Adipose Tissue Dynamics in Metabolic Regulation and Disorders
Summary
Adipose tissue is now recognised as a dynamic organ central to energy homeostasis and systemic metabolism. Beyond its role as an energy reservoir, adipose depots exert endocrine, immune and thermogenic functions that regulate glucose and lipid handling, inflammation and energy expenditure. White adipose tissue (WAT) engages in regulated expansion through hypertrophy and hyperplasia, whereas brown adipose tissue (BAT) dissipates energy via uncoupled respiration. Plasticity between these states, including beige adipocyte recruitment and WAT remodelling, underpins adaptation to nutritional and environmental cues. Dysregulation of adipose dynamics manifests in hypertrophic obesity, impaired adipogenesis, chronic inflammation and senescence of progenitor cells, promoting insulin resistance, dyslipidaemia and cardiometabolic disorders. Aging and genetic factors further influence adipose expandability, extracellular matrix remodelling and immune cell infiltration. Understanding the cellular cross-talk among adipocytes, stromal and immune compartments has revealed new mechanistic targets for therapeutic modulation of adipose function to treat obesity, type 2 diabetes and related pathologies.
Research from Nature Portfolio
Recent studies have uncovered that sympathetic neuron-derived neuropeptide Y sustains the niche of perivascular mural cells in both white and brown adipose depots, promoting thermogenic adipocyte progenitor proliferation and protecting against diet-induced obesity by sustaining energy expenditure independently of food intake. Parallel work demonstrates that transient postprandial interleukin-1β surges directly target early-stage adipocyte precursors, rapidly upregulating C/EBPβ and C/EBPδ to enhance white adipogenesis, whereas chronic elevation of the same cytokine blunts this physiological remodelling. A foundational investigation revealed that senescence in subcutaneous adipocyte progenitors impairs their commitment and fosters hypertrophic expansion of existing adipocytes, a hallmark of metabolic dysfunction that links genetic predisposition and aging to reduced adipogenic capacity and insulin resistance.
Adipose Tissue Dynamics in Metabolic Regulation and Disorders publication trend
The graph below shows the total number of articles in adipose tissue dynamics in metabolic regulation and disorders across all publications each year (not limited to Nature Index journals).
Technical terms
Adipogenesis: Differentiation of mesenchymal precursor cells into mature fat-storing adipocytes.
Hypertrophy: Enlargement of existing adipocytes due to increased lipid accumulation.
Hyperplasia: Increase in adipocyte number through proliferation and differentiation of progenitor cells.
Lipolysis: Enzymatic hydrolysis of stored triglycerides in adipocytes, releasing glycerol and free fatty acids.
Thermogenesis: Mitochondrial uncoupling in brown or beige adipocytes that dissipates energy as heat.
Mural cells: Perivascular progenitors in adipose tissue that can differentiate into thermogenic adipocytes.
References
- Thematic review series: Adipocyte Biology. Adipose tissue function and plasticity orchestrate nutritional adaptation. Journal of Lipid Research (2007).
- Sympathetic neuropeptide Y protects from obesity by sustaining thermogenic fat. Nature (2024).
- IL-1β promotes adipogenesis by directly targeting adipocyte precursors. Nature Communications (2024).
- Reduced subcutaneous adipogenesis in human hypertrophic obesity is linked to senescent precursor cells. Nature Communications (2019).
- Adipose tissue specific CCL18 associates with cardiometabolic diseases in non-obese individuals implicating CD4+ T cells. Cardiovascular Diabetology (2023).
- Impaired Remodeling of White Adipose Tissue in Obesity and Aging: From Defective Adipogenesis to Adipose Organ Dysfunction. Cells (2024).
- Adipose Tissue Hyperplasia and Hypertrophy in Common and Syndromic Obesity—The Case of BBS Obesity. Nutrients (2023).
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