Sporting weekend in TO.

13/13 In summary, we believe that carbamazepine have the potential to be promising repurposed drugs for enhancing beta-cell survival in type 1 diabetes. However, it is important to note that further studies are required to optimize the drugs' activity and selectivity.

12/13 We propose that Na+ channels play a crucial role in the hyperexcitability observed in beta-cells when exposed to high glucose, and suggest that targeting Na+ channels could be a promising approach to modulate this hyperexcitability.

11/13 Our findings now indicate the need for a re-evaluation of the role of Na+ channels in pancreatic beta-cells.

10/13 By investigating electrophysiological properties of individual cells, we aimed to understand how Na+ channel inhibitors could potentially contribute to mitigating this excitotoxicity.

9/13 Our results indicate that the potential beneficial effects of Na+ channel inhibitors are mediated through the Nav1.7 channel, contributing to the mitigation of excitotoxicity. Excitotoxicity is a phenomenon associated with excessive stimulation and cell death.

8/13 To assess the contribution of Nav1.7 to the development of diabetes, we conducted our experiments in vivo using the NOD background. Interestingly, our findings revealed a protective effect against type 1 diabetes in NOD mice with beta-cell specific knockout of scn9a.

7/13 This was achieved by utilizing mice with a floxed Scn9a gene (scn9aflox/flox) and introducing a Ins1Cre knock-in allele (Ins1Cre/wt) for lifelong deletion. Alternatively, timed deletion was facilitated by delivering Cre through an AAV8 virus.

6/13 To investigate the target of Na+ channel inhibitors, we focused on a specific Na+ channel called Nav1.7, which is encoded by the gene scn9a. We knocked out the scn9a gene specifically in beta-cells of Non-obese diabetic (NOD) mice.

5/13 We initially focused on showing that the pro-survival properties of the Nav channel inhibitor Carbamazepine could be translated to human islet cells –We have previously demonstrated this in Min6- and mouse islet cells Ref. ( https://t.co/oKddXIwvLu).

4/13 The main aim of our paper was therefore to explore the significance of repurposed drugs that can enhance beta-cell survival and function in type 1 diabetes.

3/13 Now on to the findings…. So despite significant progress in type 1 diabetes management and beta-cell replacement therapies, there is currently no effective preventative treatment that targets beta-cell loss.

2/13 A especially big thanks to @natnahirney, Sophia Provenzano and my mentor @JimJohnsonSci who were a vital part in the project. Also appreciate the collaboratory work done by @bcellorg and Xiaio-Qing Dai. Big thank you to all the co-authors and funding.

1/13 I’m excited to share the pre-print of the main part of my PhD project titled “Pharmacological or genetic inhibition of Scn9aprotects beta-cells while reducing insulin secretion in type 1 diabetes” Click here:

@PeterOverby4 giving his talk at #ABC2023

@SisSkovsoe⁩ and ⁦@PeterOverby4⁩ paper is this week’s Featured Article in ⁦@TheEndoSociety⁩ journal Endocrinology! It describes how a Cre knockin NOD mouse line designed as a research tool actually prevented type 1 diabetes in its own.

We are hiring a post doc. If you have an interest in Molecular Biology, Primary Cilia, alpha cells and islet biology, this might be the perfect position for you.

Strategic wording from @UBC’s survey on allocation of yet another tuition increase. ‘Understanding’ student affordability? It isn’t affordable. Invest in actually fixing it, which wasn’t an option. Do better. #PhDlife

🚨🚨The University of Michigan Caswell Diabetes Institute is recruiting new faculty to join us in lovely Ann Arbor. Please RT, apply, or share with colleagues who might be interested! #GoBlue

Excited for all the exciting talks #EASD2022 @EASDnews! Come attend my talk Tuesday, 20th, OP6 11:15 am, titled "Quantification of the dynamics of Ins2 gene activity". Grateful to @JimJohnsonSci and organizers for the opportunity to present! https://t.co/ynPWX7SwI4