Male Obesity and Cardiometabolic Risk: Inflammatory Mechanisms and Clinical Implications
Rodolfo de Oliveira Medeiros, Cristiano Machado Galhardi, Carlos Horacio Vargas Urzagaste, Camila Menon Oliveros, Gustavo Silveira Pires, Vinícius Willian Calderon da Silva, Felipe Quieregati de Novaes, Isabela Gazola Suzuki, Hugo Calesso dos Reis, José Antonio Pizzolato Neto, Felipe Ravazzi Guzzo, Marcus Vinicius da Silva Zanelato, Rafael Ignácio dos Santos, Pedro Henrique Lima Domingues, Bruna Gonçalves Manzoni, Melissa Antunes, Teófilo Augusto Araújo Tiradentes, Victor Cáppia, Thiago Luengo Tavares, Altair Martins BarasuolObesity is a major global health challenge strongly associated with increased cardiometabolic morbidity and mortality. In men, obesity is characterized by a predominance of visceral adiposity, which is metabolically active and closely linked to systemic inflammation, hormonal dysregulation, and adverse cardiovascular outcomes. Despite its clinical relevance, male obesity remains underrecognized as a distinct pathophysiological condition. This study aimed to analyze the inflammatory mechanisms underlying male obesity and their relationship with cardiometabolic risk. A structured narrative review was conducted based on a PICo-guided research question, with literature searches performed in PubMed/MEDLINE, Scopus, Web of Science, Embase, and ScienceDirect, covering publications from 2015 to 2026. Studies focusing on male obesity, inflammatory pathways, and cardiometabolic outcomes were included. Evidence indicates that visceral adipose tissue acts as an active endocrine organ, releasing pro-inflammatory cytokines such as TNF-α and IL-6, contributing to chronic low-grade inflammation. This inflammatory state is associated with insulin resistance (IR), endothelial dysfunction, and oxidative stress, mediated by intracellular pathways including NF-κB and JNK. Additionally, adipokine imbalance, characterized by reduced adiponectin and increased leptin levels, further exacerbates metabolic and vascular impairment. Hormonal alterations, particularly reduced testosterone levels, play a key role in amplifying visceral fat accumulation and inflammation, creating a bidirectional relationship between hypogonadism and metabolic dysfunction. Clinically, these mechanisms highlight the importance of integrating inflammatory biomarkers, body composition assessment, and hormonal evaluation into the management of male obesity. Emerging therapies, including GLP-1 receptor agonists and immunometabolic interventions, offer promising strategies for reducing cardiometabolic risk. In conclusion, male obesity represents a complex, inflammation-driven condition requiring a comprehensive and mechanism-based approach to improve clinical outcomes and guide future therapeutic developments.