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Interactions Between the Gravitostat and the Fibroblast Growth Factor System for the Regulation of Body Weight

Artikel i vetenskaplig tidskrift
Författare Vilborg Palsdottir
Sara H Windahl
Daniel Hägg
Hanna Keantar
Jakob Bellman
A. Buchanan
T. J. Vaughan
Daniel Lindén
John-Olov Jansson
Claes Ohlsson
Publicerad i Endocrinology
Volym 160
Nummer/häfte 5
Sidor 1057-1064
ISSN 0013-7227
Publiceringsår 2019
Publicerad vid Institutionen för neurovetenskap och fysiologi
Centre for Bone and Arthritis Research
Sidor 1057-1064
Språk en
Länkar dx.doi.org/10.1210/en.2018-01002
Ämnesord recombinant leptin, fgf21, obese, gene, mass, Endocrinology & Metabolism
Ämneskategorier Endokrinologi och diabetes

Sammanfattning

Both fibroblast growth factors (FGFs), by binding to FGF receptors (FGFRs), and activation of the gravitostat, by artificial loading, decrease the body weight (BW). Previous studies demonstrate that both the FGF system and loading have the capacity to regulate BW independently of leptin. The aim of the current study was to determine the possible interactions between the effect of increased loading and the FGF system for the regulation of BW. We observed that the BW-reducing effect of increased loading was abolished in mice treated with a monoclonal antibody directed against FGFR1c, suggesting interactions between the two systems. As serum levels of endocrine FGF21 and hepatic FGF21 mRNA were increased in the loaded mice compared with the control mice, we first evaluated the loading response in FGF21 over expressing mice with constant high FGF21 levels. Leptin treatment, but not increased loading, decreased the BW in the FGF21-overexpressing mice, demonstrating that specifically the loading effect is attenuated in the presence of high activity in the FGF system. However, as FGF21 knockout mice displayed a normal loading response on BW, FGF21 is neither mediating nor essential for the loading response. In conclusion, the BW-reducing effect of increased loading but not of leptin treatment is blocked by high activity in the FGF system. We propose that both the gravitostat and the FGF system regulate BW independently of leptin and that pharmacologically enhanced activity in the FGF system reduces the sensitivity of the grayitostat.

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