Background Blood glucose fluctuations in patients with brittle diabetes have been a problem for clinicians. A recent study found that transplanting the intestinal flora of healthy people to patients with brittle diabetes can improve their blood glucose fluctuations. However, the underlying mechanism remains unclear. Methods Streptozotocin‐induced diabetic rats were assigned to receive fecal microbiota transplantation (FMT) from healthy donors or to remain untreated, while normal rats received FMT from brittle diabetes donors or remained untreated. Groups included the normal control group (NC group), the diabetic group (DM group), normal rats with FMT from brittle diabetic patients (NC‐DMFMT group), and diabetic rats with FMT from normal individuals (DM‐NCFMT group). Blood glucose variability, rat liver glucokinase, and glycogen levels, as well as intestinal short‐chain fatty acid content, were detected in each group of rats. Gut microbiota composition was analyzed using 16S rDNA sequencing. Results Compared with the standard deviation of blood glucose (SDBG) (1.664 ± 0.427 mmol/L) in the NC group, that of the DM group (6.879 ± 1.475 mmol/L) was higher. However, the DM‐NCFMT group reduced SDBG (4.387 ± 0.619 mmol/L) vs. the DM group ( p < 0.05). Hepatic glycogen (27.57 ± 5.254 mg/L) was lower in the DM group than in the NC group (55.48 ± 9.467 mg/L) but increased in the DM‐NCFMT group (37.59 ± 1.283 mg/L) vs. the DM group. The abundance of Bifidobacteria in the DM group was decreased compared to that in the NC group. In contrast, Bifidobacterium abundance in the DM‐NCFMT group increased after standard human flora transplants ( p < 0.05). Correlation and stepwise regression analysis indicated that Bifidobacteria reduced SDBG partly by promoting hepatic glycogen synthesis, with an effect share of 23.01%. Conclusion Normal individual fecal microbiota transplantation improves glucose variability in DM rats, potentially mediated by enhanced hepatic glycogen synthesis.
Dou et al. (2026) studied this question.