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- Publisher
- CSIRO Publishing
- Copyright
- Copyright © The Author(s). Published by CSIRO Publishing
- ISSN
- 1031-3613
- eISSN
- 1448-5990
- DOI
- 10.1071/RD16301
- pmid
- 28672116
- Publisher site
- See Article on Publisher Site
Abstract
Visfatin and resistin appear to interfere with reproduction in the gonads, but their potential action at the hypothalamicpituitary level is not yet known. The aim of the present study was to investigate the mRNA and protein expression of these adipokines in murine gonadotroph cells and to analyse the effects of different concentrations of recombinant mouse visfatin and resistin (0.01, 0.1, 1 and 10ngmL1) on LH secretion and signalling pathways in LT2 cells and/or in primary female mouse pituitary cells. Both visfatin and resistin mRNA and protein were found in vivo in gonadotroph cells. In contrast with resistin, the primary tissue source of visfatin in the mouse was the skeletal muscle, and not adipose tissue. Visfatin and resistin both decreased LH secretion from LT2 cells after 24h exposure of cells (P<0.03). These results were confirmed for resistin in primary cell culture (P<0.05). Both visfatin (1ngmL1) and resistin (1ngmL1) increased AMP-activated protein kinase phosphorylation in LT2 cells after 5 or 10min treatment, up to 60min (P<0.04). Extracellular signal-regulated kinase 1/2 phosphorylation was transiently increased only after 5min resistin (1ngmL1) treatment (P<0.01). In conclusion, visfatin and resistin are expressed in gonadotroph cells and they may affect mouse female fertility by regulating LH secretion at the level of the pituitary.
Journal
Reproduction Fertility and Development – CSIRO Publishing
Published: Jul 4, 2017