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Activation of Canonical Wingless-type MMTV Integration Site Family (Wnt) Signaling in Mature Adipocytes Increases Beta-Catenin Levels and Leads to Cell Dedifferentiation and Insulin Resistance

Artikel i vetenskaplig tidskrift
Författare Birgit Gustafson
Ulf Smith
Publicerad i The Journal of Biological Chemistry
Volym 285
Sidor 14031-14041
ISSN 0021-9258
Publiceringsår 2010
Publicerad vid Institutionen för medicin, avdelningen för molekylär och klinisk medicin
Sidor 14031-14041
Språk en
Länkar dx.doi.org/10.1074/jbc.M110.102855
Ämnesord Adipose Tissue, Diabetes, Differentiation, Glucose Transport, PPAR, Transformation, Tumor Necrosis Factor
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

Canonical Wnt ligands are secreted by several cell types in the adipose tissue. We examined if mature adipocytes can also be target cells and found that canonical Wnt activation by Wnt3a induced a marked dedifferentiation of both 3T3-L1 and human adipocytes. Typical adipogenic markers were reduced while undifferentiated cell markers like Pref-1/Dlk1, Wnt10b, and Gata2 were increased. The cells also became insulin-resistant with impaired upstream insulin signaling and reduced glucose uptake. Wnt3a stabilized B-catenin in the absence of the LRP6 receptor and with maintained axin and Dickkopf-1 protein expression. PPARgamma was repressed and PPARgamma ligands could not restore the adipogenic markers or reduce the B-catenin levels. The dedifferentiated adipocytes expressed the myofibroblast marker alpha-smooth muscle actin and were also susceptible to osteogenic transdifferentiation. These results identify a novel pathway in mature adipose cells that is critical for maintaining the normal adipocyte phenotype and insulin sensitivity.

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