The Wnt antagonist and secreted frizzled-related protein 5: implications on lipid metabolism, inflammation, and type 2 diabetes mellitus | Zendy

Lingbin Liu | Zendy; Xiaohong Chen | Zendy; Xiangyu Zhou | Zendy; Qing Zhu | Zendy

Open Access

The Wnt antagonist and secreted frizzled-related protein 5: implications on lipid metabolism, inflammation, and type 2 diabetes mellitus

Author(s) -

Lingbin Liu,

Xiaohong Chen,

Xiangyu Zhou,

Qing Zhu

Publication year - 2018

Publication title -

bioscience reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.938

H-Index - 77

eISSN - 1573-4935

pISSN - 0144-8463

DOI - 10.1042/bsr20180011

Subject(s) - wnt signaling pathway , frizzled , microbiology and biotechnology , inflammation , signal transduction , biology , adipokine , insulin receptor , lipid signaling , endocrinology , medicine , insulin resistance , insulin , immunology

Various reports have suggested that secreted frizzled-related protein (SFRP) 5 (SFRP5) plays a regulatory role in the processes of cellular proliferation and differentiation, by means of inactivating the Wnt/β-catenin signaling pathway. Recently, SFRP5 has been identified as an anti-inflammatory adipokine, which may be induced during preadipocyte proliferation, differentiation, and maturation. This review aims to identify the recent progress in the research and development of SFRP5 that can play a role in influencing lipid metabolism, inflammation, and type 2 diabetes mellitus (T2DM). Recent evidence has indicated that SFRP5 is capable of stimulating adipocyte differentiation via inhibition of the Wnt/β-catenin signaling pathway. In addition, SFRP5 binding with wingless-type murine mammary tumor virus integration site family, member 5A (Wnt5a), inhibits the activation of c-Jun N-terminal kinase (JNK) downstream of the Wnt signaling pathway. An antagonistic relationship has been found between the reductions in inflammatory cytokine production and serine phosphorylation of insulin receptor substrate-1 (IRS-1) in regard to inhibition of insulin signaling network. By this mechanism, SFRP5 exerts its influence on metabolic function. Based on our review of the current available literature, we support the notion that SFRP5 can be used as a therapeutic target in the treatment of T2DM.

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