Research
Hormonal
Chronic structural damage in visceral fat, characterized by adipocyte death and senescence, shifts inflammation from protective to detrimental by recruiting circulating immune cells and causing fibrosis.
When fat cells die or become senescent, they release signals that attract immune cells, leading to chronic inflammation and scarring (fibrosis). This is the stage where metabolic health typically declines.
GoodSupportsHIGH confidence
With chronic overnutrition, these protective actions are insufficient, and death of adipocytes as well as senescence of several tissue cell types is seen. This structural damage causes the expression or release of immunostimulatory cell components resulting in influx and activation of monocytes and many other immune cell types... possibly detrimental fibrosis.
Why this rating
Well-supported by molecular and histological evidence in the review.
Source
Obese visceral fat tissue inflammation: from protective to detrimental?
Hubert Kolb · BMC Medicine · 2022
DOI 10.1186/s12916-022-02672-y
narrative_reviewCited 330×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Obese visceral fat inflammation is an initially protective adaptive response to restore metabolic homeostasis, but becomes detrimental when structural damage and senescence trigger chronic immune infiltration.Good
- Adipocyte hypertrophy and subsequent endoplasmic reticulum stress trigger a pro-inflammatory response (metaflammation) that initially preserves metabolic control by promoting lipolysis and tissue remodeling.Good
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