Lipopolysaccharide influence on leptin hormone and tumor necrosis factor-alpha release from human adipose tissue. (3rd May 2018)

• Record Type: Journal Article
• Authors: Al-Lahham, Sa'ad; Jaradat, Nidal; Al-Qub, Malik; Hamayel, Abdallah; Assaassa, Abdalrahman; Hammad, Faris; Mosa, Ahmed; Nafaa, Fouad; Barqawi, Abdelkarem; Abdeen, Ziad
• Is Part Of: European journal of inflammation. Volume 16(2018)
• Publication Date: 2018-05-03
• Subjects: adipose tissue -- leptin -- lipopolysaccharide -- low-grade inflammation -- obesity -- TNF-α; Inflammation -- Periodicals; Anti-Inflammatory Agents -- therapeutic use -- Periodicals; Immunotherapy -- Periodicals; Inflammation -- Periodicals; Anti-inflammatory agents -- Periodicals; Immunotherapy -- Periodicals; Anti-inflammatory agents; Immunotherapy; Inflammation; Periodicals; 616.0473
• DOI: 10.1177/2058739218774975
• Languages: English
• ISSNs: 1721-727X

Abstract

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/m 2, 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.