Adipocytokines as mediators of metabolic role of adipose tissue

The discovery of adipocytokines, products of adipose tissue, has been a turning point in the understanding of metabolic disorders. Historically considered as a passive depot of energy, adipose tissue has become an important active participant and adipocytokines crucial mediators of its metabolic rol...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Acta medica Croatica 2010-10, Vol.64 (4), p.253-262
1. Verfasser: Pandzić Jaksić, Vlatka
Format: Artikel
Sprache:hrv
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:The discovery of adipocytokines, products of adipose tissue, has been a turning point in the understanding of metabolic disorders. Historically considered as a passive depot of energy, adipose tissue has become an important active participant and adipocytokines crucial mediators of its metabolic role. Among a number of adipose tissue products, leptin and adiponectin are exclusively secreted by adipocytes. Leptin regulates energy homeostasis and interferes with several neuroendocrine and immune functions. Adiponectin is an intriguing adipocytokine with its serum level inversely correlated with fatness. It has been related to enhanced insulin sensitivity, anti-inflammatory and anti-atherogenic actions. Recent investigations have also emphasized the important role of resistin, visfatin, retinol binding protein 4, and of a whole list of cytokines like interleukin-6, tumor necrosis factor a, plasminogen activator inhibitor-1, or a chemokine, monocyte chemoattractant protein-1. The fact that secretory balance of adipose tissue in obesity is shifted towards the proinflammatory spectrum has supported the hypothesis on the development of dysfunctional adipose tissue in these circumstances. It contributes to the state of chronic inflammation and insulin resistance, and it seems to be a fundamental link between obesity and atherosclerosis.
ISSN:1330-0164