Current obesity reports · 2026
Adipose Tissue Remodeling Beyond Weight Loss: New Insights Into Incretin-Based Therapies and Bariatric Surgery.
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Abud Gabriela Ferreira, de Freitas Ellen Cristini, Stanford Kristin I
Аннотация
PURPOSE OF THE REVIEW: This review summarizes obesity-induced adaptations in subcutaneous and visceral white adipose tissue (WAT) depots and discusses how incretin-based pharmacotherapies and bariatric surgery may influence WAT remodeling beyond weight loss, drawing on evidence from animal models and human studies.
RECENT FINDINGS: In obesity, adipose tissue undergoes pathological remodeling characterized by structural and cellular changes, extracellular matrix (ECM) remodeling, altered endocrine signaling, and impaired mitochondrial function that contribute to metabolic comorbidities. Weight-loss interventions, including incretin-based therapies and bariatric surgery, are associated with improvements in adiposity and metabolic outcomes, and multiple studies suggest accompanying changes in inflammatory, mitochondrial/thermogenic, and endocrine pathways within WAT; however, mechanistic evidence in humans remains heterogeneous and is often limited by tissue accessibility and study design. This review highlights candidate cellular and molecular mechanisms through which incretin-based pharmacotherapies and bariatric surgery may modulate WAT plasticity, emphasizing convergent and distinct effects across depots and the need for more longitudinal, tissue-level human studies to define weight-dependent remodeling versus changes not fully explained by weight loss.
RECENT FINDINGS: In obesity, adipose tissue undergoes pathological remodeling characterized by structural and cellular changes, extracellular matrix (ECM) remodeling, altered endocrine signaling, and impaired mitochondrial function that contribute to metabolic comorbidities. Weight-loss interventions, including incretin-based therapies and bariatric surgery, are associated with improvements in adiposity and metabolic outcomes, and multiple studies suggest accompanying changes in inflammatory, mitochondrial/thermogenic, and endocrine pathways within WAT; however, mechanistic evidence in humans remains heterogeneous and is often limited by tissue accessibility and study design. This review highlights candidate cellular and molecular mechanisms through which incretin-based pharmacotherapies and bariatric surgery may modulate WAT plasticity, emphasizing convergent and distinct effects across depots and the need for more longitudinal, tissue-level human studies to define weight-dependent remodeling versus changes not fully explained by weight loss.