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The WNT inhibitor Dickkopf-Related Protein 1 and Bone Morphogenetic Protein 4 rescue adipogenesis in hypertrophic obesity in man.

Artikel i vetenskaplig tidskrift
Författare Birgit Gustafson
Ulf Smith
Publicerad i Diabetes
Volym 61
Nummer/häfte 5
Sidor 1217-1224
ISSN 0012-1797
Publiceringsår 2012
Publicerad vid Institutionen för medicin, avdelningen för molekylär och klinisk medicin
Sidor 1217-1224
Språk en
Ämneskategorier Cell- och molekylärbiologi

Sammanfattning

Overweight characterized by inappropriate expansion of adipose cells (hypertrophic obesity) is associated with the metabolic syndrome and is caused by an inability to recruit and differentiate new precursor cells. We examined the role of bone morphogenetic protein 4 (BMP4) and WNT activation in the regulation of human adipose cell differentiation. Cluster of differentiation (CD)14+/45+ and CD31+ cells were first removed before the remaining stromal vascular cells of human subcutaneous biopsy specimens were differentiated with/without different WNT inhibitors and/or BMP4. Inhibition of WNT and induction of Dickkopf 1 (DKK1) were markers of precursor cells undergoing excellent differentiation. The addition of DKK1 inhibited WNT activation and promoted adipogenesis in cells with a low degree of differentiation. The positive effect of DKK1, inhibiting cellular WNT activation by binding to the Kremen/LDL receptor–related protein receptors, was not seen with inhibitors of secreted WNT ligands. BMP4 increased differentiation, and BMP4 in the presence of DKK1 produced an additive effect. There was an apparent cross-talk between differentiation and commitment because BMP4 expression increased in differentiating adipocytes, and the addition of the BMP4 inhibitor, Noggin, reduced precursor cell differentiation. Thus, differentiated human adipose cells can promote adipogenesis via endogenous BMP4 activation, and the impaired adipogenesis in hypertrophic obesity is mainly due to an inability to suppress canonical WNT and to induce DKK1.

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