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HAMSAB supplement enhances SCFA production associated with microbiota and immune modulation in type 1 diabetes

ABSTRACT: Purpose: Short chain fatty acids (SCFAs) produced by the gut microbiota have dual beneficial anti-inflammatory and anti-dysbiotic effects associated with the prevention of type 1 diabetes (T1D) in mice. We have conducted a single-arm trial of a dietary supplement (HAMSAB), to determine the effects of increasing SCFA delivery in adults with long-standing T1D. Particularly, we examined blood transcriptome in these patients using RNA-seq. Methods: Blood was collected from patients at baseline and after 6 weeks of HAMSAB supplementation. Whole blood was collected directly into Paxgene or Tempus tubes containing RNA stabilisers and extracted according to the manufacturer's protocol. Next-gene sequencing of patients’ whole blood transcriptome was performed by Genewiz using Illumina NovaSeq platform obtaining sequence depth of 50 million reads/sample. Results: Several signalling pathways including fatty acid oxidation were found to be regulated by HAMSAB

ORGANISM(S): Homo sapiens

PROVIDER: GSE176230 | GEO | 2022/01/26

REPOSITORIES: GEO

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Project description:Objective: We hypothesized that type 1 diabetes (T1D) is accompanied by changes in gene expression in peripheral blood mononuclear cells (PBMCs) due to dysregulation of adaptive and innate immunity, counterregulatory responses to immune dysregulation, insulin deficiency and hyperglycemia. Research Design and Methods: Microarray analysis was performed on PBMCs from 43 patients with newly diagnosed T1D, 12 patients with newly diagnosed type 2 diabetes (T2D) and 24 healthy controls. One and four month follow-up samples were obtained from 20 of the T1D patients. Results: Microarray analysis identified 282 genes differing in expression between newlydiagnosed T1D patients and controls at a false discovery rate of 0.05. Changes in expression of interleukin-1Î² (IL1B), early growth response gene 3 (EGR3), and prostaglandin-endoperoxide; synthase 2 (PTGS2) resolved within four months of insulin therapy and were also observed in T2D suggesting that they resulted from hyperglycemia. With use of a knowledge base, 81/282 genes could be placed within a network of interrelated genes with predicted functions including apoptosis and cell proliferation. IL1B and the MYC oncogene were the most highly-connected genes in the network. IL1B was highly overexpressed in both T1D and T2D, whereas MYC was dysregulated only in T1D. Conclusion: T1D and T2D likely share a final common pathway for beta cell dysfunction that includes secretion of interleukin-1Î² and prostaglandins by immune effector cells, exacerbating existing beta cell dysfunction, and causing further hyperglycemia. The results identify several targets for disease-modifying therapy of diabetes and potential biomarkers for monitoring treatment efficacy. Experiment Overall Design: We obtained blood samples from 24 healthy volunteers, 43 newly diagnosed T1D patients and 12 newly diagnosed T2D patients. All study participants were between the ages of 2 and 18 years. We collected samples one and four months after diagnosis from the last 20 of the T1D patients. For each time point one sample did not pass quality control and was dropped from the analysis. Patients with T2D were distinguished from T1D on the basis of age, body habitus, Experiment Overall Design: presence (11/12 patients) of acanthosis nigricans, family history of type 2 diabetes (11/12 patients), and absence of autoantibodies to insulin, IA-2, and GAD65. We allowed low titers of insulin antibodies in T2D patients (< 4 U/mL), which have been previously reported. All but two Experiment Overall Design: of the T1D patients with positive anti-insulin antibodies were also positive for at least one additional autoantibody.

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HAMSAB supplement enhances SCFA production associated with microbiota and immune modulation in type 1 diabetes

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