Abstract
A highly complex network of organ communication plays a key role in regulating metabolic homeostasis, specifically due to the modulation of the insulin signaling machinery. As a paradigm, the role of adipose tissue in organ crosstalk has been extensively investigated, but tissues such as muscles and the liver are equally important players in this scenario. Perturbation of organ crosstalk is a hallmark of insulin resistance, emphasizing the importance of crosstalk molecules in the modulation of insulin signaling, potentially leading to defects in insulin action. Classically secreted proteins are major crosstalk molecules and are able to affect insulin signaling in both directions. In this review, we aim to focus on some crosstalk mediators with an impact on the early steps of insulin signaling. In addition, we also summarize the current knowledge on the role of extracellular vesicles in relation to insulin signaling, a more recently discovered additional component of organ crosstalk. Finally, an attempt will be made to identify inter-connections between these two pathways of organ crosstalk and the potential impact on the insulin signaling network.
Highlights
Organ crosstalk represents a system of biological communication that makes it possible for cells in one tissue to send information to cells in another tissue, even at relatively long distances
The insulin signaling network comprises a complex machinery consisting of a wide range of genes and proteins that regulate metabolic homeostasis
We summarized novel molecules derived from organ crosstalk that modify the insulin signaling network at different levels
Summary
Organ crosstalk represents a system of biological communication that makes it possible for cells in one tissue to send information to cells in another tissue, even at relatively long distances. A complex scenario of crosstalk mediators involving nutrients and metabolites, extracellular vesicles (EVs), and peptides and proteins that may be collectively called “organokines” needs to be considered, and many of these players are known to modify insulin signaling [1,2]. The seminal work published by Spiegelman and co-workers nearly 30 years ago identified the cytokine TNFα as a critical signal released by adipose tissue, inducing skeletal muscle insulin resistance [7,8] These findings triggered a tremendous and still ongoing interest in organ crosstalk as a major element of metabolic homeostasis and a key driver for metabolic diseases. An attempt will be made to identify such points of convergence, shedding some new light on insulin signaling in the context of organ crosstalk
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