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Type 1 Diabetes Baby

Type 1 Diabetes Originates in the Gut But Probiotics Could Offer Cure

Two separatType 1 Diabetes Babye pieces of research have found that the development of type 1 diabetes is likely caused by the gut, and therefore, a type of probiotic could be the cure.

Scientists from several European and US institutions studied 33 Finnish infants over three years from birth who were genetically predisposed to type 1 diabetes.

Their study, entitled “The Dynamics of the Human Infant Gut Microbiome in Development and in Progression toward Type 1 Diabetes” is published in the journal Cell Host & Microbe.

They discovered that four children in the group that developed type 1 diabetes had 25% less types of bacteria in their guts than other children.

The same four infants were also found to have more amounts of a specific bacteria that is known to trigger gut inflammation. This could be a prelude to type 1 diabetes as the bacteria causes the immune system to mistakenly attack and destroy beta cells in the pancreas that usually make insulin and monitor glucose levels.

“We know from previous human studies that changes in gut bacterial composition correlate with the early development of type 1 diabetes, and that the interactions between bacterial networks may be a contributing factor in why some people at risk for the disease develop type 1 diabetes and others don’t,” said Jessica Dunne, Director of Discovery Research at Juvenile Diabetes Research Foundation (JDRF), a UK charity which funded the study.

“This is the first study to show how specific changes in the microbiome are affecting the progression to symptomatic T1D.”

By being able to understand how the community of microorganisms in our guts (known as a microbiome) and which species are absent in the gastrointestinal tracts of children, the researchers believe they can slow down the progression of type 1 diabetes.

Probiotics could be the cure for type 1 diabetes

Cornell University researchers have a similar idea, but they have been working on a treatment that involves regulating insulin by engineering the bacteria found in our guts.

Their study, entitled “Engineered Commensal Bacteria Reprogram Intestinal Cells Into Glucose-Responsive Insulin-Secreting Cells for the Treatment of Diabetes” is published in the journal Diabetes.

The scientists took a strain of bacteria known as Lactobacillus gasseri – a type of bacteria found in probiotic yoghurts – and engineered the bacteria to be able to secrete a hormone called glucagon-like peptide-1 (GLP-1).

When they fed this engineered probiotic to a group of diabetic rats for 90 days, they discovered that the bacteria triggered the upper intestinal epithelial cells in the rats to convert into cells that acted a lot like the pancreatic beta cells.

The rats had up to 30% lower high blood glucose than diabetic rats that did not receive the probiotic, and the probiotic was shown to reduce glucose levels in diabetic rats the same way the levels would be reduced in normal rats.

“The amount of time to reduce glucose levels following a meal is the same as in a normal rat… and it is matched to the amount of glucose in the blood. It’s moving the centre of glucose control from the pancreas to the upper intestine,” said John March, professor of biological and environmental engineering at Cornell University and the paper’s senior author.

The next step for March and his team is to prove that their method of engineering bacteria to move insulin production to the intestine will work in humans too.

They aim to develop a pill that patients suffering from both type 1 and type 2 diabetes can take daily, that will be available within the next two years.

 

To learn how you can get more involved in the DRC’s research projects visit: Support a Diabetes Research Project

 

Source:

http://www.ibtimes.co.uk/type-1-diabetes-originates-gut-probiotics-could…

 

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Role of the integrated stress response in type 1 diabetes pathogenesis
In individuals with type 1 diabetes (T1D), the insulin-producing beta cells are spontaneously destroyed by their own immune system. The trigger that provokes the immune system to destroy the beta cells is unknown. However, accumulating evidence suggest that signals are perhaps first sent out by the stressed beta cells that eventually attracts the immune cells. Stressed cells adapt different stress mitigation systems as an adaptive response. However, when these adaptive responses go awry, it results in cell death. One of the stress response mechanisms, namely the integrated stress response (ISR) is activated under a variety of stressful stimuli to promote cell survival. However, when ISR is chronically activated, it can be damaging to the cells and can lead to cell death. The role of the ISR in the context of T1D is unknown. Therefore, in this DRC funded study, we propose to study the ISR in the beta cells to determine its role in propagating T1D.
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