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Altered Subcutaneous Adipose Tissue Response to Systemic LPS Administration in Patients with Type 2 Diabetes | OMICS International | Abstract
ISSN: 2155-6156

Journal of Diabetes & Metabolism
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Research Article

Altered Subcutaneous Adipose Tissue Response to Systemic LPS Administration in Patients with Type 2 Diabetes

Mathur N1, Andreasen AS1,2, Berg RMG1, Pedersen M1, Møller K1,2,3, Pedersen BK1* and Laye MJ1

1Centre of Inflammation and Metabolism, Department of Infectious Diseases and CMRC, Rigshospitalet, University of Copenhagen, Denmark

2Intensive Care Unit 4131, University Hospital Rigshospitalet, Copenhagen, Denmark

3Neurointensive Care Unit, Department of Neuroanaesthesiology, University Hospital Rigshospitalet, Copenhagen, Denmark

*Corresponding Author:
Bente Klarlund Pedersen
Centre of Inflammation and Metabolism
Rigshospitalet- Section 7641
Blegdamsvej 9, DK-2100, Copenhagen, Denmark
Tel: +45 35457797
Fax: +45 35 45 76 44
E-mail: [email protected]

Received date August 16, 2012; Accepted date October 11, 2012; Published date October 17, 2012

Citation: Mathur N, Andreasen AS, Berg RMG, Pedersen M, Møller K, et al. (2012) Altered Subcutaneous Adipose Tissue Response to Systemic LPS Administration in Patients with Type 2 Diabetes. J Diabetes Metab 3:217. doi:10.4172/2155-6156.1000217

Copyright: © 2012 Mathur N, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Aim: Inflammation is thought to play a major role in impaired metabolism. However, the metabolic and inflammatory response of adipose tissue, to a pro-inflammatory stimulus is poorly defined in patients with Type 2 Diabetes Mellitus (T2DM). We therefore aimed to investigate whether adipose tissue in T2DM would display an altered response to E. coli LipoPolySaccharide (LPS).
Materials and methods: Twelve patients with T2DM and 12 control subjects received an intravenous bolus injection of LPS (0.3 ng/kg). Abdominal subcutaneous adipose tissue biopsies, serum and plasma were obtained at 0, 2, 4, 6 and 8 hours after LPS. The gene expression of Tumour Necrosis Factor-α (TNF), InterLeukin-6 (IL-6), lipoprotein lipase (LPL), hormone sensitive lipase (HSL), fatty acid synthase (FASN), adiponectin and peroxisome proliferator-activated recptor γ (PPARγ) was analysed by real time reverse transcription Polymerase Chain Reaction (PCR).
Results: The expression of TNF and IL-6 in adipose tissue increased after LPS administration without any difference between groups (2-way ANOVA, effect of time: p<0.001 and p=0.0001, respectively). In contrast, the expression of LPL, HSL and adiponectin in adipose tissue increased only in control subjects (2-way ANOVA, effect of time X group: p=0.03; p=0.02 and p=0.02, respectively). There was no effect of LPS on FASN or PPARγ in either group.
Conclusion: Patients with T2DM demonstrate a resistance to LPS in terms of inducing important mediators of lipolysis and lipogenesis, although the expression of TNF and IL-6 in adipose tissue increased in both groups. And thus, adipose tissue may contribute to the acute inflammation-related metabolic complications seen in T2DM.

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