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Updated: Oct 1, 2026

Evaluation of Hepatic Glucose Production in a Polycystic Ovary Syndrome Mouse Model
Published on: March 5, 2022
Effect of 2-deoxy-D-glucose on gonadotropins, prolactin and serum glucose concentrations in the mare
Christina J McManus1, Laurie A Davison, Barry P Fitzgerald
1Department of Veterinary Science, Maxwell Gluck Equine Research Center, University of Kentucky, Lexington, KY 40546-0099, USA.
Abstract:
In a variety of species, glucoprivation results in the suppression of the reproductive axis. Two experiments were performed to test the hypothesis that blockade of glucose metabolism via administration of the glucose inhibitor 2-deoxy-D-glucose (2DG) to mares would cause a modification in gonadotropin and prolactin secretion. Long-term ovariectomized mares (Experiment 1, n=4) or ovary-intact mares during the follicular phase of a synchronized estrous cycle (Experiment 2, n=4 per dose) were treated with 2DG. The dose of 2DG used in Experiment 1 was 100mg 2DG/kg BW, but because severe behavioral responses occurred, lower doses (50, 25, and 12.5mg 2DG/kg BW) were used for Experiment 2. In addition to the effects of 2DG, the pituitary responsiveness after glucoprivation was determined by an injection of gonadotropin-releasing hormone (100 microg) 6h post-treatment. In both experiments, treatment with 2DG was unaccompanied by changes in gonadotropin secretion or pituitary responsiveness. Mares treated with 100 mg 2DG/kg BW exhibited a significant increase in prolactin and mares treated with 100mg 2DG or 50mg 2DG/kg BW exhibited a significant increase in serum glucose concentrations, suggesting that glucoprivation was detected at these doses. Lower doses of 2DG did not cause significant alterations in prolactin or glucose levels. These results indicate that 2DG inhibits glucose utilization, but short-term glucoprivation via this metabolic inhibitor does not alter gonadotropin secretion in the mare. This lack of response to glucoprivation may reflect species differences in the response to glucoprivation or may be due to metabolic responses to the inhibition of glucose availability.
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