To the top

Page Manager: Webmaster
Last update: 9/11/2012 3:13 PM

Tell a friend about this page
Print version

Lysyl oxidase and adipose… - University of Gothenburg, Sweden Till startsida
To content Read more about how we use cookies on

Lysyl oxidase and adipose tissue dysfunction

Journal article
Authors E. Pastel
E. Price
Kajsa Sjöholm
L. J. McCulloch
N. Rittig
N. Liversedge
B. Knight
N. Moller
Per-Arne Svensson
K. Kos
Published in Metabolism - Clinical and Experimental
Volume 78
Pages 118-127
ISSN 0026-0495
Publication year 2018
Published at Institute of Medicine
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 118-127
Language en
Keywords Obesity, Fibrosis, Diabetes, Bariatric surgery, Inflammation, extracellular-matrix, insulin-resistance, metabolic profile, liver, fibrosis, weight-loss, obesity, hypoxia, expression, macrophages, adipocytes, Endocrinology & Metabolism
Subject categories Endocrinology and Diabetes


Background/objectives. Lysyl oxidase (LOX) is an enzyme crucial for collagen fibre crosslinking and thus for fibrosis development. Fibrosis is characterised by a surplus of collagen fibre accumulation and is amongst others also a feature of obesity-associated dysfunctional adipose tissue (AT) which has been linked with type 2 diabetes. We hypothesised that in type 2 diabetes and obesity LOX expression and activity will be increased as a consequence of worsening AT dysfunction. This study aimed to provide a comprehensive characterisation of LOX in human AT. Methods. LOX mRNA expression was analysed in omental and abdominal subcutaneous AT obtained during elective surgery from subjects with a wide range of BMI, with and without diabetes. In addition, LOX expression was studied in subcutaneous AT before and 9.5 months after bariatric surgery. To study the mechanism of LOX changes, its expression and activity were assessed after either hypoxia, recombinant human leptin or glucose treatment of AT explants. In addition, LOX response to acute inflammation was tested after stimulation by a single injection of lipopolysaccharide versus saline solution (control) in healthy men, in vivo. Quantity of mRNA was measured by RT-qPCR. Results. LOX expression was higher in obesity and correlated with BMI whilst, in vitro, leptin at high concentrations, as a potential feedback mechanism, suppressed its expression. Neither diabetes status, nor hyperglycaemia affected LOX. Hypoxia and lipopolysaccharide-induced acute inflammation increased LOX AT expression, latter was independent of macrophage infiltration. Conclusions. Whilst LOX may not be affected by obesity-associated complications such as diabetes, our results confirm that LOX is increased by hypoxia and inflammation as underlying mechanism for its upregulation in adipose tissue with obesity. (C) 2017 Elsevier Inc. All rights reserved.

Page Manager: Webmaster|Last update: 9/11/2012

The University of Gothenburg uses cookies to provide you with the best possible user experience. By continuing on this website, you approve of our use of cookies.  What are cookies?