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"The human gastrointestinal tract (GIT) harbours a very complex and dynamic microbial community, the so called gastrointestinal microbiota. This complex microbial ecosystem exceeds the number of host cells1. It contains a gene set 100 times larger than that of the human genome, carrying out many functions that are not encoded in our own genome2. The bacterial colonization of the human gut with this microbiota plays an essential role for the development and maintenance of an appropriate metabolic and immune homeostasis in the host3,4.
An increasing body of scientific evidence has arisen during the last years indicating that the microbiota-host interaction affects not just the gut environment but also distal organs5,6,7. Among these, several studies strongly suggest that the intestinal microbiota may interplay with the nervous system and the brain8. Animal studies have evidenced the potential of the gut microbiota to modulate pain perception9,10,11, behaviour, mood and stress response5,12,13. The gut microbiota is able to produce neuroactive molecules such as histamine, acetylcholine or GABA, among others14. Actually, the gut is the second organ with more nerve cells in our body, behind the brain, and it has its own nervous system, the Enteric Nervous System (ENS), which has led to the concept of the Gut Brain15. However, the role of the microbiota in this context, especially regarding the neuro-muscular diseases, is only barely known. Several studies have focused on autoimmune diseases such as inflammatory bowel disease (IBD), rheumatoid arthritis or multiple sclerosis but, to date, there are no data available on other pathologies such as myasthenia gravis (MG)"
"To the best of our knowledge this is the first study assessing the intestinal microbiota composition in AChR-MG patients as compared with matched healthy controls. Our results indicate a severe dysbiosis in the gut microbiota of these patients. This is in line with the recent evidence indicating the association of intestinal microbiota aberrancies and different autoimmune diseases such as allergy20,21, Type-1 diabetes22, inflammatory bowel disease23,24, lupus erythematosus25, multiple sclerosis26,27, rheumatoid arthritis28,29 or spondyloarthritis29, among others. However, there is not a common microbial dysbiosis pattern associated with these different autoimmune conditions and, therefore, the microbiota alterations found in MG patients do not seem to be extrapolated to other autoimmune conditions."
https://www.nature.com/articles/s41598-018-32700-y
I just wonder if MG is assosiated with reduced or altered gut biome diversity how this may effect my diabetes and blood sugar control as the gut biome must play a significant role in diabetes generally.
Here is something regarding this and T1D
Distinct fecal and oral microbiota composition in human type 1 diabetes, an observational study
"
Results
Oral microbiota were markedly different in T1D (eg abundance of Streptococci) compared to HC. Fecal analysis showed decreased butyrate producing species in T1D and less butyryl-CoA transferase genes. Also, plasma levels of acetate and propionate were lower in T1D, with similar fecal SCFA. Finally, fecal strains Christensenella and Subdoligranulum correlated with glycemic control, inflammatory parameters and SCFA.
Conclusions
We conclude that T1D patients harbor a different amount of intestinal SCFA (butyrate) producers and different plasma acetate and propionate levels. Future research should disentangle cause and effect and whether supplementation of SCFA-producing bacteria or SCFA alone can have disease-modifying effects in T1D."
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0188475
An increasing body of scientific evidence has arisen during the last years indicating that the microbiota-host interaction affects not just the gut environment but also distal organs5,6,7. Among these, several studies strongly suggest that the intestinal microbiota may interplay with the nervous system and the brain8. Animal studies have evidenced the potential of the gut microbiota to modulate pain perception9,10,11, behaviour, mood and stress response5,12,13. The gut microbiota is able to produce neuroactive molecules such as histamine, acetylcholine or GABA, among others14. Actually, the gut is the second organ with more nerve cells in our body, behind the brain, and it has its own nervous system, the Enteric Nervous System (ENS), which has led to the concept of the Gut Brain15. However, the role of the microbiota in this context, especially regarding the neuro-muscular diseases, is only barely known. Several studies have focused on autoimmune diseases such as inflammatory bowel disease (IBD), rheumatoid arthritis or multiple sclerosis but, to date, there are no data available on other pathologies such as myasthenia gravis (MG)"
"To the best of our knowledge this is the first study assessing the intestinal microbiota composition in AChR-MG patients as compared with matched healthy controls. Our results indicate a severe dysbiosis in the gut microbiota of these patients. This is in line with the recent evidence indicating the association of intestinal microbiota aberrancies and different autoimmune diseases such as allergy20,21, Type-1 diabetes22, inflammatory bowel disease23,24, lupus erythematosus25, multiple sclerosis26,27, rheumatoid arthritis28,29 or spondyloarthritis29, among others. However, there is not a common microbial dysbiosis pattern associated with these different autoimmune conditions and, therefore, the microbiota alterations found in MG patients do not seem to be extrapolated to other autoimmune conditions."
https://www.nature.com/articles/s41598-018-32700-y
I just wonder if MG is assosiated with reduced or altered gut biome diversity how this may effect my diabetes and blood sugar control as the gut biome must play a significant role in diabetes generally.
Here is something regarding this and T1D
Distinct fecal and oral microbiota composition in human type 1 diabetes, an observational study
"
Results
Oral microbiota were markedly different in T1D (eg abundance of Streptococci) compared to HC. Fecal analysis showed decreased butyrate producing species in T1D and less butyryl-CoA transferase genes. Also, plasma levels of acetate and propionate were lower in T1D, with similar fecal SCFA. Finally, fecal strains Christensenella and Subdoligranulum correlated with glycemic control, inflammatory parameters and SCFA.
Conclusions
We conclude that T1D patients harbor a different amount of intestinal SCFA (butyrate) producers and different plasma acetate and propionate levels. Future research should disentangle cause and effect and whether supplementation of SCFA-producing bacteria or SCFA alone can have disease-modifying effects in T1D."
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0188475
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