Table 1 Key messages and gaps of knowledge

• In normal non-inflamed fat tissue, resident immune cells interact with adipocytes and stromal cells for metabolic homeostasis, thermogenesis, and cell turnover.

• Adipocytes deal with excess ambient nutrients by increased lipid storage (hypertrophy) and proliferation (hyperplasia). Resident pro-inflammatory macrophages support matrix remodeling required for adipocyte hyperplasia.

• Excessive enlargement of adipocytes causes metabolic stress and the release of pro-inflammatory mediators which activate resident immune cells for enhanced production of immune mediators, resulting in enhanced sympathetic tone, lipolysis in adipocytes, lipid uptake in macrophages, matrix remodeling, and angiogenesis.

• Chronic overnutrition eventually leads to structural/functional damage, i.e., adipocyte death and accumulation of senescent cells. Both are strong immunostimulatory processes causing the influx of monocytes and many other immune cell types from circulation. There is further enhanced matrix remodeling including fibrosis, angiogenesis, lipid uptake by macrophages, clearing of the tissue from cell debris, and spread of senescent state from affected to neighboring cells by the release of microRNA-containing vesicles.

• Although tissue inflammation serves the restoration of a physiological functional state it is not known at which stage and by what quality chronic inflammation may mediate detrimental effects.

• The role of senescent cells in supporting or damaging tissue functions requires further research.

• Subtypes of visceral obesity remain to be defined, with age, sex and genetic background as important parameters. The protective versus detrimental functions of inflammation may differ between subtypes.

• Molecular mechanisms are often deduced from animal studies. Differences between animal models and obese humans must be taken into account.