Diabesity is a global epidemic and a complex disorder caused by a decrease in beta-cell function and leptin resistance. Several factors contribute to the pathophysiology of this disease. To preserve endocrine function, it is critical to understand the cause and mechanisms of the progressive deterioration of the endocrine function and how non-endocrine factors like immune cells and neuronal cells regulate its function. Due to the disease's complexity, the in-depth understanding of the mechanism leading to the pathophysiological conditions of diabesity is yet to be understood properly. The field of inter-organ interaction or cell-to-cell interaction studies has grown significantly over the past decade and shows many promising results of how inter-organ interaction influences cellular function. Moreover, these studies have reported several seminal findings on how cell-to-cell interaction or non-endocrine cells influences and plays important role in maintaining energy and metabolic homeostasis. Therefore, to understand diabesity more mechanistically, we should understand how non-endocrine cell populations affect endocrine cell function.
This research theme aims to explore the crosstalk amongst endocrine, neuronal, and immune cells mediated critical factors in the development of diabetes and obesity, with a focus on the mechanisms underlying the pathogenesis of diabetes and obesity. In this submission, we welcome the original paper, basic study, clinical research, and reviews focusing on diabesity. Organ crosstalk assays like organ on chip or organoid system which focuses on understanding the mechanism of diabesity using immune cells or brain cells will also be considered. Further, it’s not limited to type-2 diabetes, type1 diabetes studies are also welcomed. We would like to suggest themes for the authors but are not restricted to these themes only.
• Role of various immune cells in the mechanism of diabetes (1 and 2) or obesity or diabesity.
• Characterization of the central nervous system in the mechanism of diabetes (1 and 2) or obesity or diabesity.
• Role of HPA axis in diabetes (1 and 2) or obesity or diabesity.
• Identification of critical crosstalk between brain cells and immune cells leading to diabetes (1 and 2) or obesity or diabesity.
Keywords:
Diabesity, immune cells, neuronal cells, HPA axis, diabetes, obesity
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Diabesity is a global epidemic and a complex disorder caused by a decrease in beta-cell function and leptin resistance. Several factors contribute to the pathophysiology of this disease. To preserve endocrine function, it is critical to understand the cause and mechanisms of the progressive deterioration of the endocrine function and how non-endocrine factors like immune cells and neuronal cells regulate its function. Due to the disease's complexity, the in-depth understanding of the mechanism leading to the pathophysiological conditions of diabesity is yet to be understood properly. The field of inter-organ interaction or cell-to-cell interaction studies has grown significantly over the past decade and shows many promising results of how inter-organ interaction influences cellular function. Moreover, these studies have reported several seminal findings on how cell-to-cell interaction or non-endocrine cells influences and plays important role in maintaining energy and metabolic homeostasis. Therefore, to understand diabesity more mechanistically, we should understand how non-endocrine cell populations affect endocrine cell function.
This research theme aims to explore the crosstalk amongst endocrine, neuronal, and immune cells mediated critical factors in the development of diabetes and obesity, with a focus on the mechanisms underlying the pathogenesis of diabetes and obesity. In this submission, we welcome the original paper, basic study, clinical research, and reviews focusing on diabesity. Organ crosstalk assays like organ on chip or organoid system which focuses on understanding the mechanism of diabesity using immune cells or brain cells will also be considered. Further, it’s not limited to type-2 diabetes, type1 diabetes studies are also welcomed. We would like to suggest themes for the authors but are not restricted to these themes only.
• Role of various immune cells in the mechanism of diabetes (1 and 2) or obesity or diabesity.
• Characterization of the central nervous system in the mechanism of diabetes (1 and 2) or obesity or diabesity.
• Role of HPA axis in diabetes (1 and 2) or obesity or diabesity.
• Identification of critical crosstalk between brain cells and immune cells leading to diabetes (1 and 2) or obesity or diabesity.
Keywords:
Diabesity, immune cells, neuronal cells, HPA axis, diabetes, obesity
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.