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.
In addition, glycation was also shown to induce morphological and functional alterations 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 alterations 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.