GUT: Dung transplants can stop the progression of new type 1 diabetes

Type 1 diabetes (T1D) is an autoimmune disease characterized by β cell damage.
T1D-induced T-cell-mediated autoimmunity has prompted attempts to prevent disease progression by targeting T lymphocytes with immunosuppressive drugs such as cyclosporine, anti-CD3 antibodies, anti-thymus cell globulin 3 and anti-CD80 antibody therapy, among others.
, however, these treatment strategies have at best a temporary improvement in the progression of the disease, have no effect on long-term progression, and are accompanied by serious side effects.
, there is an urgent need to learn more about T1D pathophysiology in order to find new treatments.
T1D pathophysiology was associated with changes in the gut bacteriobi.
in mice with non-obesity diabetes (NOD), the interaction of gut microbes with the innocid immune system is a key factor in T1D development and can be improved by fecal microbial transplantation (FMT) and specific microorganisms.
study explores the effects of fecal microbiome transplantation (FMT) on disease progression in people with type 1 diabetes.
researchers randomly divided patients with T1D (18-30 years of age) who had been on the disease for six weeks into two groups, one receiving three autobiographic or foreign (healthy supply) FMT treatments over a four-month 100-month time and the other in a control group.
observational endpoint was the retention of stimulated C peptide releases over a 12-month period through mixed dietary testing.
secondary results were changes in blood sugar control, fasting plasma metabolites, T-cell autoimmunity, small intestine gene expression spectrum, and intestinal bacterial composition.
at 12 months, the stimulating C peptide levels were significantly retained compared to the healthy provider FMT group (n s 10 subjects).
the bacterial concentration in the small intestine is inversely inversely related to the remaining β cell function (r - -0.55, p - 0.02), while plasma metabolites 1-peanut tyrene-GPC and 1-nutmeg base The level of -2-peanut tyrenic acid-GPC is linearly related to the preservation of residual β cells (r s 0.56, p s 0.01, r s 0.46, p s 0.042).
, the baseline CD4 plus CXCR3 plus T cell count in the heteroential biopsy, the level of vibrio desulfurization in the small intestine, and the expression of the CCL22 and CCL5 genes predicted the β cell function retained after FMT.
study, the authors say FMT aborted endo-endo-insulin production in newly diagnosed T1D patients within 12 months of the onset of T1D.
and bacterial strains from several microbial sources are associated with retained residual β cell function.
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