Sprangers S A, Piacsek B E
Department of Biology, Marquette University, Milwaukee, Wisconsin 53201-1881, USA.
Proc Soc Exp Biol Med. 1997 Dec;216(3):398-403. doi: 10.3181/00379727-216-44188.
Reduced caloric intake has been shown to inhibit reproductive cycles in females of several mammalian species. Previous studies have shown that increased negative feedback efficacy of estrogen on gonadotropin secretion may be responsible. The present study was designed to test the alternate hypothesis that caloric restriction alters the positive feedback efficacy of estrogen on gonadotropin secretion. Adult, cycling female rats were placed on reduced food intake (R) equal to 50% of that consumed by ad/libitum-fed controls (C). When R rats stopped cycling, both R and C rats were ovariectomized (OVX) and immediately implanted subcutaneously with a Silastic capsule containing 100 microg 17beta-estradiol (E2). Blood samples were obtained at 0900-1000 hr and 1600-1730 hr on Days 2, 4, 6, 8, 10, 12, and 14 after OVX and implantation. Follicle-stimulating hormone (FSH), luteinizing hormone (LH), and E2 were measured by radioimmunoassay in duplicate aliquots. Results indicate that underfed female rats retain the ability to respond to elevated estrogen levels with an afternoon surge of gonadotropin which is present for at least 14 days for LH. By contrast, FSH surges in R rats became progressively smaller and were no longer significant after Day 10. The present results also demonstrate that the response of R rats to elevated estrogen levels is significantly greater than that of C rats on Days 2-4 for FSH and 2-14 for LH. It is concluded that an inability to respond to elevated estrogen levels with an afternoon LH surge is not the cause of the cessation of normal estrous cycles. The progressive decrease in the afternoon surge of FSH may be, at least partly, responsible for the decreased follicular development observed in underfed rats. Possible explanations of the enhanced LH response to the positive feedback of estrogen are discussed.
热量摄入减少已被证明会抑制几种哺乳动物雌性的生殖周期。先前的研究表明,雌激素对促性腺激素分泌的负反馈效能增加可能是原因所在。本研究旨在检验另一种假设,即热量限制会改变雌激素对促性腺激素分泌的正反馈效能。将成年的、处于发情周期的雌性大鼠置于食物摄入量减少(R)的状态,其摄入量相当于自由进食对照组(C)的50%。当R组大鼠停止发情周期时,将R组和C组大鼠都进行卵巢切除(OVX),并立即皮下植入一个含有100微克17β-雌二醇(E2)的硅橡胶胶囊。在卵巢切除和植入后的第2、4、6、8、10、12和14天的0900 - 1000时和1600 - 1730时采集血样。通过放射免疫分析法对两份等分试样进行促卵泡激素(FSH)、促黄体生成素(LH)和E2的测定。结果表明,进食不足的雌性大鼠保留了对升高的雌激素水平产生促性腺激素下午高峰的反应能力,LH的这种高峰至少持续14天。相比之下,R组大鼠的FSH高峰逐渐变小,在第10天后不再显著。本研究结果还表明,在第2 - 4天对于FSH以及第2 - 14天对于LH,R组大鼠对升高的雌激素水平的反应显著大于C组大鼠。得出的结论是,无法通过下午LH高峰对升高的雌激素水平做出反应不是正常发情周期停止的原因。FSH下午高峰的逐渐下降可能至少部分地导致了在进食不足的大鼠中观察到的卵泡发育减少。讨论了对雌激素正反馈的LH反应增强的可能解释。