Visfatin and resistin in gonadotroph cells: expression, regulation of LH secretion and signalling pathways
Virginie Maillard A B , Sébastien Elis A , Alice Desmarchais A , Céline Hivelin A , Lionel Lardic A , Didier Lomet A , Svetlana Uzbekova A , Philippe Monget A and Joëlle Dupont AA UMR85 PRC, INRA, CNRS, IFCE, Université de Tours, 37380 Nouzilly, France.
B Corresponding author. Email: virginie.maillard@inra.fr
Reproduction, Fertility and Development 29(12) 2479-2495 https://doi.org/10.1071/RD16301
Submitted: 4 August 2016 Accepted: 21 May 2017 Published: 4 July 2017
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 10 ng mL−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 24 h exposure of cells (P < 0.03). These results were confirmed for resistin in primary cell culture (P < 0.05). Both visfatin (1 ng mL−1) and resistin (1 ng mL−1) increased AMP-activated protein kinase α phosphorylation in LβT2 cells after 5 or 10 min treatment, up to 60 min (P < 0.04). Extracellular signal-regulated kinase 1/2 phosphorylation was transiently increased only after 5 min resistin (1 ng mL−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.
Additional keywords: adipokine, AMP-activated protein kinase, extracellular signal-regulated kinase, gonadotrophin, myokine, nicotinamide phosphoribosyltransferase (NAMPT), RETN, tissue expression.
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