Obesity is associated with low-grade inflammation that originates mainly from adipose tissue. This is implicated in the
pathogenesis of type-2 diabetes and cardiovascular diseases. Strong evidence indicates that chronically elevated systemic
low-grade lipopolysaccharide (LPS), elicits low-grade inflammation. However, evidence on LPS effect on adipokines’
level, such as leptin, is scarce, and it has never been investigated ex vivo in human subcutaneous adipose tissue (SAT)
and therefore we aim to investigate this. To achieve our aim, SAT explants were obtained from 12 patients (50% males)
and were treated with/without LPS. Protein concentration was determined by enzyme-linked immunosorbent assay
(ELISA). We found that the average age and body mass index (BMI) of included patients were 58.6 years and 28.6 kg/
m2, respectively. LPS induced significantly (~3×, P < 0.0001) the secretion of tumor necrosis factor (TNF)-α from SAT,
and it was not associated with age or BMI. However, leptin secretion was inhibited slightly (~20%), but significantly.
Interestingly, leptin release was significantly inhibited (~50%) in SAT from lean but not from obese patients, and there
was an association between leptin response and BMI (R = 0.8), but no association with age. In this study, we found, for
the first time, that LPS suppresses the release of leptin hormone from SAT obtained from lean patients, while it induces
TNF-α release. Our findings provide extra evidence and confirm earlier studies regarding the role of LPS in low-grade
inflammation. Further investigations are essential to identify factors that inhibit LPS passage through intestinal barrier in
order to prevent or reduce the development of obesity and its associated chronic diseases.

Title

European Journal of Inflammation

Publisher

Sage

Publisher Country

United States of America

Indexing

Thomson Reuters

Impact Factor

0.936

Publication Type

Prtinted only

Volume

16

Year

2018

Pages

1-5