Hormonal
Obesity exacerbates cardiovascular disease (CVD) risk and mortality through structural and metabolic mechanisms, including visceral fat deposition, pro-inflammatory cytokine release (TNF-α, IL-1, IL-6), and lipotoxicity from free fatty acids and ceramides.
Obesity is not just about weight; it is a state of chronic inflammation and metabolic signaling disruption that directly harms the heart and blood vessels. Managing obesity requires addressing these underlying biological mechanisms, such as reducing visceral fat and inflammation, to lower cardiovascular risk.
The metabolic effects associated with obesity-related complications are primarily caused by the stimulation of pro-inflammatory cytokines (such as TNF-α, IL-1, IL-6) and lipotoxicity resulting from increased levels of free fatty acids (FFAs) and lipid intermediates like ceramides, which are implicated in insulin resistance, DM, MASLD and CVDs.
Why this rating
The paper is a comprehensive review citing multiple prospective studies and mechanistic animal models, though it lacks a single primary clinical trial.
Source
The signaling pathways in obesity‐related complications
Preethi Chandrasekaran et al. · Journal of Cell Communication and Signaling · 2024
DOI 10.1002/ccs3.12039
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