The global increase in the incidence of metabolic diseases such as obesity and type 2 diabetes has led numerous studies in this field and provided evidence for pancreatic beta cell dysfunction and death to be one of the major culprits for both type 1 and type 2 diabetes. During onset of diabetes, glucotoxicity, lipotoxicity, oxidative stress and in later situation chronic inflammation has been implicated for insulin secretory defect as well as insulin resistance. Thus preservation, expansion and improving function of beta cell has been one of the major therapeutic approaches past several years in the context of type 2 diabetes.
To preserve beta cell function it is important to understand the cause and mechanisms about the progressive deterioration of beta cell. In-depth mechanism of beta cell injury and the relative contribution of each of the processes (glucotoxicity, lipotoxicity, oxidative stress, inflammation etc) and their physiological effect is yet to be understood properly.
This research topic will be dedicated to updating current knowledge on islet dysfunction with special reference to molecular processes that influence the decline of islet health, mass and function and potential intervention to beta cell preservation in the context of obesity and type 2 diabetes. Original paper, basic study, clinical research and reviews are all welcomed. The subtopics of interest include but not limit to:
• Islet inflammation: mechanism and therapeutics
• Insulin granule exocytosis
• Islet macrophage heterogeneity
• Beta cell ER stress
• Crosstalk between islet and other organs
• Potential drugs for islet preservation
• Apoptosis
The global increase in the incidence of metabolic diseases such as obesity and type 2 diabetes has led numerous studies in this field and provided evidence for pancreatic beta cell dysfunction and death to be one of the major culprits for both type 1 and type 2 diabetes. During onset of diabetes, glucotoxicity, lipotoxicity, oxidative stress and in later situation chronic inflammation has been implicated for insulin secretory defect as well as insulin resistance. Thus preservation, expansion and improving function of beta cell has been one of the major therapeutic approaches past several years in the context of type 2 diabetes.
To preserve beta cell function it is important to understand the cause and mechanisms about the progressive deterioration of beta cell. In-depth mechanism of beta cell injury and the relative contribution of each of the processes (glucotoxicity, lipotoxicity, oxidative stress, inflammation etc) and their physiological effect is yet to be understood properly.
This research topic will be dedicated to updating current knowledge on islet dysfunction with special reference to molecular processes that influence the decline of islet health, mass and function and potential intervention to beta cell preservation in the context of obesity and type 2 diabetes. Original paper, basic study, clinical research and reviews are all welcomed. The subtopics of interest include but not limit to:
• Islet inflammation: mechanism and therapeutics
• Insulin granule exocytosis
• Islet macrophage heterogeneity
• Beta cell ER stress
• Crosstalk between islet and other organs
• Potential drugs for islet preservation
• Apoptosis
