The increasing global type 1 diabetes (T1D) incidence cannot be explained by changes in genetic susceptibility as it is happening too fast. Thus, environmental factors are most likely important determinants of the rising incidence. A variety of both food and microbial molecules (from diet, virus infection, microbiome changes etc.) have been associated with T1D. Some of these factors can increase the intestinal permeability, which is already increased in people with pre- and manifest T1D, and thereafter cross the intestinal barrier where they can cause damage. Studies in primarily the NOD mouse model for T1D have revealed how many different environmental factors can potentially contribute to disease by affecting the microbiome, systemic and local inflammation, pancreas morphology, beta-cell stress, among others. Such changes may lead to beta-cell autoimmunity and T1D. Further strengthening the gut-pancreas axis hypothesis, islet infiltrating lymphocytes express the gut homing receptor a4ß7 integrin in NOD mice. For some environmental factors there seem to be certain time windows (pre- and postnatally) for which genetically predisposed individuals are particularly vulnerable to exposure. Although intense research, the mechanisms by which the different environmental factors may contribute to beta-cell autoimmunity and T1D are still unexplored, and there may very well be unknown environmental factors that can be behind the increasing T1D incidence.
The overall aim of this research topic is to direct attention to T1D, a disease with an unexplained global rise in incidence and consequently increased suffering from disease complication. T1D is a disease that does not only affect the pancreatic beta cells but is also associated with increased intestinal permeability, enteropathy, and microbiota changes across different disease endotypes. Thus, T1D affects the intestine and possibly also other organ systems, and with this research theme’s focus on the gut-pancreas axis, we hope to provide a more complete picture of T1D. Intervention studies in NOD mice have identified several possible diabetogenic environmental factors (diet, virus, bacteria) and associated mechanism. However, intervention studies in humans aiming at evading these environmental factors to prevent T1D have overall been discouraging. This is indicating that there are diabetogenic environmental factors which have not been identified yet, that combinations of certain environmental factors may be particularly diabetogenic, that exposure during yet unidentified time windows may be causative, among other possible explanations that we hope to highlight with this research topic.
We welcome submission of all article types accepted in Frontiers of Endocrinology such as original research articles, systematic reviews, methods, reviews, mini reviews, perspectives, and opinion articles on the scope “gut-pancreas axis in type 1 diabetes – focus on environmental factors”. We accept contributions to, but not limited to, the following themes:
o Role of environmental factors in T1D, hereunder pre- and postnatal exposure to diet, viruses, bacteria etc.
o Contribution of intestinal barrier dysfunction, hereunder increased intestinal permeability in T1D
o The innate immune system in pancreas and intestine, its (dys)regulation, communication with the adaptive immune system, and response towards environmental factors
o Beta-cell stress and induction of autoimmunity
o Treatment aimed at preventing or reverting T1D
o Association between T1D and celiac disease
o Effects of incretins on islet function in T1D
The increasing global type 1 diabetes (T1D) incidence cannot be explained by changes in genetic susceptibility as it is happening too fast. Thus, environmental factors are most likely important determinants of the rising incidence. A variety of both food and microbial molecules (from diet, virus infection, microbiome changes etc.) have been associated with T1D. Some of these factors can increase the intestinal permeability, which is already increased in people with pre- and manifest T1D, and thereafter cross the intestinal barrier where they can cause damage. Studies in primarily the NOD mouse model for T1D have revealed how many different environmental factors can potentially contribute to disease by affecting the microbiome, systemic and local inflammation, pancreas morphology, beta-cell stress, among others. Such changes may lead to beta-cell autoimmunity and T1D. Further strengthening the gut-pancreas axis hypothesis, islet infiltrating lymphocytes express the gut homing receptor a4ß7 integrin in NOD mice. For some environmental factors there seem to be certain time windows (pre- and postnatally) for which genetically predisposed individuals are particularly vulnerable to exposure. Although intense research, the mechanisms by which the different environmental factors may contribute to beta-cell autoimmunity and T1D are still unexplored, and there may very well be unknown environmental factors that can be behind the increasing T1D incidence.
The overall aim of this research topic is to direct attention to T1D, a disease with an unexplained global rise in incidence and consequently increased suffering from disease complication. T1D is a disease that does not only affect the pancreatic beta cells but is also associated with increased intestinal permeability, enteropathy, and microbiota changes across different disease endotypes. Thus, T1D affects the intestine and possibly also other organ systems, and with this research theme’s focus on the gut-pancreas axis, we hope to provide a more complete picture of T1D. Intervention studies in NOD mice have identified several possible diabetogenic environmental factors (diet, virus, bacteria) and associated mechanism. However, intervention studies in humans aiming at evading these environmental factors to prevent T1D have overall been discouraging. This is indicating that there are diabetogenic environmental factors which have not been identified yet, that combinations of certain environmental factors may be particularly diabetogenic, that exposure during yet unidentified time windows may be causative, among other possible explanations that we hope to highlight with this research topic.
We welcome submission of all article types accepted in Frontiers of Endocrinology such as original research articles, systematic reviews, methods, reviews, mini reviews, perspectives, and opinion articles on the scope “gut-pancreas axis in type 1 diabetes – focus on environmental factors”. We accept contributions to, but not limited to, the following themes:
o Role of environmental factors in T1D, hereunder pre- and postnatal exposure to diet, viruses, bacteria etc.
o Contribution of intestinal barrier dysfunction, hereunder increased intestinal permeability in T1D
o The innate immune system in pancreas and intestine, its (dys)regulation, communication with the adaptive immune system, and response towards environmental factors
o Beta-cell stress and induction of autoimmunity
o Treatment aimed at preventing or reverting T1D
o Association between T1D and celiac disease
o Effects of incretins on islet function in T1D
