Salk Institute researchers have described a potential new approach to treating diabetes by protecting beta cells – the cells in the pancreas that produce, store and release the hormone insulin.
When the beta cells become dysfunctional, the body may • Lead insulin to control blood sugar (glucose) and glucose levels can lead to dangerous, even deadly concentrations
The researchers reached their destination with an unexpected source: Vitamin D. Vitamin D in cells and mouse models proved beneficial in the treatment of damaged beta cells. It also provided new insights into gene regulation that could be used in developing treatments for other diseases, including cancer.
"We know that diabetes is a disease caused by inflammation," said senior author Ronald Evans. "In this study, we identified the vitamin D receptor as an important modulator for both inflammation and survival of beta cells."
Using embryonic stem cell beta cells, researchers were able to identify a compound, iBRD9, that potentiates activation of the vitamin D receptor when combined with vitamin D to improve survival of beta cells.
The team achieved this through a screening test to search for compounds that improved survival of beta cells in a dish. They then tested the combination in a mouse model of diabetes and showed that it can bring glucose back to normal in the animals.
"This study began by studying the role of vitamin D in beta cells," said lead author Zong Wei. "Epidemiological studies in patients suggest a correlation between high levels of vitamin D in the blood and a lower risk of diabetes, but the underlying mechanism was poorly understood and it was difficult to protect beta cells with the vitamin alone. We now have some ideas on how we can use this compound. "
The underlying process has to do with transcription, how genes are translated into proteins. By combining the new compound with vitamin D, certain protective genes could be expressed in much higher amounts than in diseased cells.
"Activation of the vitamin D receptor can trigger the anti-inflammatory function of genes that help cells survive under stress conditions," said Michael Downes. "By using a screening system we developed in the lab, we were able to identify an important piece of this puzzle that allows for superactivation of the vitamin D signaling pathway."
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The implications of the discovery can have far-reaching implications: it identifies a fundamental mechanism that can put many different drug targets in the clinic.
"In this study, we looked at diabetes, but because this is an important receptor, it could possibly be universal for all treatments where you need to boost the effects of vitamin D," adds Ruth Yu, one of the authors of the study. "For example, we are particularly interested in studying it for pancreatic cancer, a disease our laboratory is already investigating."
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The team said that although the new compound apparently does not cause any side effects in the mice, more tests are needed before clinical Experiments can begin.
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Released: May 1