We are back today after a 1.5-month hiatus, and I apologize for that – it has most definitely been the busiest semester of my life! Words of advice for any future students planning to do an honor’s project: try to gather and finish the data analysis as early as possible (harder than it sounds because experiments sometimes often do not go as planned) and begin writing your thesis as soon as possible! As the thesis writing really requires reading a lot of literature, critically thinking about results, and really organizing ideas, it takes a lot of time. With anything else you might have going on in 4th year, such as graduate/professional school/job applications, course studies, etc, you will really want to manage your time efficiently! Luckily, today, we will be glancing over a very promising article very recently published in Nature: Diabetes relief in mice by glucose-sensing insulin – secreting human a-cells (Furuyama et. al., 2019). Once again, the article link will be provided on the bottom of this page, and I really want to emphasize how amazing it is that being a student at uOttawa allows us to access such fantastic resources for free, which otherwise would cost a fee!
In case you did not have a chance to read the September blog, I mentioned that insulin is secreted by beta cells in the pancreas. Well, what if I told you that the researchers for this paper actually found a way to reprogram alpha (α) cells and pancreatic polypeptide (PPY)-producing γ-cells such that they can make insulin in response to glucose too! That is an absolute breakthrough! Imagine the possibilities! The first one that I think of right away relates to Type 1 (T1) diabetes. T1 diabetes is characterized by one’s own immune system targeting its own pancreatic beta cells for destruction, resulting in an insulin deficiency. Now what if other cell types can possibly make up for that deficiency?! By reprogramming the α and γ cells with transcription factors, a special protein that controls how genes are expressed, these cells were actually able to make glucose within a living mouse for up to 6 months after they were transplanted inside them!
Pancreatic beta, alpha, and gamma cells, are a part of clusters of cells in the pancreas, called islets. Therefore, these cells all fall under the category of “islet cells.” Alpha cells, normally, are the cells that produce glucagon, which has the opposite effect of insulin: to increase blood glucose levels. A very significant aspect that the authors have shown is that islet cells displays potential for plasticity even when mature. Plasticity is the ability of something to change/adapt itself in response to some form of stimulus. In this case, the stimuli were the transcription factors. This breakthrough lends great potential for the interconversion of islet cells between their different forms and functions. Alpha and gamma cells are great targets for reprogramming to beta cells, because they are very genetically similar, are in the same region, and have been shown to produce insulin more efficiently than other cell types. The article mentions that it remains “to be seen if diabetes therapies that modulate islet-cell interconversion without side effects are possible,” but what has been discovered still a huge stepping-stone towards any clinical applications in the future.
I wish you all a fantastic midterm season and hope no one loses out on too much sleep. The end of the semester is in sight, and I know we can all make it through! If you have any questions about the article, diabetes, or our club, feel free to send our club an email!
Until next time,
VP Research, uOttawa Team Diabetes
Article Link (or search it up on Google -> https://biblio.uottawa.ca/en/find/search-plus)
Furuyama, K., Chera, S., van Gurp, L., Oropeza, D., Ghila, L., Damond, N., Vethe, H., Paulo, J., Joosten, A., Berney, T., Bosco, D., Dorrell, C., Grompe, M., Ræder, H., Roep, B., Thorel, F. and Herrera, P. (2019). Diabetes relief in mice by glucose-sensing insulin-secreting human α-cells. Nature, 567(7746), pp.43-48.