GLUT1-mediated glycolysis supports GnRH-induced secretion of luteinizing hormone from female gonadotropes

Dequina A. Nicholas, Vashti S. Knight, Karen J. Tonsfeldt, Tomohiro Terasaka, Olivia Molinar-Inglis, Shannon B.Z. Stephens, Jo Ann Trejo, Alexander S. Kauffman, Pamela L. Mellon, Mark A. Lawson

Research output: Contribution to journalArticlepeer-review

Abstract

The mechanisms mediating suppression of reproduction in response to decreased nutrient availability remain undefined, with studies suggesting regulation occurs within the hypothalamus, pituitary, or gonads. By manipulating glucose utilization and GLUT1 expression in a pituitary gonadotrope cell model and in primary gonadotropes, we show GLUT1-dependent stimulation of glycolysis, but not mitochondrial respiration, by the reproductive neuropeptide GnRH. GnRH stimulation increases gonadotrope GLUT1 expression and translocation to the extracellular membrane. Maximal secretion of the gonadotropin Luteinizing Hormone is supported by GLUT1 expression and activity, and GnRH-induced glycolysis is recapitulated in primary gonadotropes. GLUT1 expression increases in vivo during the GnRH-induced ovulatory LH surge and correlates with GnRHR. We conclude that the gonadotropes of the anterior pituitary sense glucose availability and integrate this status with input from the hypothalamus via GnRH receptor signaling to regulate reproductive hormone synthesis and secretion.

Original languageEnglish
Article number13063
JournalScientific reports
Volume10
Issue number1
DOIs
Publication statusPublished - Dec 1 2020
Externally publishedYes

ASJC Scopus subject areas

  • General

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