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Obesity has been associated with an inflammatory state, but it is unique because it causes a state of chronic, low-grade inflammation, known as meta-inflammation.[1][2] Meta-inflammation is unique because it is subclinical meaning that while there is an increase in circulating pro-inflammatory factors, no clinical signs of inflammation, heat, pain, and redness, are seen with meta-inflammation. [3] Based on the immune system cells involved, both innate and adaptive immunity are involved in meta-inflammation. There are different types of obesity depending on where fat cells are stored. Abdominal obesity, excess fat cell accumulation in adipose tissue of the abdomen, is associated more strongly with meta-inflammation.[4]
Evolutionarily, adipose tissue has been shown to function as an immune organ.[3] The immune cells located in adipose tissue are important for maintaining metabolic homeostasis. With obesity, the immune cells important for maintaining metabolic homeostasis are suppressed because immune cell function and immune cell amount are affected by excess fat accumulation in adipose tissue.[2] [3] Excess fat accumulation can lead to insulin resistance, and insulin resistance has been linked to meta-inflammation.[3] With insulin resistance, there is an increase in macrophages, mast cells, neutrophils, T lymphocytes, and B lymphocytes, and a decrease in eosinophils and some T lymphocytes.[3]
Obesity has also been shown to induce hypoxic conditions in adipose cells.[1][4] Hypoxic conditions result from fat cells expanding, and this decreases vascularization to surrounding fat cells.[1][2][3] Decreased vascularization results in decreased amounts of oxygen in adipose tissue so adipose cells have to switch to anaerobic metabolism for energy production.[4] Anaerobic metabolism stimulates inflammation caused by macrophages.[4] There are two types of macrophages, classically activated M1 macrophages that increase inflammation and alternatively activated M2 macrophages that decrease inflammation. In animal studies, obesity has been shown to cause a shift from M2 to M1 macrophages in adipose tissue, causing an increase in inflammation.[2][3][4]
- ^ a b c Segovia, SA; Vickers, MH; Reynolds, CM (October 2017). "The impact of maternal obesity on inflammatory processes and consequences for later offspring health outcomes". Journal of developmental origins of health and disease. 8 (5): 529–540. doi:10.1017/S2040174417000204. PMID 28343461.
- ^ a b c d Lumeng, CN; Saltiel, AR (June 2011). "Inflammatory links between obesity and metabolic disease". The Journal of clinical investigation. 121 (6): 2111–7. doi:10.1172/JCI57132. PMID 21633179.
- ^ a b c d e f g Mraz, M; Haluzik, M (September 2014). "The role of adipose tissue immune cells in obesity and low-grade inflammation". The Journal of endocrinology. 222 (3): R113-27. doi:10.1530/JOE-14-0283. PMID 25006217.
- ^ a b c d e de Heredia, Fátima Pérez; Gómez-Martínez, Sonia; Marcos, Ascensión (May 2012). "Obesity, inflammation and the immune system". The Proceedings of the Nutrition Society. 71 (2): 332–338. doi:10.1017/S0029665112000092. ISSN 1475-2719. PMID 22429824.