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Lipedema is a chronic, progressive disorder of adipose tissue that predominantly affects women, characterized by symmetrical fat accumulation in the extremities, pain, and resistance to caloric restriction. Recent insights suggest that lipedema represents a hormone-driven gynecological fat disorder, in which estrogen receptor (ER) imbalance plays a central role. The predominance of ERβ activity and suppression of ERα signaling are hypothesized to drive adipose hypertrophy, fibrosis, and inflammation, particularly in the context of intracrine estradiol excess. This model aligns lipedema with other estrogen-sensitive conditions, such as endometriosis and uterine fibroids, and provides a novel framework for understanding its pathophysiology. Therapeutically, this reframing opens new perspectives for hormonal modulation using selective progestins (drospirenone, gestrinone) and metabolic adjuncts such as tirzepatide, beyond the current symptomatic or surgical approaches.
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Lipedema is a chronic, progressive adipose tissue disorder that affects up to 10% of women and is characterized by disproportionate lower-limb fat accumulation, pain, edema, and resistance to conventional weight-loss approaches. Its pathophysiology involves a complex interplay of adipocyte hypertrophy, chronic inflammation, extracellular matrix fibrosis, mitochondrial dysfunction, and sex steroid imbalance, highlighting the need for disease-modifying therapies. This narrative review synthesizes mechanistic, translational, and clinical evidence linking metabolic, inflammatory, and fibrotic pathways to lipedema and tirzepatide's potential therapeutic relevance. Tirzepatide, a dual GLP-1 (Glucagon-Like Peptide-1)/GIP (Glucose-Dependent Insulinotropic Polypeptide) receptor agonist, has demonstrated unprecedented efficacy in obesity and diabetes, alongside pleiotropic actions on inflammation, fibrosis, and adipose remodeling. Mechanistic studies reveal favorable effects on macrophage polarization, cytokine signaling, extracellular matrix turnover, and thermogenesis, suggesting potential relevance to lipedema biology. Translational evidence from related fibro-inflammatory conditions such as steatohepatitis and heart failure further supports its antifibrotic and immunomodulatory plausibility. Although direct clinical evidence in lipedema is lacking, the convergence of mechanistic pathways provides a strong rationale to investigate tirzepatide as a disease-modifying candidate. If future clinical studies confirm these mechanisms, tirzepatide could represent a novel metabolic-hormonal therapy capable of modifying the natural course of lipedema.
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- Lipedema (2)
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