡萄糖（2DG），雌激素以剂量依赖方式抑制去卵巢大鼠LH脉冲释放，雌激素增强2DG对LH脉冲的抑制作用。此外，2DG诱导去甲肾上腺素释放的PVN，和局部注射的儿茶酚胺合成抑制剂到PVN阻断2DG诱导的LH分泌的抑制。这些结果表明，LH释放的抑制葡萄糖的可用性降低介导的去甲肾上腺素能神经元投射PVN。

Fasting-stress profoundly suppresses luteinizing hormone (LH) secretion in the rat in a estrogen dependent manner. It has been demonstrated that this suppression is mediated by noradrenergic neurons projecting to the hypothalamic paraventricular nucleus (PVN). The present research aimed to investigate further brain mechanism mediating the fasting-induced suppression of LH release.Forty-eight h fasting significantly increased numbers of estrogen receptor-containing cells in both the PVN and A2 region of solitary tract nucleus (NTS) in the lower brain stem. Acute infusion of estrogen into the PVN caused an inhibition of pulsatile LH release only in the 48-h fasted ovariectomized (OVX) rats, but not in the ad lib-fed OVX rats. On the other hand, the estrogen infusion into the NTS did not affect LH secretion. The estrogen infusion into the both nuclei did not affect the noradrenaline release in the PVN.These results suggest that fasting induces estrogen receptor expression in the PVN where estrogen acts to suppresses LH secretion without affecting noradrenaline release.It has demonstrated that intravenous injection of 2-deoxyglucose (2DG), a glucose antagonist, suppressed pulsatile LH release in OVX rats in a dose-dependent manner and that estrogen enhanced the inhibitory effect of 2DG on LH pulses. Furthermore, 2DG induced noradrenaline release in the PVN,and local injection of catecholamine synthesis inhibitor into the PVN blocked 2DG-induced suppression of LH secretion. These results suggest that suppression of LH release by lowered glucose availability is mediated y noradrenergic neurons projecting the PVN.