One of the key mechanisms that lead to the development of obesity complications is the inflammatory reaction that occurs at the level of adipose tissue.
At the origin of this inflammation there is the abnormal increase in the volume of fat cells, which fill up with lipids almost to burst; since the capillaries fail to offer enough oxygen to support this abnormal growth of adipose tissue, adipocytes begin to suffer from hypoxia and to secrete pro-inflammatory substances. In turn, these cytokines recall immune cells that engulf the dying adipocytes, supporting and amplifying inflammation.
Increasing the vascularization of adipose tissue would therefore be a protective factor against the complications of obesity. Having more capillaries and blood available to the adipose tissue means in fact increasing the amount of oxygen available for the adipocytes, consequently attenuating the systemic inflammatory response.
It has been shown for some time that physical exercise can induce angiogenesis, the formation of new blood vessels (capillaries). Recently it has been seen that this activity of exercise-dependent capillarization also occurs at the level of adipose tissue, increasing:
- the number of capillaries
- gene expression of endothelial growth factors and their receptors;
- the amount of blood that actually perfuses adipose tissue.
All this has been demonstrated on obese rats subjected to physical exercise, but presumably the results can also be transferred to humans. We recall that aerobic training of medium-low intensity duration represents the greatest stimulus for the creation of new capillaries; clearly constancy is needed, since these circulatory adaptations require a few months to manifest.
Effects of adipose tissue angiogenesis and hypoxia in obese rats.
Disanzo BL1, You T2.
