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The extracellular signal-regulated kinase isoform ERK1 is specifically required for in vitro and in vivo adipogenesis.
Bost F., Aouadi M., Caron L., Even P., Belmonte N., Prot M., Dani C., Hofman P., Pagès G., Pouysségur J. et al
Diabetes 54, 2 (2005) 402-11 - http://hal.archives-ouvertes.fr/hal-00304208
Articles dans des revues avec comité de lecture
Sciences du Vivant/Biochimie, Biologie Moléculaire
Sciences du Vivant/Biologie du développement
The extracellular signal-regulated kinase isoform ERK1 is specifically required for in vitro and in vivo adipogenesis.
F. Bost 1, M. Aouadi 1, L. Caron 1, P. Even 2, N. Belmonte 3, M. Prot 1, C. Dani 3, P. Hofman 4, G. Pagès 3, J. Pouysségur 3, Y. Le Marchand-Brustel 1, B. Binétruy ( ) 1
1 :  Signalisation moléculaire et obésité
INSERM : U568 – IFR50 – Université Nice Sophia Antipolis [UNS]
Faculte de Medecine Avenue de Valombrose 06107 NICE CEDEX 2
France
2 :  Unité mixte de recherche de physiologie de la nutrition et du comportement alimentaire
Institut national de la recherche agronomique (INRA) – Institut National Agronomique Paris-Grignon
75231 Paris
France
3 :  Institut de signalisation, biologie du développement et cancer (ISBDC)
http:// www.unice.fr/ISDBC
CNRS : UMR6543 – Université Nice Sophia Antipolis [UNS]
Centre Antoine lacassagne 33 Avenue de volombrose 06189 NICE CEDEX 2
France
4 :  Immunité muqueuse et vaccination
INSERM : E0215
Faculté de Médecine 28 Avenue de Valombrose 06103 Nice Cedex 2
France
Hyperplasia of adipose tissue is critical for the development of obesity, but molecular mechanisms governing normal or pathological recruitment of new adipocytes remain unclear. The extracellular signal-regulated kinase (ERK) pathway plays a pivotal role in many essential cellular functions, such as proliferation and differentiation. Using ERK1(-/-) mice, we investigated the role of this isoform in adipose tissue development. Mice lacking ERK1 have decreased adiposity and fewer adipocytes than wild-type animals. Furthermore, ERK1(-/-) mice challenged with high-fat diet are resistant to obesity, are protected from insulin resistance, and have a higher postprandial metabolic rate. To get insights into cellular mechanisms implicated in reduced adiposity in ERK1(-/-) animals, we analyzed adipocyte differentiation in ERK1(-/-) cells. Compared with wild-type control cells, mouse embryo fibroblasts and cultures of adult preadipocytes isolated from ERK1(-/-) adult animals exhibit impaired adipogenesis. An inhibitor of the ERK pathway does not affect the residual adipogenesis of the ERK1(-/-) cells, suggesting that ERK2 is not implicated in adipocyte differentiation. Our results clearly link ERK1 to the regulation of adipocyte differentiation, adiposity, and high-fat diet-induced obesity. This suggests that a therapeutic approach of obesity targeting specifically the ERK1 isoform and not ERK2 would be of particular interest.
Anglais

Diabetes (Diabetes)
Publisher American Diabetes Association
ISSN 0012-1797 (eISSN : 0012-1797)
internationale
02/2005
54
2
402-11

Adipocytes – Adipose Tissue – Animals – Blood Glucose – Cell Differentiation – Crosses – Genetic – Dietary Fats – Embryo – Mammalian – Energy Metabolism – Glucose Tolerance Test – Insulin – Isoenzymes – MAP Kinase Signaling System – Mice – Inbred C57BL – Knockout – Mitogen-Activated Protein Kinase 3 – Motor Activity – Stem Cells