It is now established that obesity, especially visceral, represents an important risk factor for the appearance of insulin resistance and type 2 diabetes.
In recent years, adipose tissue has been the subject of numerous studies that have highlighted the important endocrine activity, such that today we prefer to talk about the adipose organ .
In obese subjects it happens that the adipocytes (so called the cells of adipose tissue) are filled with fats "almost to burst". This filling causes a lot of damage to the cell, as it compresses the nucleus and the organelles against the plasma membrane and creates problems of hypoxia (oxygen shortage). Consequently, the adipocyte enters a state of stress and secretes inflammatory cytokines that attract phagocytes (immune cells responsible for the digestion of pathogens); these particular white blood cells attack the dying cell just as they normally do with a pathogen. In turn, macrophages and other phagocytes secrete further pro-inflammatory cytokines, which recall new immune cells by perpetuating the ongoing inflammation.
The organism thus enters a state of chronic inflammation and the immune hyperactivity also ends up damaging healthy tissues, which reduce its sensitivity to insulin. In fact, inflammatory cytokines such as tumor necrosis factor alpha (TNF?), Interleukine 6 (IL-6) and interleukin 1 alpha (IL-1?) Have been shown to interfere negatively with activity of insulin receptors.
As anticipated, the most dangerous obesity is that in which the adipose mass is concentrated above all at the abdominal level. In fact, we have seen how this tissue is characterized by poor capillarization and reduced hyperplastic capacity (see the hyperplasia of adipocytes article); consequently it is more likely to suffer from hypoxia, from which all the other potential pathogenetic events listed above develop.
