Ependymal denudation in the fourth ventricle attenuates glucoprivic feeding without altering blood glucose and luteinizing hormone responses in female rats
Abstract
The hindbrain plays a critical role in regulating feeding, glucose metabolism, and reproductive function during malnutrition, and our previous studies suggest that hindbrain ependymal cells lining the fourth ventricle (4V) potentially contribute to the physiological responses to hindbrain glucoprivation. The present study aimed to examine the effects of 4V ependymal denudation on counterregulatory responses to hindbrain glucoprivation. Neuraminidase, an enzyme that induces ependymal denudation, was administered into the 4V of ovariectomized rats implanted with a silicone tube containing a negative feedback level of estradiol-17β (OVX + low E2 rats) to generate an ependymal cell-disrupted model, whereas vehicle administration served as the control condition. Following 4V administration of neuraminidase or vehicle, OVX + low E2 rats received 4V administration of 2-deoxy-D-glucose (2DG), a glucose utilization inhibitor, or xylose as an osmotic control, and food intake, blood glucose levels, and luteinizing hormone (LH) concentrations were measured. Administration of 2DG into the 4V increased food intake in control rats, whereas this response was absent in rats with ependymal denudation. In contrast, 4V administration of 2DG increased blood glucose levels and suppressed LH secretion in both control rats and rats with ependymal denudation. Taken together, these findings indicate that 4V ependymal cells may, at least in part, contribute to feeding responses during hindbrain glucoprivation.
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BibTeX
@article{sato2026ependymal,
title = {{Ependymal denudation in the fourth ventricle attenuates glucoprivic feeding without altering blood glucose and luteinizing hormone responses in female rats}},
author = {Marimo Sato and Fumie Magata and Hiroko Tsukamura and Fuko Matsuda},
journal = {Endocrine Journal},
year = {2026},
month = sep,
doi = {10.1507/endocrj.ej26-0074},
url = {https://www.jstage.jst.go.jp/article/endocrj/advpub/0/advpub_EJ26-0074/_article},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Ependymal denudation in the fourth ventricle attenuates glucoprivic feeding without altering blood glucose and luteinizing hormone responses in female rats
AU - Marimo Sato
AU - Fumie Magata
AU - Hiroko Tsukamura
AU - Fuko Matsuda
PY - 2026
DA - 2026/09/26
JO - Endocrine Journal
DO - 10.1507/endocrj.ej26-0074
UR - https://www.jstage.jst.go.jp/article/endocrj/advpub/0/advpub_EJ26-0074/_article
AB - The hindbrain plays a critical role in regulating feeding, glucose metabolism, and reproductive function during malnutrition, and our previous studies suggest that hindbrain ependymal cells lining the fourth ventricle (4V) potentially contribute to the physiological responses to hindbrain glucoprivation. The present study aimed to examine the effects of 4V ependymal denudation on counterregulatory responses to hindbrain glucoprivation. Neuraminidase, an enzyme that induces ependymal denudation, was administered into the 4V of ovariectomized rats implanted with a silicone tube containing a negative feedback level of estradiol-17β (OVX + low E2 rats) to generate an ependymal cell-disrupted model, whereas vehicle administration served as the control condition. Following 4V administration of neuraminidase or vehicle, OVX + low E2 rats received 4V administration of 2-deoxy-D-glucose (2DG), a glucose utilization inhibitor, or xylose as an osmotic control, and food intake, blood glucose levels, and luteinizing hormone (LH) concentrations were measured. Administration of 2DG into the 4V increased food intake in control rats, whereas this response was absent in rats with ependymal denudation. In contrast, 4V administration of 2DG increased blood glucose levels and suppressed LH secretion in both control rats and rats with ependymal denudation. Taken together, these findings indicate that 4V ependymal cells may, at least in part, contribute to feeding responses during hindbrain glucoprivation.
SN - 1348-4540
SN - 0918-8959
ER -