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The Extracellular Signal–Regulated Kinase Isoform ERK1 Is Specifically Required for In Vitro and In Vivo Adipogenesis

¹ Institut National de la Santé et de la Recherche Médicale (INSERM) Unité 568, IFR 50, Faculté de Médecine, Université de Nice Sophia Antipolis, Nice, France
² Unité Mixte de Recherche (UMR) INRA/INA Physiologie de la Nutrition et du Comportement, Paris, France
³ Centre National de la Recherche Scientifique (CNRS) Unité Mixte de Recherche (UMR) 6543, Faculté des Sciences, Université de Nice Sophia Antipolis, Nice, France
⁴ Institut National de la Santé et de la Recherche Médicale (INSERM) E 0215 and Laboratory of Clinical and Experimental Pathology, Faculté de Médecine and Pasteur Hospital, Université de Nice Sophia Antipolis, Nice, 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.

Abbreviations: ERK, extracellular signal–regulated kinase; JNK, c-Jun NH₂-terminal kinase; MEK, mitogen-activated protein/ERK kinase; PPAR, peroxisome proliferator–activated receptor; RQ, respiratory quotient

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