Although effects of dietary, environmental or genetic changes on gut bacterial diversity are extensively researched, the mechanisms by which these dysbiosis related changes affect host functions remains incompletely defined. Intestinal barrier dysfunction is being increasingly recognized as an early or initiating step in communicating bacterial diversity-dependent changes to the host. Continuous translocation of LPS from the leaky gut to the liver results in liver damage or dysfunction that leads to the development of type 2 diabetes, atherosclerosis, heart disease, heart failure and also neurological diseases, such as Alzheimer’s and Parkinson’s disease. In addition, changes in gut barrier function also affects the intestinal absorption of dietary lipids and consequently the plasma lipid profiles resulting in modulation of lipid homeostasis-associated metabolic diseases. Collectively, these new developments underscore the importance of more detailed understanding of the role of intestinal barrier function in the development of diet-induced metabolic diseases.
The overall goal of this research topic is to expand our continuing understanding of the critical role of intestine in modulating development of metabolic diseases. While diet-dependent gut dysbiosis is extensively researched (and NOT the focus of this Research Topic), recent developments have established the role of intestinal barrier function and gut dysbiosis is most likely to influence disease development via modifying one or more functional layers of the intestinal barrier. Furthermore, recent advances have also provided novel links between intestinal barrier function and dietary lipid absorption although the underlying mechanisms remain undefined. Therefore, detailed understanding of the role of one or more functional layers of intestinal barrier in affecting intestinal permeability and/or dietary lipid absorption is critical for the development of novel therapeutic strategies. Scientific advancement focused on targeted modulation of intestinal barrier, defining the mechanisms linking intestinal permeability to metabolic disturbances and subsequent disease development are some of the specific goals to be addressed by this Research Topic.
Manuscripts addressing any or all of the following topics will be within the scope of this Research Topic:
1) Detailed understanding of the structural and functional components of the intestinal barrier including not only the integrity of the intestinal epithelial cell monolayer but also Intestinal Alkaline phosphatase, the mucin layer and lamina propria.
2) Effects of targeted manipulation of the “layers” of the intestinal barrier on the overall barrier function and disease development.
3) Delineation of mechanisms that link intestinal barrier function to intestinal lipid absorption/intestinal inflammation and how these mechanisms are altered during disease development.
4) Direct consequences of diet-induced intestinal barrier dysfunction on metabolic diseases.
Although effects of dietary, environmental or genetic changes on gut bacterial diversity are extensively researched, the mechanisms by which these dysbiosis related changes affect host functions remains incompletely defined. Intestinal barrier dysfunction is being increasingly recognized as an early or initiating step in communicating bacterial diversity-dependent changes to the host. Continuous translocation of LPS from the leaky gut to the liver results in liver damage or dysfunction that leads to the development of type 2 diabetes, atherosclerosis, heart disease, heart failure and also neurological diseases, such as Alzheimer’s and Parkinson’s disease. In addition, changes in gut barrier function also affects the intestinal absorption of dietary lipids and consequently the plasma lipid profiles resulting in modulation of lipid homeostasis-associated metabolic diseases. Collectively, these new developments underscore the importance of more detailed understanding of the role of intestinal barrier function in the development of diet-induced metabolic diseases.
The overall goal of this research topic is to expand our continuing understanding of the critical role of intestine in modulating development of metabolic diseases. While diet-dependent gut dysbiosis is extensively researched (and NOT the focus of this Research Topic), recent developments have established the role of intestinal barrier function and gut dysbiosis is most likely to influence disease development via modifying one or more functional layers of the intestinal barrier. Furthermore, recent advances have also provided novel links between intestinal barrier function and dietary lipid absorption although the underlying mechanisms remain undefined. Therefore, detailed understanding of the role of one or more functional layers of intestinal barrier in affecting intestinal permeability and/or dietary lipid absorption is critical for the development of novel therapeutic strategies. Scientific advancement focused on targeted modulation of intestinal barrier, defining the mechanisms linking intestinal permeability to metabolic disturbances and subsequent disease development are some of the specific goals to be addressed by this Research Topic.
Manuscripts addressing any or all of the following topics will be within the scope of this Research Topic:
1) Detailed understanding of the structural and functional components of the intestinal barrier including not only the integrity of the intestinal epithelial cell monolayer but also Intestinal Alkaline phosphatase, the mucin layer and lamina propria.
2) Effects of targeted manipulation of the “layers” of the intestinal barrier on the overall barrier function and disease development.
3) Delineation of mechanisms that link intestinal barrier function to intestinal lipid absorption/intestinal inflammation and how these mechanisms are altered during disease development.
4) Direct consequences of diet-induced intestinal barrier dysfunction on metabolic diseases.
