Immunometabolism in Adipose Tissue Inflammation

Adipose tissue serves not only as an energy reservoir but also as a dynamic immunoregulatory site. In the context of positive energy balance, adipocytes undergo hypertrophy and metabolic stress, triggering a shift in local immune cell populations and activating proinflammatory programmes. This bidirectional crosstalk, coined immunometabolism, encompasses metabolic rewiring of immune cells—such as macrophages, neutrophils and T lymphocytes—within visceral and subcutaneous fat depots. Chronic low-grade inflammation emerging from these processes underpins insulin resistance, type 2 diabetes and cardiovascular disease. Advances in single-cell profiling and metabolic tracing have revealed how nutrient fluxes, lipid intermediates and adipokines shape immune cell fate and function. Understanding the molecular basis of adipose immunometabolism holds promise for interventions aimed at restoring tissue homeostasis and improving metabolic health globally.

Research from Nature Portfolio

Recent studies have demonstrated that the interaction between host diet and the gut microbiome can dictate neutrophil recruitment into visceral adipose tissue. In experimental models, transfer of microbiome from individuals with obesity combined with high-fat feeding led to a transient surge in neutrophils, subsequent expansion of Th1 cells and diminution of regulatory T cells, culminating in adipose inflammation and impaired insulin sensitivity. Parallel work has identified antigen presentation by adipocytes themselves as a critical determinant of T cell subset balance. Genetic ablation of major histocompatibility complex class II on adipocytes prevented the usual shift towards interferon-γ-producing Th1 cells and preserved regulatory T cell abundance, thereby attenuating diet-induced adipose inflammation and systemic insulin resistance. These findings position both neutrophil dynamics and adipocyte antigen presentation as tractable targets for restoring immunometabolic equilibrium.

Immunometabolism in Adipose Tissue Inflammation publication trend

The graph below shows the total number of articles in immunometabolism in adipose tissue inflammation across all publications each year (not limited to Nature Index journals).

Technical terms

Adipocyte: A fat cell specialised for lipid storage and endocrine signalling.

Immunometabolism: The interplay between immune cell function and metabolic pathways.

Visceral adipose tissue (VAT): Fat depot surrounding internal organs, prone to inflammatory changes in obesity.

Regulatory T cell (Treg): A T lymphocyte subset that suppresses excessive immune responses.

Th1 cell: A T helper cell subset that produces interferon-γ and promotes inflammation.

Neutrophil: A granulocytic leukocyte that acts as an early responder in inflammation.

Major histocompatibility complex class II (MHCII): A protein complex on antigen-presenting cells that activates CD4+ T cells.

Gut microbiome: The community of microorganisms in the gastrointestinal tract influencing host immunity and metabolism.

Insulin resistance: A pathological state in which cells fail to respond effectively to insulin, leading to impaired glucose uptake.

References

1. Obesity-associated microbiomes instigate visceral adipose tissue inflammation by recruitment of distinct neutrophils. Nature Communications (2024).
2. Adipocyte adaptive immunity mediates diet-induced adipose inflammation and insulin resistance by decreasing adipose Treg cells. Nature Communications (2017).
3. Orchestration of the Adipose Tissue Immune Landscape by Adipocytes. Annual Review of Physiology (2024).
4. Adipose failure through adipocyte overload and autoimmunity. Autoimmunity Reviews (2023).
5. Adipose Tissue-Resident Immune Cells in Obesity and Type 2 Diabetes. Frontiers in Immunology (2019).