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Lysyl oxidase and adipose tissue dysfunction

Artikel i vetenskaplig tidskrift
Författare E. Pastel
E. Price
Kajsa Sjöholm
L. J. McCulloch
N. Rittig
N. Liversedge
B. Knight
N. Moller
Per-Arne Svensson
K. Kos
Publicerad i Metabolism - Clinical and Experimental
Volym 78
Sidor 118-127
ISSN 0026-0495
Publiceringsår 2018
Publicerad vid Institutionen för medicin
Sidor 118-127
Språk en
Länkar https://doi.org/10.1016/j.metabol.2...
Ämnesord Obesity, Fibrosis, Diabetes, Bariatric surgery, Inflammation, extracellular-matrix, insulin-resistance, metabolic profile, liver, fibrosis, weight-loss, obesity, hypoxia, expression, macrophages, adipocytes, Endocrinology & Metabolism
Ämneskategorier Endokrinologi och 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.

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