Loss of periostin ameliorates adipose tissue inflammation and fibrosis in vivo View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-06-04

AUTHORS

Fumiko Nakazeki, Masataka Nishiga, Takahiro Horie, Hitoo Nishi, Yasuhiro Nakashima, Osamu Baba, Yasuhide Kuwabara, Tomohiro Nishino, Tetsushi Nakao, Yuya Ide, Satoshi Koyama, Masahiro Kimura, Shuhei Tsuji, Naoya Sowa, Shigeo Yoshida, Simon J. Conway, Motoko Yanagita, Takeshi Kimura, Koh Ono

ABSTRACT

Recent evidence suggests that the accumulation of macrophages as a result of obesity-induced adipose tissue hypoxia is crucial for the regulation of tissue fibrosis, but the molecular mechanisms underlying adipose tissue fibrosis are still unknown. In this study, we revealed that periostin (Postn) is produced at extraordinary levels by adipose tissue after feeding with a high-fat diet (HFD). Postn was secreted at least from macrophages in visceral adipose tissue during the development of obesity, possibly due to hypoxia. Postn−/− mice had lower levels of crown-like structure formation and fibrosis in adipose tissue and were protected from liver steatosis. These mice also showed amelioration in systemic insulin resistance compared with HFD-fed WT littermates. Mice deficient in Postn in their hematopoietic compartment also had lower levels of inflammation in adipose tissue, in parallel with a reduction in ectopic lipid accumulation compared with the controls. Our data indicated that the regulation of Postn in visceral fat could be beneficial for the maintenance of healthy adipose tissue in obesity. More... »

PAGES

8553

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41598-018-27009-9

DOI

http://dx.doi.org/10.1038/s41598-018-27009-9

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1104306748

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29867212


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