A functional role for the p62-ERK1 axis in the control of energy homeostasis and adipogenesis.
In vivo genetic inactivation of the signalling adapter p62 leads to mature-onset obesity and insulin resistance, which correlate with reduced energy expenditure (EE) and increased adipogenesis, without alterations in feeding or locomotor functions. Enhanced extracellular signal-regulated kinase (ERK) activity in adipose tissue from p62-knockout (p62(-/-)) mice, and differentiating fibroblasts, suggested ... an important role for this kinase in the metabolic alterations of p62(-/-) mice. Here, we show that genetic inactivation of ERK1 in p62(-/-) mice reverses their increased adiposity and adipogenesis, lower EE and insulin resistance. These results establish genetically that p62 is a crucial regulator of ERK1 in metabolism.
Mesh Terms:
Adipocytes, Adipogenesis, Animals, Cell Differentiation, Extracellular Signal-Regulated MAP Kinases, Fibroblasts, Humans, Insulin, Mice, Mice, Inbred C57BL, Mice, Knockout, Models, Genetic, Obesity, Recombinant Proteins, Transcription Factors
Adipocytes, Adipogenesis, Animals, Cell Differentiation, Extracellular Signal-Regulated MAP Kinases, Fibroblasts, Humans, Insulin, Mice, Mice, Inbred C57BL, Mice, Knockout, Models, Genetic, Obesity, Recombinant Proteins, Transcription Factors
EMBO Rep.
Date: Mar. 01, 2010
PubMed ID: 20154642
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