Although the transcription factor Sox8 is broadly expressed during embryogenesis in developing ectodermal and mesodermal tissues, mice develop surprisingly normally in the absence of Sox8. Phenotypes in adult Sox8-deficient mice include mild osteopenia, late-onset male infertility, and reduced weight. We show here that progressive degeneration of adipose tissue in adult Sox8-deficient mice significantly contributes to weight reduction. Although serum levels of leptin, IGF-1, and noradrenaline were altered in Sox8-deficient mice, these changes could not explain the observed phenotype. Other serum parameters, including indicators of glucose metabolism, were largely normal. However, expression of the preadipocyte marker Pref-1 was elevated in adipose tissues of Sox8-deficient mice. This increase correlated with an impaired differentiation of Sox8-deficient fibroblasts to adipocytes in culture, a defect that could be rescued by reintroducing Sox8 into the cells. Furthermore, Sox8 levels were higher in mesodermal precursors than in mature adipocytes. We postulate a precursor-intrinsic role of Sox8 during replenishment of the adipocyte pool in adult mice and assume that disturbance of this function significantly contributes to adipose tissue degeneration in Sox8-deficient mice.
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rdfs:comment |
Although the transcription factor Sox8 is broadly expressed during embryogenesis in developing ectodermal and mesodermal tissues, mice develop surprisingly normally in the absence of Sox8. Phenotypes in adult Sox8-deficient mice include mild osteopenia, late-onset male infertility, and reduced weight. We show here that progressive degeneration of adipose tissue in adult Sox8-deficient mice significantly contributes to weight reduction. Although serum levels of leptin, IGF-1, and noradrenaline were altered in Sox8-deficient mice, these changes could not explain the observed phenotype. Other serum parameters, including indicators of glucose metabolism, were largely normal. However, expression of the preadipocyte marker Pref-1 was elevated in adipose tissues of Sox8-deficient mice. This increase correlated with an impaired differentiation of Sox8-deficient fibroblasts to adipocytes in culture, a defect that could be rescued by reintroducing Sox8 into the cells. Furthermore, Sox8 levels were higher in mesodermal precursors than in mature adipocytes. We postulate a precursor-intrinsic role of Sox8 during replenishment of the adipocyte pool in adult mice and assume that disturbance of this function significantly contributes to adipose tissue degeneration in Sox8-deficient mice.
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skos:exactMatch | |
uniprot:name |
J. Lipid Res.
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uniprot:author |
Guth S.I.,
Hess A.,
Schmidt K.,
Wegner M.
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uniprot:date |
2009
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uniprot:pages |
1269-1280
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uniprot:title |
Adult-onset degeneration of adipose tissue in mice deficient for the Sox8 transcription factor.
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uniprot:volume |
50
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dc-term:identifier |
doi:10.1194/jlr.M800531-JLR200
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