Periostin Promotes White Adipose Tissue Fibrosis By Altering The Functions Of Adipose-Derived Stem Cells And Macrophages

Obesity is one of main challenges of human health in modern society.However,we do not fully understand the cellular origin of WAT fibrosis.Here,we show that adipocyte progenitor-derived extracellular matrix(ECM)protein periostin expression is increased in the fibrotic eWAT of mice either fed high-fat diet(HFD)or intraperitoneally injected lipopolysaccharide(LPS).Periostin plays important roles in the development of AT fibrosis.Periostin accelerates the accumulation of local macrophages in eWAT through activated their proliferation and recruitment.Meanwhile,periostin promotes a phenotypic shift toward CD9high fibrogenic cells,driving pathological remodeling and altering WAT function in obesity.In addition,knockout of POSTN gene weakens the pro-inflammation ability of BMDM from LPS injected mice.These findings correlates the expression level of periostin in white adipose tissue(WAT)with WAT fibrosis level,insulin-resistance severity,and type 2 diabetes.Collectively,our data suggest that in addition to representing a WAT adipogenic niche,different periostin expression levels modulate WAT fibrogenesis and are associated with loss of metabolic fitness.