Adipose Tissue Metabolic Evolution from Birth to Adulthood: Tracing Adipose Tissue Dysfunction from Early Life to Aging

Adipose tissue is not a static energy depot but a dynamic endocrine organ whose lipid composition, cellular architecture, and secretory profile evolve substantially across the life course. From fetal and perinatal development through childhood, adulthood, and aging, adipose tissue undergoes profound remodeling that shapes systemic energy balance, insulin sensitivity, and inflammatory tone. When this developmental trajectory is disrupted, the consequences extend well beyond adipose tissue itself, contributing to childhood and adult obesity, insulin resistance, and accelerated metabolic aging. Understanding the molecular and cellular mechanisms that govern this evolution – and identifying the points at which it goes awry – is central to explaining why some individuals develop metabolic disease early in life while others remain protected into adulthood.Recent research has begun to resolve this trajectory in increasing molecular detail. Lipidomic and multi-omics profiling of perinatal biospecimens has linked early growth parameters to specific lipid signatures, pointing to metabolic programming that begins before birth and shapes later adiposity. In pediatric and adult cohorts, comparative lipidomic and transcriptomic analyses across adipose depots have identified age- and depot-specific molecular signatures of dysfunction, suggesting that the mechanisms driving pediatric obesity are not simply a smaller-scale version of adult disease. This depot- and age-specific vulnerability extends to tissue composition: immune cell populations, including distinct macrophage subsets, accumulate differentially across adipose depots and life stages in obesity, and several genes and signaling pathways have recently been identified as regulators of adipose inflammation, fibrosis, and adipocyte differentiation – mechanistic links between tissue remodeling and the chronic low-grade inflammation that characterizes metabolic dysfunction. Beyond the fat depot itself, adipose-dispose-derived secreted mediators have been shown to propagate metabolic signals to distal organs such as the liver, illustrating how local adipose dysfunction can drive systemic disease, while recent reviews have synthesized how white adipose tissue dysfunction evolves across obesity and the aging process more broadly.This Research Topic invites contributions that trace the metabolic and cellular evolution of adipose tissue from birth to adulthood and identify the mechanisms linking early-life adipose programming to later metabolic pathology. We welcome Original Research, Reviews, and Perspective articles addressing, but not limited to, the following themes:• Perinatal and early-life adipose tissue programming, including cord blood and birth-parameter lipidomics• Comparative adipose tissue biology across childhood, adulthood, and aging• Adipose tissue immune cell heterogeneity, including macrophage subsets, in obesity and metabolic disease• Molecular regulators of adipose inflammation, fibrosis, and adipocyte differentiation• Adipose tissue-derived mediators and inter-organ crosstalk linking adipose dysfunction to systemic damage• Adipokine and lipid signaling in the transition from pediatric to adult obesity• Mechanisms of white adipose tissue dysfunction in aging and age-related metabolic decline• Multi-omics (lipidomics, transcriptomics, proteomics) approaches to adipose tissue remodeling across the life course Topic editors: David Sanchez-Infantes, Marijana Todorcevic, Bruno Ramos-Molina Source: https://www.frontiersin.org/research-topics/87135/adipose-tissue-metabolic-evolution-from-birth-to-adulthood-tracing-adipose-tissue-dysfunction-from-early-life-to-aging