DRC & Research News

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gut microbiome

Prolonged Antibiotic Treatment Induces A Diabetogenic Intestinal Microbiome That Accelerates Diabetes In NOD Mice

gut-microbiomeOriginal article published by the ISME Journal on August 14, 2015. Click here to read the original article.

Accumulating evidence supports that the intestinal microbiome is involved in Type 1 diabetes (T1D) pathogenesis through the gut-pancreas nexus. Our aim was to determine whether the intestinal microbiota in the non-obese diabetic (NOD) mouse model played a role in T1D through the gut.

To examine the effect of the intestinal microbiota on T1D onset, we manipulated gut microbes by: (1) the fecal transplantation between non-obese diabetic (NOD) and resistant (NOR) mice and (2) the oral antibiotic and probiotic treatment of NOD mice. We monitored diabetes onset, quantified CD4+T cells in the Peyer’s patches, profiled the microbiome and measured fecal short-chain fatty acids (SCFA). The gut microbiota from NOD mice harbored more pathobionts and fewer beneficial microbes in comparison with NOR mice.

Fecal transplantation of NOD microbes induced insulitis in NOR hosts suggesting that the NOD microbiome is diabetogenic. Moreover, antibiotic exposure accelerated diabetes onset in NOD mice accompanied by increased T-helper type 1 (Th1) and reduced Th17 cells in the intestinal lymphoid tissues. The diabetogenic microbiome was characterized by a metagenome altered in several metabolic gene clusters. Furthermore, diabetes susceptibility correlated with reduced fecal SCFAs.

In an attempt to correct the diabetogenic microbiome, we administered VLS#3 probiotics to NOD mice but found that VSL#3 colonized the intestine poorly and did not delay diabetes. We conclude that NOD mice harbor gut microbes that induce diabetes and that their diabetogenic microbiome can be amplified early in life through antibiotic exposure. Protective microbes like VSL#3 are insufficient to overcome the effects of a diabetogenic microbiome.

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Bacteria That Prevents Type 1 Diabetes

Original article published by Inserm on May 8, 2015. Click here to read the original article.

Our bodies have ten times the amount of microbes than human cells. This set of bacteria is called microbiota. In some instances, bacteria known as pathogens can cause infectious diseases. However, these micro-organisms can also protect us from certain diseases. Researchers from Inserm, Paris Descartes University and the CNRS (French National Centre for Scientific Research), through collaboration with teams from China and Sweden, have recently shown how microbiota protects against the development of type 1 diabetes. This research is published in the Immunity journal, 4 August 2015.

A pancreatic islet of Langerhans expressing the immunoregulator antimicrobial peptide CRAM (in red). The insulin-producting beta-cells are in green and the glucagon-producting alpha-cells are in blue. © Julien Diana

To combat pathogens, the immune system has developed various mechanisms to detect, defend against and even destroy micro-organisms that are harmful to the body. This includes antimicrobial peptides and natural proteins that destroy pathogenic bacteria by disrupting their cellular membrane. Not only are they produced by immune cells, they are also produced by cells whose functions are not immune-related.

A research team coordinated by Julien Diana, an Inserm Research Fellow at Inserm Unit 1151 “Institut Necker-Enfant Malades” [Necker Institute for Sick Children] (Inserm/CNRS/Université Paris Descartes), is focussing on a category of antimicrobial peptides, i.e. cathelicidins. Apart from their protective function, these peptides have also exhibited immunoregulatory abilities against several autoimmune diseases. As such, scientists hypothesise that cathelicidins may be involved in the control of type 1 diabetes, an autoimmune disease where certain cells in the immune system attack beta cells in the pancreas which secrete insulin.

Firstly, they observed that beta pancreatic cells in non-diseased mice produce cathelicidins and that, interestingly, this production is impaired in diabetic mice.

To test this hypothesis, they are injecting diabetic mice with cathelicidins where production is defective.

“Injecting cathelicidins inhibits the development of pancreatic inflammation and, as such, suppresses the development of autoimmune disease in these mice” states Julien Diana.

Given that the production of cathelicidins is controlled by short-chain fatty acids produced by gut bacteria, Julien Diana’s team are studying the possibility that this may by the cause of the cathelicidin deficiency associated with diabetes. Indeed, researchers have observed that diabetic mice have a lower level of short-chain fatty acids than that found in healthy mice.

By transferring part of the gut bacteria from healthy mice to diabetic mice, they are re-establishing a normal level of cathelicidin. Meanwhile, the transfer of micro-organisms reduces the occurrence of diabetes.

For the authors, “this research is further evidence of the undeniable role microbiota plays in autoimmune diseases, particularly in controlling the development of autoimmune diabetes”.

Preliminary data, as well as scientific literature, suggest that a similar mechanism may exist in humans, paving the way for new therapies against autoimmune diabetes.

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How Can YOU Influence the Future of Type 1 Diabetes Research?

DRC Logo for NewsWritten by Christie Auyeung on August 9, 2015 via diaTribe. Click here to read original article.

The Diabetes Research Connection (DRC) has created a novel crowdfunding platform which directly connects donors with early-career scientists, enabling them to perform peer-reviewed, innovative research in type 1 diabetes. DRC, which was first established in 2012 and recently had its official launch, is dedicated to supporting exciting ideas of these younger scientists, who often have difficulties securing funding. Through DRC, scientists can receive up to $50,000 to support new research designed to prevent, cure, or better treat type 1 diabetes. We had the chance to discuss the DRC’s goals with its President, Dr. Alberto Hayek, and Board Chair, Mr. David Winkler. See below for our fascinating interview!

