ArticlemSystems2026
Gut microbiota translocation contributes to early islet apoptosis in streptozotocin-induced diabetes.
Article in mSystems, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
Abstract
Dysbiosis of the gut microbiota and impaired intestinal barrier are associated with diabetes development. The translocation of gut microbiota induced by streptozotocin (STZ) has been confirmed to damage pancreatic islets. However, it remains uncertain whether dysregulated gut microbiota plays an essential role in the translocation leading to pancreatic injury. In specific pathogen-free (SPF) and germ-free (GF) mice treated with STZ, we measured glucose metabolism levels, pancreatic islet damage, intestinal barrier integrity, and bacterial content in the pancreas to investigate the role of gut microbiota translocation in diabetes development. Shotgun metagenomic sequencing was used to analyze the impact of STZ on gut microbiota structure and function. Fecal microbiota transplantation was performed to explore if gut microbiota translocation depends on STZ-induced structural dysregulation. STZ induced intestinal damage in SPF mice, resulting in gut microbiota translocation to the pancreas, pancreatic apoptosis, and dysregulated glucose metabolism. Despite inherent intestinal barrier damage, absence of pancreatic apoptosis in GF mice further indicates that gut microbiota translocation is an essential prerequisite for STZ-induced pancreatic islet apoptosis. STZ significantly altered mouse gut microbiota composition and function. Transplantation of fecal microbiota from STZ-treated or saline-treated mice into STZ-induced GF mice also resulted in microbial translocation and pancreas apoptosis. Apoptosis of β cells in STZ-treated mice results from gut microbiota translocating to the pancreas through impaired intestinal barrier caused by STZ treatment independent of alterations in the gut microbial community.IMPORTANCEIn our study, the apoptosis of β cells in STZ-treated mice is the result of the translocation of gut microbiota to the pancreas through the impaired intestinal barrier induced by STZ, independent of alterations in the gut microbiota. These findings proposed the potential role of compounds in impairing the intestinal barrier integrity, promoting microbiota migration and finally damaging pancreatic islets.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.