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黄体生成素（LH）的分泌。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。本研究旨在进一步探讨空腹抑制黄体生成素释放的脑机制。禁食48小时显著增加下脑干孤立束核（NTS） PVN区和A2区雌激素受体细胞数量。急性输注雌激素至PVN只在禁食48小时的去卵巢大鼠（OVX）中引起脉动性LH释放的抑制，而在自由喂养的OVX大鼠中则没有。另一方面，雌激素输注NTS不影响LH分泌。雌激素输注到两核对PVN内去甲肾上腺素的释放没有影响。这些结果表明，禁食诱导PVN中雌激素受体的表达，其中雌激素抑制LH分泌而不影响去甲肾上腺素的释放。研究表明，静脉注射葡萄糖拮抗剂2-脱氧葡萄糖（2DG）以剂量依赖的方式抑制OVX大鼠脉动性LH释放，雌激素增强了2DG对LH脉冲的抑制作用。此外，2DG诱导PVN释放去甲肾上腺素，局部向PVN注射儿茶酚胺合成抑制剂可阻断2DG诱导的LH分泌抑制。这些结果表明，降低葡萄糖可用性对LH释放的抑制是由投射PVN的去甲肾上腺素能神经元介导的。

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.