Neuroendocrine mechanism mediating the nutritional infertility

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Glucose availability would be one of the major factors involved in the suppressed reproductive functions under malnutrition in mammalian species. In the present study, the role of glucose availability in regulating gonadotropin-releasing hormone (GnRH)/Iuteinizing hormone (LH) release in female rats. The sensors for detecting the blood glucose level to regulate LH secretion and feeding behavior have been considered to be located in the hypothalamus and medulla oblongata in rats. The present study focussed on the localization of glucose sensors in the area postrema using Fos immunohistochemistry as a marker of neuronal activation.Peripheral administration of a glucose antagonist, 2-deoxyglucose (2DG), induced a massive expression of Fos protein in the area postrema (AP), solitary tract nucleus (NTS) and paraventricular nucleus of the hypothalamus in ovariectomized and estradiol-primed ovariectomized rats. Dual immunohistochemistry with Fos and various cell markers, such as GFAP and MAP-2, showed that Fos-expressing cells in the AP would be neuronal but not glial cells. These cell were not catecholaminergic because any Fos-like immunoreactivities in the AP were not co-localized with tyrosine hydroxy lase immunoreactivity. A part of the Fos-expressing neruons in the NTS was catecholaminergic.These results indicate that a population of non-catecholaminergic neurons in the AP could be involved in sensing low glucose availability to regulate reproductive functions as well as feeding behavior n female rats.