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1 CNRS 8090, Institute of Biology, Pasteur Institute, Lille, France
2 Lille, France; CNRS 8090, Institute of Biology, Pasteur Institute, Lille, France
3 ERIT-M 0106, INSERM, Lille, France
4 Department of Endocrinology, Clinica Universitaria de Navarra, Spain
5 CNRS 8090, Institute of Biology, Pasteur Institute, Lille, France; Genomic Medicine, Imperial College London, London, United Kingdom
* To whom correspondence should be addressed. E-mail: odile.poulain{at}good.ibl.fr.
Obesity is characterized by systemic low-grade inflammation where adipose tissue, especially the omental depot, is thought to play a key role. We have previously shown that inflammation impairs 3T3-L1 preadipocyte cell line differentiation. To explore whether this interaction takes also place in vivo, the expression of several genes related to inflammation and adipocyte differentiation was assessed in human samples. Paired adipose tissue biopsies (from omental and subcutaneous depots) were obtained from 24 women: 6 lean normoglycaemic and 18 obese volunteers with different glycaemic states (normoglycaemic, glucose intolerant or type 2 diabetic). The expression levels of CD14, IL-18, leptin, adiponectin, SREBP1, PPAR
, PBEF1 (visfatin), GPD1, LPL, FABP4 and HIF1
were determined by quantitative real time PCR. CD14 and IL-18 were overexpressed in omental adipose tissue as compared to the subcutaneous depot irrespective of the subjects obesity or diabetes status. A significant decrease of LPL, GPD1 and leptin expression was observed in omental tissue and an inverse correlation between expression of CD14 and IL-18 and that of PPAR
, LPL and FABP4 was observed. The underexpression of omental lipogenic markers was more accentuated in the presence of glucose intolerance. Furthermore, adiponectin and SREBP1 expressions were also significantly decreased in omental tissue of type 2 diabetic patients. PBEF1 and HIF1
expressions remained comparable in all samples. Therefore, in humans, inflammation is increased in the omental depot as evidenced by CD14 and IL-18 expression. In this localisation, the inflammatory state is associated with a decreased expression of lipogenic markers, which is more pronounced in diabetic subjects.
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