Increasing obesity is a global epidemic that threatens human health. Accompanied by the expansion of adipose tissue, it becomes a high-risk factor for the development of metabolic disorders such as fatty liver, cardiovascular disease, and type 2 diabetes mellitus.
Adipose tissue is not only the largest depot of triglycerides in the body, but also an endocrine organ regulating energy and metabolic homeostasis by secreting various adipokines, including exosomes from adipose tissue. Adipokines can be involved in regulating the function of adipose tissue itself and other metabolic organs, such as liver and pancreatic islets, by autocrine, paracrine and endocrine. In obesity, leptin increased in adipose tissue while adiponectin decreased. The abnormal secretion of these adipokines may participate in the occurrence and development of metabolic diseases such as diabetes and non-alcoholic fatty liver disease (NAFLD). For example, brown adipose tissue can secrete adipokines, such as FGF21, NRG4, and VEGF, which are different with those from white adipose tissue to regulate NAFLD.
Adipokines from different depots or different types of adipocytes can regulate many processes, including adipose tissue browning, angiogenesis, inflammatory response, central food intake, and gut microbiota. Therefore, how adipokines and adipose tissue exosomes regulate the function of metabolic organs in metabolic diseases requires more research.
This Research Topic aims to discover new adipokines or exosomes from adipose tissue, and reveal the roles and mechanisms of which in metabolic diseases.
Potential sub-topics include:
• Cohort and observational studies on the link between adipokines and metabolic diseases;
• Discovery of new adipokines or exosomes from different adipose depots;
• How the adipokines regulate adipose tissue functions, adipocyte differentiation and adipose microenvironment;
• How the adipokines re-modulate the immune system;
• The roles of adipokines on fatty liver and diabetes;
• The interaction between adipokines and gut microbiota.
Increasing obesity is a global epidemic that threatens human health. Accompanied by the expansion of adipose tissue, it becomes a high-risk factor for the development of metabolic disorders such as fatty liver, cardiovascular disease, and type 2 diabetes mellitus.
Adipose tissue is not only the largest depot of triglycerides in the body, but also an endocrine organ regulating energy and metabolic homeostasis by secreting various adipokines, including exosomes from adipose tissue. Adipokines can be involved in regulating the function of adipose tissue itself and other metabolic organs, such as liver and pancreatic islets, by autocrine, paracrine and endocrine. In obesity, leptin increased in adipose tissue while adiponectin decreased. The abnormal secretion of these adipokines may participate in the occurrence and development of metabolic diseases such as diabetes and non-alcoholic fatty liver disease (NAFLD). For example, brown adipose tissue can secrete adipokines, such as FGF21, NRG4, and VEGF, which are different with those from white adipose tissue to regulate NAFLD.
Adipokines from different depots or different types of adipocytes can regulate many processes, including adipose tissue browning, angiogenesis, inflammatory response, central food intake, and gut microbiota. Therefore, how adipokines and adipose tissue exosomes regulate the function of metabolic organs in metabolic diseases requires more research.
This Research Topic aims to discover new adipokines or exosomes from adipose tissue, and reveal the roles and mechanisms of which in metabolic diseases.
Potential sub-topics include:
• Cohort and observational studies on the link between adipokines and metabolic diseases;
• Discovery of new adipokines or exosomes from different adipose depots;
• How the adipokines regulate adipose tissue functions, adipocyte differentiation and adipose microenvironment;
• How the adipokines re-modulate the immune system;
• The roles of adipokines on fatty liver and diabetes;
• The interaction between adipokines and gut microbiota.