Type 2 diabetes (T2DM) is a multi-organ disease that results from the combination of central and peripheral insulin resistance and a secretory defect in beta-cells resulting in chronic hyperglycemia. While insulin resistance of tissue affects other tissues and organs, it is of vital importance to understand how organs communicate under normal conditions and T2DM. Accumulating data suggest that either these communications are impaired or altered in a way that exacerbates T2DM. As we know of today, communication could be via neural circuits and a variety of soluble mediators such as hormones, small molecules, lipids, and extracellular vesicles (EV). Secretome analysis from mice and humans suggests that thousands of peptides and proteins are released from adipocytes, hepatocytes, myocytes other cell types regulating glucose and lipid metabolism. In addition, autonomic neurons in the hypothalamus and brainstem play crucial roles in regulating feeding, glucose homeostasis, and pancreatic function through neural and hormonal signals. Metabolites produced by gut microbiota vary in T2DM adding one more layer of complexity to inter-organ crosstalk during T2DM.
This collection aims to address the current understanding of organ crosstalk and how it is impaired under the condition of T2DM. We will accept both original research and reviews on the following, but not limited to, subjects:
- how different organs interconnect, communicate and influence each other in normal vs Type 2 diabetes;
- new information on both neural circuits and peripheral “organokines” regulating glucose and lipid metabolism;
- the molecular basis of different therapeutic strategies targeting organ-organ communication in T2DM.
Type 2 diabetes (T2DM) is a multi-organ disease that results from the combination of central and peripheral insulin resistance and a secretory defect in beta-cells resulting in chronic hyperglycemia. While insulin resistance of tissue affects other tissues and organs, it is of vital importance to understand how organs communicate under normal conditions and T2DM. Accumulating data suggest that either these communications are impaired or altered in a way that exacerbates T2DM. As we know of today, communication could be via neural circuits and a variety of soluble mediators such as hormones, small molecules, lipids, and extracellular vesicles (EV). Secretome analysis from mice and humans suggests that thousands of peptides and proteins are released from adipocytes, hepatocytes, myocytes other cell types regulating glucose and lipid metabolism. In addition, autonomic neurons in the hypothalamus and brainstem play crucial roles in regulating feeding, glucose homeostasis, and pancreatic function through neural and hormonal signals. Metabolites produced by gut microbiota vary in T2DM adding one more layer of complexity to inter-organ crosstalk during T2DM.
This collection aims to address the current understanding of organ crosstalk and how it is impaired under the condition of T2DM. We will accept both original research and reviews on the following, but not limited to, subjects:
- how different organs interconnect, communicate and influence each other in normal vs Type 2 diabetes;
- new information on both neural circuits and peripheral “organokines” regulating glucose and lipid metabolism;
- the molecular basis of different therapeutic strategies targeting organ-organ communication in T2DM.
