Hormonal
Hypoxia in expanded white adipose tissue directly stimulates the expression and secretion of pro-inflammatory adipokines (e.g., IL-6, leptin, VEGF) and inhibits anti-inflammatory adiponectin, thereby driving the chronic inflammation associated with obesity.
This paper explains that as fat cells grow too large, they run out of oxygen (hypoxia), which triggers them to release inflammatory chemicals. This is a mechanical consequence of tissue expansion, not just 'bad diet'. While you cannot directly 'treat' hypoxia with a pill, reducing adipose tissue mass is the primary way to alleviate the physical crowding that causes this hypoxic inflammatory response.
Cell- culture studies on murine and human adipocytes show that hypoxia (induced by low O2 or chemically) leads to stimulation of the expression and secretion of a number of inflammation-related adipokines, including angiopoietin-like protein 4, IL-6, leptin, macrophage migration inhibitory factor and vascular endothelial growth factor. Hypoxia also stimulates the inflammatory response of macrophages and inhibits adipocyte differentiation from preadipocytes.
Why this rating
Strong molecular and cell-culture evidence, supported by in vivo mouse models, though human causal data is less direct.
Source
Hypoxia in adipose tissue: a basis for the dysregulation of tissue function in obesity?
Paul Trayhurn et al. · British Journal Of Nutrition · 2008
DOI 10.1017/s0007114508971282
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