January 24, 2017
2 min read
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‘Strong link’ observed between gut inflammation, type 1 diabetes

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Adults with type 1 diabetes have an “inflammatory signature” that characterizes their duodenal mucosa and sets them apart from adults with celiac disease, although whether the inflammation is a cause or consequence of the autoimmune process remains unclear, study findings show.

“Our findings indicate the individuals with type 1 diabetes have an inflammatory signature and microbiome that differ from what we see in people who do not have diabetes or even in those with other autoimmune conditions such as celiac disease,” Lorenzo Piemonti, MD, of the Diabetes Research Institute at San Raffaele Hospital in Milan, said in a press release. “Some researchers have theorized that the gut may contribute to the development of type 1 diabetes, so it is important to understand how the disease affects the digestive system and microbiome.”

Piemonti and colleagues analyzed biopsies of the duodenal mucosa in 19 patients with type 1 diabetes, 19 patients with celiac disease and 16 healthy controls, all recruited from the San Raffaele Scientific Institute between 2005 and 2015. Researchers assessed the expression of 91 genes related to inflammation — mainly cytokines, chemokines and chemokine receptors — and immunohistochemistry to measure inflammation, as well as 16S rRNA gene sequencing to analyze microbiome composition among the three groups of patients.

Researchers observed an increased expression of 10 genes in patients with type 1 diabetes vs. patients with celiac disease or controls: CCL13, CCL19, CCL22, CCR2, COX2, IL4R, CD68, PTX3, TNF-alpha and VEGFA genes. Among these genes, CD68, PTX3, TNF-alpha and VEGFA were also down-regulated in patients with celiac disease, but not controls, according to researchers. There was no association found between gene expression and HbA1c, duration of diabetes, secondary complications or the reason that led to endoscopy.

In immunohistochemical analysis, researchers confirmed a specific inflammatory status for those with type 1 diabetes vs. tissues from patients with celiac disease or controls, characterized by an increase in monocyte/macrophage lineage infiltration (P < .01).

Researchers also observed a difference in the duodenal mucosal microbiome of patients with type 1 diabetes, noting an increase in Firmicutes, the ratio of Firmicutes to Bacteroidetes and a reduction in Proteobacteria and Bacteroidetes. The expression of genes specific for type 1 diabetes inflammation was associated with the abundance of specific bacteria in duodenum.

“We don’t know if type 1 diabetes’ signature effect on the gut is caused by or the result of the body’s own attacks on the pancreas,” Piemonti said. “By exploring this, we may be able to find new ways to treat the disease by targeting the unique gastrointestinal characteristics of individuals with type 1 diabetes.” by Regina Schaffer

Disclosure: The researchers report no relevant financial disclosures.

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