LIGHT (lymphotoxin-like inducible protein that competes with glycoprotein D for herpes virus entry on T cells) is a cytokine in the TNF ligand superfamily that is expressed on activated T cells, monocytes, granulocytes and immature dendritic cells. LIGHT can stimulate cell growth or cell death and/or induce inflammatory cytokines. A recent study reported that transgenic mice that overexpressed LIGHT on T cells developed hyperlipidemia and show elevated cholesterol and triglyceride concentrations in the blood. The aim of this study was to analyze whether LIGHT has a role in human obesity associated inflammatory status. The clinical study included 190 subjects with different degrees of obesity and glucose tolerance. Circulating LIGHT concentrations was positively associated with body mass index (BMI), fat mass, triglycerides and negatively with HDL-cholesterol. Moreover, serum LIGHT levels were significantly increased in morbidly obese subjects and in patients with type 2 diabetes. The second part of this study was conducted with in vitro experiments using human differentiated adipocytes. The results showed that adipocytes from obese subjects spontaneously released pro-inflammatory cytokines and chemokines, but levels increased after treatment with LIGHT. The authors observed that LIGHT led to phosphorylation of NF-kB in human adipocytes, which is the transcription factor responsible for the induction of proinflammatory cytokines. LIGHT also upregulated the expression and synthesis of its own receptor (herpesvirus entry mediator (HVEM)) and decreased expression of genes involved in lipid metabolism such peroxisome proliferator-activated receptor-g (PPAR-g) and fatty acid synthase. These data suggest that LIGHT may have a role in the inflammatory state and dyslipidemia associated with obesity.
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