Key result
POSTN deletion protected mice from lipopolysaccharide- and obesity-induced adipose tissue fibrosis and improved insulin resistance.
Why the study?
Periostin is a matricellular protein, but its functions in adipose fibrosis remain unclear.
Periostin deficiency protects against LPS- and obesity-induced adipose tissue fibrosis and improves insulin resistance in mice, suggesting a potential therapeutic target for type II diabetes.
Periostin (POSTN) is a type of matricellular protein, but its functions in adipose fibrosis remain unclear. Here, we found that POSTN expression is significantly increased in mouse adipose tissue after treatment with lipopolysaccharide (LPS) or a high-fat diet (HFD) and that adipose progenitor cells are the main source of POSTN. In our mouse model of fibrosis, POSTN deletion protected mice from adipose fibrosis, probably through reducing the accumulation of macrophages and promoting adipocyte differentiation of progenitor cells. Taken together, our study demonstrates that POSTN deficiency attenuates adipose tissue fibrosis and improves insulin resistance, providing new insights into the diagnosis and treatment of type II diabetes by targeting adipose tissue fibrosis.
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Yang et al. (2021) studied Adipose tissue fibrosis and insulin resistance. POSTN deletion was evaluated on Adipose tissue fibrosis and insulin resistance. POSTN deletion protected mice from lipopolysaccharide- and obesity-induced adipose tissue fibrosis and improved insulin resistance.
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