Inflammation and Metabolic Dysfunction in Obesity and Adipose Tissue

Obesity is accompanied by chronic low-grade inflammation within adipose depots. Excess energy storage drives adipocyte hypertrophy, local hypoxia and recruitment of immune cells, notably macrophages and T lymphocytes. These cells secrete pro-inflammatory cytokines such as tumour necrosis factor-α, interleukin-6 and monocyte chemoattractant protein-1, shifting the adipose microenvironment towards metabolic dysfunction. Dysregulated lipid handling in adipocytes elevates circulating free fatty acids, promoting ectopic lipid deposition in liver and muscle and disrupting insulin signalling. The ensuing insulin resistance underpins the metabolic syndrome, a cluster of central obesity, dyslipidaemia, hypertension and hyperglycaemia. Visceral adipose tissue is particularly prone to immune cell infiltration, amplifying systemic inflammation and escalating cardiometabolic risk worldwide. Advances in omics, imaging and computational approaches reveal heterogeneity within obese populations, identifying subgroups with discordant biomarker profiles and divergent disease trajectories. Interdisciplinary efforts now focus on inflammatory pathway modulation, nutritional strategies and precision risk stratification to curb obesity-related metabolic disease.

Research from Nature Portfolio

Recent studies enhance precision in cardiometabolic risk prediction by subclassifying individuals based on biomarker profiles discordant from body mass index (BMI). Unsupervised clustering in large European cohorts has revealed subpopulations whose lipid, glycaemic or inflammatory markers diverge from expected levels given their adiposity. Inclusion of these discordant profiles in predictive models improves identification of those at elevated risk of type 2 diabetes and major cardiovascular events. This approach underscores the role of inflammation-driven metabolic dysfunction beyond crude measures of adiposity, guiding more targeted interventions in obesity management.

Inflammation and Metabolic Dysfunction in Obesity and Adipose Tissue publication trend

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

Technical terms

Adipose tissue: Specialized connective tissue for energy storage, comprising adipocytes and resident immune cells.

Insulin resistance: Impaired cellular response to insulin, leading to reduced glucose uptake and elevated blood glucose.

Metabolic syndrome: Cluster of metabolic abnormalities including central obesity, dyslipidaemia, hypertension and hyperglycaemia.

Cytokines: Small signalling proteins secreted by cells to regulate immunity and inflammation.

Adipokines: Bioactive molecules released by adipose tissue that influence metabolic and inflammatory processes.

Visceral adipose tissue: Fat stored within the abdominal cavity, closely associated with systemic metabolic risk.

References

1. Subclassification of obesity for precision prediction of cardiometabolic diseases. Nature Medicine (2024).
2. Association between systemic immune-inflammation index and metabolic syndrome and its components: results from the National Health and Nutrition Examination Survey 2011–2016. Journal of Translational Medicine (2023).
3. Molecular tracking of insulin resistance and inflammation development on visceral adipose tissue. Frontiers in Immunology (2023).
4. Endothelial Dysfunction in Obesity-Induced Inflammation: Molecular Mechanisms and Clinical Implications. Biomolecules (2020).
5. Mechanisms of Obesity-Induced Inflammation and Insulin Resistance: Insights into the Emerging Role of Nutritional Strategies. Frontiers in Endocrinology (2013).