eads to endocrine tumors,’ explains Hua.
In type I diabetes, the loss of islet beta cells is the leading reason why a sufficient amount of insulin cannot be produced. ‘If we could eventually repress menin function to specifically stimulate beta-cell proliferation, this may facilitate devising new strategies to increase insulin-secreting beta cells and treating diabetes,’ notes Hua.
‘We did not expect the connection between a study about a tumor suppressor and a potential new avenue for treating diabetes,’ he adds. ‘By taking advantage of studying a genetically well-characterized tumor syndrome, MEN1, we set out to understand how the first step of benign tumor development is precisely controlled. The more we discovered about menin function, the better we understood the precise role of menin in regulating islet cell proliferation. This latest finding about the acute and specific role of menin on repressing islet cells, but not adjacent exocrine cells, led to the realization that manipulating the menin pathway might be a powerful way to stimulate islet cell proliferation to fight type I diabetes, although we are just beginning toward that goal.’
Study co-authors are Robert B. Schnepp, Ya-Xiong, Haoren Wang, Tim Cash, Albert Silva, Alan Diehl, and Eric Brown, with participation from the members of Dr. Eric Brown's lab and Dr. Alan Diehl's lab, all from Penn. This research was funded by the National Institutes of Health.
Source:Eurekalert
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