Phosphodiesterase 5 as target for adipose tissue disorders
•The importance of nitric oxide pathway in adipocyte biology is reviewed.•The role of phosphodiesterase 5 in adipocyte physiology is discussed.•The use of phosphodiesterase 5 inhibitors in adipose tissue disorders is hypothesized. Adipose tissue as an endocrine organ is responsible for the release o...
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Veröffentlicht in: | Nitric oxide 2013-11, Vol.35, p.186-192 |
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Sprache: | eng |
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Zusammenfassung: | •The importance of nitric oxide pathway in adipocyte biology is reviewed.•The role of phosphodiesterase 5 in adipocyte physiology is discussed.•The use of phosphodiesterase 5 inhibitors in adipose tissue disorders is hypothesized.
Adipose tissue as an endocrine organ is responsible for the release of multiple cytokines, which have the most diverse metabolic functions. Therefore, it is extremely important to preserve its physiological health in order to avoid local and systemic disorders. Experiments available in literature show the importance of the nitric oxide (NO)/guanosine 3′5′ cyclic monophosphate (cGMP)/protein kinase G (PKG) pathway in adipocyte biology. Phosphodiesterase 5 (PDE5) is an enzyme responsible for cGMP inactivation, and the use of its inhibitors can be an alternative in the search of a more balanced adipose tissue.
This review aims to describe the PDE5 role and the possibility of using PDE5 inhibitors in adipocyte physiology derangements and their consequences.
Studies published in the last 10years that related PDE5 and its inhibitors to adipose tissue were raised in major databases.
PDE5 is present in adipocyte, and PDE5 inhibitors can promote adipogenesis, interfere with adipokines secretion, decrease inflammatory markers expression, and increase the thermogenic potential of white adipose tissue.
PDE5 plays an important role in adipocyte physiology and the use of its inhibitors may prove a useful tool to combat adipose tissue disorders and its highest expression, metabolic syndrome. |
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ISSN: | 1089-8603 1089-8611 |
DOI: | 10.1016/j.niox.2013.10.006 |