Hormonal
Obesity induces low-grade chronic inflammation in white adipose tissue (WAT) via adipocyte death (apoptosis/necroptosis), which recruits pro-inflammatory macrophages (forming crown-like structures) and triggers systemic insulin resistance and metabolic syndrome.
Obesity is not just about storing fat; it is an active inflammatory state. Excess fat, especially visceral fat, leads to adipocyte death, which triggers an immune response (inflammation) that blocks insulin signaling. To improve metabolic health, strategies must address this underlying inflammation, not just caloric intake, by supporting adipose tissue health and reducing cytokine-driven resistance.
Obesity is a state of low-grade chronic inflammation that causes multiple metabolic diseases. During obesity, signalling via cytokines of the TNF family mediate cell death and inflammation within the adipose tissue, eventually resulting in lipid spill-over, glucotoxicity and insulin resistance.
Why this rating
Based on a comprehensive review of animal models and human studies, though specific clinical trial data is limited compared to mechanistic evidence.
Source
Cell death and inflammation during obesity: “Know my methods, WAT(son)”
Ximena Hildebrandt et al. · Cell Death and Differentiation · 2022
DOI 10.1038/s41418-022-01062-4
More from this paper
- TNF and NF-κB signaling pathways directly inhibit insulin signaling by phosphorylating IRS-1, thereby causing insulin resistance; neutralizing TNF or inhibiting IKKβ improves glucose homeostasis.Good
- Different forms of cell death (apoptosis, necroptosis, pyroptosis) in adipose tissue have distinct inflammatory consequences; necroptosis is highly inflammatory and linked to metabolic dysfunction, while apoptosis may trigger anti-inflammatory macrophage responses.Moderate
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