Cross-talk between skeletal muscle and adipose tissue: A link with obesity?

Since the discovery of leptin, the adipocyte and its products have been the subject of intensive research. Thus, it has been demonstrated that adipose tissue plays a central role in energy homeostasis, behaving as an endocrine organ that expresses molecules involved in regulation of metabolism; alte...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Medicinal research reviews 2005-01, Vol.25 (1), p.49-65
Hauptverfasser: Argilés, Josep M., López-Soriano, Joaquín, Almendro, Vanessa, Busquets, Sílvia, López-Soriano, Francisco J.
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Since the discovery of leptin, the adipocyte and its products have been the subject of intensive research. Thus, it has been demonstrated that adipose tissue plays a central role in energy homeostasis, behaving as an endocrine organ that expresses molecules involved in regulation of metabolism; alterations in the expression or activity of those molecules have a fundamental role in pathologies such as obesity and insulin resistance. However, little is known about the role played by another tissue, skeletal muscle, which may have similar functions regarding metabolism control. Indeed, some molecules expressed in this tissue have recently been shown to modulate adipose metabolism. The present review considers the metabolic interrelationships and cross‐talk of signals derived from both skeletal muscle and adipose tissue. It is suggested that cytokines derived from both tissues may have an important role in maintaining an adequate ratio of skeletal muscle to fat and thus may play an important role in the control of body weight. IL‐15 (a cytokine highly‐expressed in skeletal muscle), TNF‐α, and leptin could play a decisive role in the suggested “conversation” between adipose tissue and skeletal muscle. © 2004 Wiley Periodicals, Inc.
ISSN:0198-6325
1098-1128
DOI:10.1002/med.20010