Monday January 21, 2019

Gut Bacteria Has The Ability To Contribute to Diabetes

"Our findings show clearly how important the interaction between gut microbiota and diet is to understand our metabolism in health and disease," said Backhed

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Diabetes
Representational image. Pixabay

Gut bacteria has the ability to affect how cells respond to insulin and can thus contribute to Type-2 diabetes, says a new study.

The study explored that the gut microbiota of people with treatment-naive Type-2 diabetes can be linked to a different metabolism of the amino acid histidine, which is mainly derived from the diet.

This in turn leads to the formation of imidazole propionate, a substance that impairs the cells’ ability to respond to insulin. Therefore, reducing the amount of bacterial-produced imidazole propionate could be a new way of treating patients with such disease.

“This substance does not cause all Type-2 diabetes, but our working hypothesis is that there are sub-populations of patients who might benefit from changing their diet or altering their gut microbiota to reduce the levels of imidazole propionate,” said Fredrik Backhed, Professor at the University of Gothenburg in Sweden.

Diabetes
Representational image. Pixabay

For the study, published in the journal Cell, the research team involved 649 participants.

They used fecal samples and found that the microbiota of people with Type-2 diabetes produced imidazole propionate when histidine was added. However, this mechanism was not found in the diabetes-free control subjects.

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“Our findings show clearly how important the interaction between gut microbiota and diet is to understand our metabolism in health and disease,” said Backhed.

The result also shows that gut bacteria from different individuals can lead to the production of completely different substances that may have very specific effects in the body,” he noted. (IANS)

Next Story

Novel Hope for Stem Cell Approach to Treat Diabetes

'Another idea would be to use gene-editing tools to alter the genes of beta cells in ways that would allow them to 'hide' from the immune system after implantation.'

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Diabetes
Representational image. Pixabay

The researchers, from the Washington University School of Medicine in St. Louis, said that when they transplanted the beta cells into mice that could not make insulin, the new cells began secreting insulin within a few days, and they continued to control blood sugar in the animals for months.

‘We’ve been able to overcome a major weakness in the way these cells previously had been developed. The new insulin-producing cells react more quickly and appropriately when they encounter glucose,’ said lead author Jeffrey R. Millman, PhD, Assistant Professor.

‘The cells behave much more like beta cells in people who don’t have diabetes,’ he said.

For the study, published in the journal Stem Cell Reports, the team grew beta cells from human stem cells, but they made numerous changes to the ‘recipe’ for producing insulin-producing beta cells, treating the cells with different factors at different times as they grew and developed to help the cells mature and function more effectively.

Diabetes
Representational image. Pixabay

After that process was complete, the researchers transplanted the beta cells into diabetic mice with suppressed immune systems so that they wouldn’t reject the human cells.

Those transplanted cells produced insulin at levels that effectively controlled blood sugar in the mice, functionally curing their diabetes for several months, which, for most of the mice in the study, was about the length of their lives.

The researcher said he can’t predict exactly when such cells may be ready for human trials but believes there are at least two ways that stem cell-derived beta cells could be tested in human patients.

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‘The first would be to encapsulate the cells in something like a gel — with pores small enough to prevent immune cells from getting in but large enough to allow insulin to get out,’ he said.

‘Another idea would be to use gene-editing tools to alter the genes of beta cells in ways that would allow them to ‘hide’ from the immune system after implantation.’ (IANS)