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Visfatin and resistin in gonadotroph cells: expression, regulation of LH secretion and signalling pathways
Virginie Maillard1, Sébastien Elis1, Alice Desmarchais1
1UMR85 PRC, INRA, CNRS, IFCE, Université de Tours, 37380 Nouzilly, France.
Abstract:
Visfatin and resistin appear to interfere with reproduction in the gonads, but their potential action at the hypothalamic-pituitary 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 10ngmL-1) on LH secretion and signalling pathways in LβT2 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 LβT2 cells after 24h exposure of cells (P<0.03). These results were confirmed for resistin in primary cell culture (P<0.05). Both visfatin (1ngmL-1) and resistin (1ngmL-1) increased AMP-activated protein kinase α phosphorylation in LβT2 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 (1ngmL-1) 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.
Insights
Visfatin and resistin are found in pituitary gonadotroph cells and can reduce luteinizing hormone (LH) secretion, potentially impacting female fertility.
Area of Science:
- Endocrinology
- Reproductive Biology
- Molecular Endocrinology
Background:
- Visfatin and resistin are adipokines with known reproductive roles at the gonadal level.
- Their function within the hypothalamic-pituitary axis, specifically in gonadotroph cells, remains largely unexplored.
Purpose of the Study:
- To investigate the expression of visfatin and resistin in murine gonadotroph cells.
- To analyze the impact of visfatin and resistin on luteinizing hormone (LH) secretion and associated signaling pathways in pituitary cells.
Main Methods:
- Quantitative assessment of visfatin and resistin mRNA and protein expression in vivo and in vitro.
- Treatment of LβT2 cells and primary female mouse pituitary cells with varying concentrations of recombinant visfatin and resistin.
- Measurement of LH secretion and phosphorylation of key signaling molecules (AMPKα, ERK1/2).
Main Results:
- Visfatin and resistin were detected in gonadotroph cells in vivo.
- Both adipokines significantly decreased LH secretion from LβT2 cells and primary pituitary cells.
- Visfatin and resistin treatment led to increased phosphorylation of AMP-activated protein kinase α.
- Resistin transiently increased extracellular signal-regulated kinase 1/2 phosphorylation.
Conclusions:
- Visfatin and resistin are expressed in pituitary gonadotroph cells.
- These adipokines can modulate LH secretion at the pituitary level.
- The findings suggest a potential role for visfatin and resistin in regulating female fertility through pituitary mechanisms.
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