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LIGHT (TNFSF14) inhibits adipose differentiation without affecting adipocyte metabolism
G Tiller1, H Laumen, P Fischer-Posovszky
1Else Kröner-Fresenius-Zentrum für Ernährungsmedizin, Technische Universität München, Freising, Germany.
Objective:
The member of the tumor necrosis factor family LIGHT (lymphotoxin-like inducible protein that competes with glycoprotein D for herpesvirus entry on T cells; TNFSF14 (tumor necrosis factor super family protein 14) is primarily expressed in lymphocytes, in which it induces the expression of pro-inflammatory cytokines and alterations of lipid homeostasis. Recently, the protein was shown to be upregulated in obesity and to induce cytokine secretion from adipocytes.
Research Methods And Procedures:
Using an automated complementary DNA (cDNA) screen, LIGHT was identified to inhibit adipose differentiation. As cellular models for adipogenesis mouse 3T3-L1, human SGBS (Simpson-Golabi-Behmel syndrome) and primary human preadipocytes differentiated in vitro were used as well as primary human adipocytes to study adipocyte functions. Analysis of lipid deposition by Oil Red O staining, mRNA expression by quantitative reverse transcriptase-PCR, nuclear factor (NF)-κB activation as well as protein secretion by enzyme linked immunosorbent assay and Luminex technology was performed.
Results:
LIGHT was found to inhibit lipid accumulation in the three models of preadipocytes in a dose-dependent manner without cytotoxic effects. This inhibition of differentiation was probably because of interference at early steps of adipogenesis, as early exposure during differentiation showed the strongest effect, as assessed by decreased peroxisome proliferator-activated receptor-γ (PPARγ) and CCAAT/enhancer-binding protein-α (C/EBPα) mRNA expression. In contrast to TNFα, basal and insulin-stimulated glucose uptake and lipolysis of terminally differentiated mature adipocytes were not altered in the presence of LIGHT. At a concentration sufficient to inhibit differentiation, secretion of proinflammatory cytokines was not significantly induced and NF-κB activity was only modestly induced compared with TNFα.
Conclusion:
LIGHT is a novel inhibitor of human adipocyte differentiation without adversely influencing central metabolic pathways in adipocytes.
Insights
LIGHT (TNFSF14) inhibits human adipocyte differentiation by interfering with early adipogenesis steps. This novel inhibitor does not affect mature adipocyte functions or induce significant inflammation, offering potential therapeutic avenues.
Area of Science:
- Cell Biology
- Molecular Biology
- Endocrinology
Background:
- Tumor Necrosis Factor (TNF) family member LIGHT (TNFSF14) is expressed in lymphocytes and influences cytokine production and lipid homeostasis.
- LIGHT is upregulated in obesity and can induce cytokine secretion from adipocytes.
Purpose of the Study:
- To investigate the role of LIGHT in adipocyte differentiation and function.
- To determine if LIGHT impacts lipid accumulation and adipogenesis in cellular models.
Main Methods:
- Utilized automated cDNA screening to identify LIGHT's role in adipogenesis.
- Employed 3T3-L1, SGBS, and primary human preadipocytes/adipocytes for differentiation and function studies.
- Assessed lipid deposition, gene expression (PPARγ, C/EBPα), NF-κB activation, and protein secretion.
Main Results:
- LIGHT dose-dependently inhibited lipid accumulation in preadipocytes without cytotoxicity.
- Inhibition occurred at early adipogenesis stages, evidenced by reduced PPARγ and C/EBPα mRNA.
- Mature adipocyte functions (glucose uptake, lipolysis) and pro-inflammatory cytokine secretion were not significantly altered by LIGHT.
Conclusions:
- LIGHT is a novel inhibitor of human adipocyte differentiation.
- LIGHT does not adversely affect key metabolic pathways in mature adipocytes.
