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- Title
Enkephalin-δ Opioid Receptor Signaling Mediates Glucoprivic Suppression of LH Pulse and Gluconeogenesis in Female Rats.
- Authors
Tsuchida, Hitomi; Nonogaki, Miku; Takizawa, Marina; Inoue, Naoko; Uenoyama, Yoshihisa; Tsukamura, Hiroko
- Abstract
Energy availability is an important regulator of reproductive function at various reproductive phases in mammals. Glucoprivation induced by 2-deoxy-D-glucose (2DG), an inhibitor of glucose utilization, as an experimental model of malnutrition suppresses the pulsatile release of GnRH/LH and induces gluconeogenesis. The present study was performed with the aim of examining whether enkephalin-δ-opioid receptor (DOR) signaling mediates the suppression of pulsatile GnRH/LH release and gluconeogenesis during malnutrition. The administration of naltrindole hydrochloride (NTI), a selective DOR antagonist, into the third ventricle blocked the suppression of LH pulses and part of gluconeogenesis induced by IV 2DG administration in ovariectomized rats treated with a negative feedback level of estradiol-17 β (OVX + low E2). The IV 2DG administration significantly increased the number of Penk (enkephalin gene)-positive cells coexpressing fos (neuronal activation marker gene) in the paraventricular nucleus (PVN), but not in the arcuate nucleus (ARC) in OVX + low E2 rats. Furthermore, double in situ hybridization for Penk / Pdyn (dynorphin gene) in the PVN revealed that approximately 35% of the PVN Penk -expressing cells coexpressed Pdyn. Double in situ hybridization for Penk / Crh (corticotropin-releasing hormone gene) in the PVN and Penk / Kiss1 (kisspeptin gene) in the ARC revealed that few Penk -expressing cells coexpressed Crh and Kiss1. Taken together, these results suggest that central enkephalin-DOR signaling mediates the suppression of pulsatile LH release during malnutrition. Moreover, the current study suggests that central enkephalin-DOR signaling is also involved in gluconeogenesis during malnutrition in female rats.
- Subjects
ENKEPHALINS; GLUCONEOGENESIS; LABORATORY rats
- Publication
Endocrinology, 2023, Vol 164, Issue 3, p1
- ISSN
0013-7227
- Publication type
Article
- DOI
10.1210/endocr/bqac216