Hormonal
Obesity drives chronic low-grade inflammation through the expansion of adipose tissue, which shifts the balance of adipokines to favor proinflammatory mediators (like leptin and resistin) and recruit proinflammatory immune cells (M1 macrophages), increasing the risk of metabolic diseases.
Excess body fat, particularly visceral fat, is not just stored energy but an active organ that releases inflammatory signals. This chronic inflammation is a primary driver of type 2 diabetes and cardiovascular disease. Weight loss interventions that reduce adipose tissue mass can help restore the balance of adipokines and reduce this chronic inflammatory state.
This balance shifts to favor proinflammatory mediators as adipose tissue expands during the development of obesity. As a consequence, the proinflammatory status of adipose tissue contributes to a chronic low-grade state of inflammation and metabolic disorders associated with obesity.
Why this rating
The paper synthesizes extensive evidence from human and animal studies linking adipose expansion, adipokine profiles, and inflammatory outcomes.
Source
The role of adipokines in chronic inflammation
Peter Mancuso · ImmunoTargets and Therapy · 2016
DOI 10.2147/itt.s73223
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