Insulin plays a key role in the regulation of energy homeostasis through its anabolic action on specific target tissues. In particular, it acts, through a direct effect, by stimulating glucose uptake and storage in the skeletal muscle, promoting glycogen synthesis in the liver while suppressing lipolysis, increasing lipogenesis and glucose uptake in the adipose tissue. In addition, it also exerts very important indirect effects like the link between the adipose to hepatic tissue but not limited to.
In this context, in addition to the well-known mechanisms like increased caloric intake and decreased physical activity, a fundamental role on insulin resistance and responsiveness is played by the metabolic-mediated crosstalk among different tissues. Alteration of this process can affect insulin action, as well as beta-cell function and/or insulin clearance, and is associated to the development and worsening of many different diseases like obesity, cardiovascular disease (CVD), nonalcoholic fatty liver disease (NAFLD), metabolic syndrome, polycystic ovary syndrome (PCOS) and type 2 diabetes (T2D).
Hence, understanding the mechanisms of alteration in metabolic-mediated crosstalk among insulin-sensitive tissues, in particular focusing on the liver, adipose tissue and skeletal muscle, but also on beta-cells and gut, would be fundamental for better characterizing the etiology of many pathologic conditions as well as the development of new and effective therapeutic agents.
The Research Topic focuses on highlighting the mechanisms of alteration in the crosstalk among insulin-sensitive tissues associated to insulin resistance and its related diseases. We encourage interested scientists to submit original articles, review articles and perspectives covering the following topics but not limited to:
- Metabolic mediators activity in the crosstalk among insulin-sensitive tissues.
- Mathematical modeling of the crosstalk among insulin-sensitive tissues.
- Role of gluco-/lipo-toxicity in hepatic, adipose and skeletal muscle insulin resistance and beta-cell function.
- Metabolomics/Lipidomics of insulin resistance and gluco/lipotoxicity
- Animal models for insulin resistance and gluco-/lipotoxicity.
- Therapeutic agents for management of insulin resistance its related diseases: obesity, CVD, NAFLD, PCOS and T2D.
Insulin plays a key role in the regulation of energy homeostasis through its anabolic action on specific target tissues. In particular, it acts, through a direct effect, by stimulating glucose uptake and storage in the skeletal muscle, promoting glycogen synthesis in the liver while suppressing lipolysis, increasing lipogenesis and glucose uptake in the adipose tissue. In addition, it also exerts very important indirect effects like the link between the adipose to hepatic tissue but not limited to.
In this context, in addition to the well-known mechanisms like increased caloric intake and decreased physical activity, a fundamental role on insulin resistance and responsiveness is played by the metabolic-mediated crosstalk among different tissues. Alteration of this process can affect insulin action, as well as beta-cell function and/or insulin clearance, and is associated to the development and worsening of many different diseases like obesity, cardiovascular disease (CVD), nonalcoholic fatty liver disease (NAFLD), metabolic syndrome, polycystic ovary syndrome (PCOS) and type 2 diabetes (T2D).
Hence, understanding the mechanisms of alteration in metabolic-mediated crosstalk among insulin-sensitive tissues, in particular focusing on the liver, adipose tissue and skeletal muscle, but also on beta-cells and gut, would be fundamental for better characterizing the etiology of many pathologic conditions as well as the development of new and effective therapeutic agents.
The Research Topic focuses on highlighting the mechanisms of alteration in the crosstalk among insulin-sensitive tissues associated to insulin resistance and its related diseases. We encourage interested scientists to submit original articles, review articles and perspectives covering the following topics but not limited to:
- Metabolic mediators activity in the crosstalk among insulin-sensitive tissues.
- Mathematical modeling of the crosstalk among insulin-sensitive tissues.
- Role of gluco-/lipo-toxicity in hepatic, adipose and skeletal muscle insulin resistance and beta-cell function.
- Metabolomics/Lipidomics of insulin resistance and gluco/lipotoxicity
- Animal models for insulin resistance and gluco-/lipotoxicity.
- Therapeutic agents for management of insulin resistance its related diseases: obesity, CVD, NAFLD, PCOS and T2D.