Key Insight: A modified form of immunoglobulin G (IgG), known as fucosylated IgG, has been identified as a factor contributing to adipose tissue dysfunction during aging.

Study Reveals Fucosylated IgG as Key Driver of Age-Related Metabolic Decline

A study published in the journal Engineering has identified a modified form of immunoglobulin G (IgG), known as fucosylated IgG, as a factor contributing to adipose tissue dysfunction during aging. The research, conducted using mouse models, suggests that modulating the fucosylation of IgG may represent a potential avenue for addressing age-related metabolic disorders.

Study Details and Methods

Researchers from North China University of Technology (also reported as North China University of Science and Technology) and Capital Medical University analyzed epididymal white adipose tissue (eWAT) from young and aged mice. The team employed RNA sequencing to examine gene expression and conducted comprehensive N- and O-glycoproteomic profiling to identify changes in protein glycosylation patterns. Findings from the RNA sequencing were confirmed using quantitative polymerase chain reaction.

Key Findings

Gene Expression and Glycosylation

• RNA sequencing revealed a significant downregulation of adipogenic genes (genes involved in fat cell development) and an upregulation of inflammatory and fibrotic markers in the adipose tissue of aged mice.
• Glycoproteomic profiling showed widespread changes in glycosylation. The differentially glycosylated proteins identified were primarily located outside of cells and were involved in functions including innate immune responses, transport, signal transduction, and extracellular matrix-receptor interaction.
• Levels of IgG glycosylation were significantly increased in aged mice. Specifically, N-fucosylation of IgG1, IgG2a, and IgG3 was elevated. Increased O-fucosylation was detected only in IgG2a.

In Vivo Experiments

• In experiments with aged mice, reducing IgG levels through B-cell depletion led to an increase in adipogenic gene expression and a decrease in the expression of fibrotic markers.
• These effects were reversed when the mice were given either fucosylated or nonfucosylated IgG.
• When comparing the two forms, fucosylated IgG was found to exacerbate inflammation and fibrosis and more strongly inhibit adipogenesis than nonfucosylated IgG.

Conclusions and Implications

The authors concluded that the fucosylation of IgG contributes to metabolic decline, chronic inflammation, and fibrosis in aging adipose tissue. They proposed that modulating IgG fucosylation may represent a strategy to alleviate age-related metabolic disorders.

Publication Information

The paper, titled "Fucosylated IgG Contributes to Adipose Tissue Dysfunction During Aging," is authored by Jingyu Wang, Wei Su, Haotian Wang, Licui Liu, Jinlong Li, and Youxin Wang. It is available via the DOI: 10.1016/j.eng.2025.10.008.