Key result
Obesity drives metabolic comorbidities via chronic inflammation from adipose tissue dysfunction and gut dysbiosis.
Why the study?
Chronic low-grade inflammation is a key mechanism in the development and persistence of obesity and its metabolic and organ-related complications, but its pathophysiological mechanisms and clinical implications require comprehensive analysis.
Recognizing obesity as a chronic inflammatory disease shifts the treatment paradigm towards therapies that restore immunological and metabolic balance, such as GLP-1 receptor agonists.
Answers are grounded in this paper and cite their sources.
Supports viewing obesity as inflammatory; leaves open whether targeting this pathway improves outcomes beyond weight loss.
Obesity is currently recognized as one of the greatest global public health challenges and is increasingly referred to as the pandemic of the 21st century[1,2]. The results of recent analyses confirm that one of the main mechanisms responsible for the development and persistence of obesity and its metabolic and organ-related complications is chronic inflammation in the body[3]. In obesity, one observes immunological remodeling of adipose tissue, increased activation of inflammatory pathways[4], disturbances in adipokine secretion[5], as well as gut dysbiosis and increased intestinal barrier permeability, which exacerbate metabolic endotoxemia and systemic inflammation[6]. These mechanisms contribute to the development of insulin resistance, endothelial dysfunction, and numerous comorbidities, such as type 2 diabetes, cardiovascular diseases, MASLD, neurodegenerative diseases, and cancer[7,8]. Adipose tissue thus functions as an active endocrine-immunological organ that, through the production of inflammatory mediators, influences the metabolic homeostasis of the entire body[9,10]. Recognizing obesity as an inflammatory disease is changing the current treatment paradigm - the goal of therapy is not only weight reduction but also the restoration of immunological and metabolic balance and the mitigation of the long-term consequences of chronic inflammation[11,12]. The development of targeted therapies, modulation of the gut microbiota, and the use of epigenetic mechanisms may represent important avenues for future research and treatment of obesity[13–15]. GLP-1 receptor agonists and multireceptor drugs, which, in addition to their metabolic effects, also exhibit anti-inflammatory properties, are currently showing particularly promising results[7]. The aim of this study is to analyze and summarize the current state of knowledge regarding the role of low-grade chronic inflammation (LGCI) in the pathogenesis of obesity, with particular emphasis on inflammatory mechanisms, the role of adipokines and immune cells, as well as clinical consequences and potential therapeutic strategies.
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Kuba et al. (2026) conducted a review in Obesity. Obesity-induced chronic low-grade inflammation was evaluated. Obesity acts as a chronic low-grade inflammatory disease driven by adipose tissue dysfunction and gut dysbiosis, leading to insulin resistance and numerous metabolic comorbidities.
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