Editorial
Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. May 15, 2015; 6(4): 548-553
Published online May 15, 2015. doi: 10.4239/wjd.v6.i4.548
Adipose tissue fibrosis
Christa Buechler, Sabrina Krautbauer, Kristina Eisinger
Christa Buechler, Sabrina Krautbauer, Kristina Eisinger, Department of Internal Medicine I, University Hospital of Regensburg, 93042 Regensburg, Germany
Author contributions: All authors contributed to this manuscript.
Supported by A grant of the German Research Foundation (BU 1141/8-1).
Conflict-of-interest: The authors certify that there is no conflict of interest in relation to this article.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Christa Buechler, PhD, Department of Internal Medicine I, University Hospital of Regensburg, Franz-Josef-Strauß-Allee 11, 93042 Regensburg, Germany. christa.buechler@klinik.uni-regensburg.de
Telephone: +49-941-9447009 Fax: +49-941-9447019
Received: November 10, 2014
Peer-review started: November 11, 2014
First decision: December 26, 2014
Revised: January 12, 2015
Accepted: February 9, 2015
Article in press: February 11, 2015
Published online: May 15, 2015
Processing time: 186 Days and 0.6 Hours
Abstract

The increasing prevalence of obesity causes a major interest in white adipose tissue biology. Adipose tissue cells are surrounded by extracellular matrix proteins whose composition and remodeling is of crucial importance for cell function. The expansion of adipose tissue in obesity is linked to an inappropriate supply with oxygen and hypoxia development. Subsequent activation of hypoxia inducible factor 1 (HIF-1) inhibits preadipocyte differentiation and initiates adipose tissue fibrosis. Thereby adipose tissue growth is limited and excess triglycerides are stored in ectopic tissues. Stressed adipocytes and hypoxia contribute to immune cell immigration and activation which further aggravates adipose tissue fibrosis. There is substantial evidence that adipose tissue fibrosis is linked to metabolic dysfunction, both in rodent models and in the clinical setting. Peroxisome proliferator activated receptor gamma agonists and adiponectin both reduce adipose tissue fibrosis, inflammation and insulin resistance. Current knowledge suggests that antifibrotic drugs, increasing adipose tissue oxygen supply or HIF-1 antagonists will improve adipose tissue function and thereby ameliorate metabolic diseases.

Keywords: Collagen; Hypoxia; Insulin resistance; Immune cells; Adipocyte

Core tip: The close association of adipose tissue fibrosis and metabolic complications in obesity has been corroborated in rodent and human studies. Adipose tissue hypoxia initiates fibrosis which is further aggravated by inflammation. In adipose tissue preadipocytes, adipocytes and resident macrophages produce collagen showing that the fibrotic process differs from the extensively studied scar formation in the liver. Strategies to resolve fibrosis in fat tissues thereby promoting healthy adipose tissue growth are suggested to improve metabolic situation in obese patients.