How glycation and low oxygen levels (hypoxia) cause fat tissue inflammation and contribute to cellulite

  • Adipose (fat) tissue hypoxia, i.e. low oxygen levels in the fat tissue, is an important cause of fat tissue dysfunction and inflammation
  • Hypoxia is caused by the enlargement of fat cells which compress blood vessels and thereby inhibit nourishment and oxygenation of the fat tissue, leading to a partial "suffocation" of the fat tissue and consequent inflammation
  • Blood vessel dysfunction due to other reasons (poor diet, lack of exercise, increased blood coagulation due to hormonal contraception etc.) also contributes to hypoxia
  • Adipose tissue glycation, i.e. the damage of proteins by sugar derivatives such as methylglyoxal, is also responsible for the metabolic dysfunction of fat tissue we often see in obesity and in cellulite
  • Moreover, glycation degrades the blood vessels of adipose tissue, leading to hypoxia, mentioned above, and inflammation
  • Finally, glycation degrades the collagen fibres found in and around fat tissue of the legs and other body areas, thereby contributing to the creation of the hardened connective tissue nodules we see in cellulite
  • The low grade inflammation caused by both glycation and hypoxia spreads throughout the body, via inflammatory fat cell hormones called adipokines and it is a major cause of cardiovascular and other disease
  • At skin level, the combination of fat tissue hypoxia and glycation and the low grade inflammation they cause, also contributes to the development of cellulite
  • Source: Glycation and hypoxia: two key factors for adipose tissue dysfunction
  • Abstract: Many aspects of adipose tissue pathophysiology in metabolic diseases have been described in the last years. One of such aspects is certainly hypoxia, which was shown to develop in adipose tissue of obese individuals and animal models. Recent data suggest two main factors for adipose tissue hypoxia: adipocyte hypertrophy and vascular dysfunction. Accordingly, glycation was also shown to induce morphological and functional alteration in adipose tissue. In particular, methylglyoxal directly formed from glucose was shown to potently induce AGE formation in vivo and to contribute to metabolic and vascular alteration in adipose tissue. Glycation and hypoxia are both thought to be on the basis of low grade inflammatory activation, further increasing metabolic dysregulation in adipose tissue. This review summarizes the current knowledge about the factors that contribute for tissue hypoxia and the role of glycation, not only at the vascular level, but also at the metabolic, oxidative and inflammatory levels.