In case you’ve never heard of crowdfunding (e.g., KickStarterIndiegogo), here’s how it works with DRC:

  • Scientists submit project proposals through the DRC website, which then undergo extensive review by a panel of over 80 leading diabetes experts for innovation, feasibility, value, and achievability.
  • In as few as 12 weeks, the most promising projects are selected and posted on DRC’s website.
  • Donors can choose projects they wish to fund (see the current projects available for support here) and donate right on the website.
  • Each researcher provides project updates and final outcomes to ensure transparency and adding to the body of diabetes research knowledge.

Back in March, we reviewed the Journal of the American Medical Association’s (JAMA) “Special Communication” paper titled “The Anatomy of Medical Research,” which pointed to the fact that diabetes and chronic illnesses are tremendously underfunded compared to other disease areas like cancer and HIV/AIDS. DRC provides one unique and complementary way of addressing this challenge, joining other efforts to increase diabetes research funding such as:

Bonus! Our Interview with Diabetes Research Connection’s Chair Mr. David Winkler and President Dr. Alberto Hayek

Q: What is so special or particularly advantageous about using a crowdfunding model to fund type 1 diabetes research?

Mr. Winkler: One serious problem is the dearth of funding for early-stage research, often the source of some of the best creativity. Mainstream funding sources such as JDRF, ADA, and NIH don’t provide grants in the range of $50,000, and many early-stage researchers who are in serious need of funding have difficulty obtaining grants. So we thought, why not go to the general public and enable DRC to complement these mainstream funding sources? In this way, we are broadening the base for donations, and the donor knows exactly to whom and what research project the funds are going.

Dr. Hayek: By following the instructions on the website, people can directly participate in the research of their choice. Right now when someone gives money to mainstream funding sources, they don’t have much choice as to how the money will be spent. That is why crowdfunding is ideal. We’re also hoping that through crowdfunding, we can increase engagement with the public and cause more people to become involved in diabetes research.

Q: What qualities distinguish early-career scientists, and why is it so important for DRC to focus on them?

Dr. Hayek: It is very difficult for an early investigator like a PhD student to apply for funding, especially young scientists who have out-of-the-box, creative, and risky ideas. Most PIs [“principal investigators,” essentially the lead researchers] are not willing to take on such risks, and that is where DRC provides a credible solution.

Mr. Winkler: We hope we can provide seed money so that researchers can generate preliminary data to begin to show proof of a principle that will then enable the researcher to apply for larger grants. Research funds are often focused on the translational back end of research, but if we fail to feed the front end of the pipeline, we won’t have much future research to drive the back end clinical studies. That is why we need to support exciting, early-stage, innovative ideas.

Q: What are you most proud of? What do you consider the DRC’s biggest successes thus far?

Dr. Hayek: We have 80 of the top scientists in diabetes research in the United States endorsing us and reviewing each project submitted. When we first told them of our idea, they were so overwhelmingly curious, interested and supportive.

Mr. Winkler: We’ve already fully funded two projects and we approved nine more projects this year.

Q: What are your short term and long term goals for DRC?

Mr. Winkler: We’re hopeful that we will fund at least ten projects this year, which would equal a half million dollars. I’d like to see DRC fund at least one million dollars in research next year. Our ultimate goal  to find new ways to prevent, cure, and care for people with diabetes. We hope our grants will provide the foundation for other researchers to pursue avenues they might not have considered, adding to the body of knowledge, and engage more people in the process.

Q: How can we motivate more young people to become engaged in diabetes/endocrinology?

Mr. Winkler: The best way to motivate a researcher is to provide funding. If the funding is not there, they may turn to other diseases, away from diabetes. In terms of motivation for donors and others, DRC provides the only platform where you can directly influence the future of diabetes research and be assured that 100% of your donation goes directly to the research you designate. It’s also very important for DRC supporters to get the word out about this platform via social networking and direct contact with those involved in the diabetes fight for better solutions.

Q: What do you think is the most solvable problem in diabetes?

Mr. Winkler: One of the biggest problems in type 1 diabetes is blood glucose variability. The advent of CGMs has made a huge difference in blood sugar control. That combined with a low glycemic diet produces considerably less variability in glucose levels. It’s not a cure or permanent solution, but it enables any person with type 1 diabetes to keep their blood glucose levels within a tighter bandwidth. Better glucose sensors would be great as well as faster insulins. Ultimately, an artificial pancreas will help further enhance blood glucose range control in the near future, or increasing access to those as well. Also, using CGM’s should be made available now and result immediately in better hospital outcomes.

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See our approved research projects and campaigns.

Role of the integrated stress response in type 1 diabetes pathogenesis
In individuals with type 1 diabetes (T1D), the insulin-producing beta cells are spontaneously destroyed by their own immune system. The trigger that provokes the immune system to destroy the beta cells is unknown. However, accumulating evidence suggest that signals are perhaps first sent out by the stressed beta cells that eventually attracts the immune cells. Stressed cells adapt different stress mitigation systems as an adaptive response. However, when these adaptive responses go awry, it results in cell death. One of the stress response mechanisms, namely the integrated stress response (ISR) is activated under a variety of stressful stimuli to promote cell survival. However, when ISR is chronically activated, it can be damaging to the cells and can lead to cell death. The role of the ISR in the context of T1D is unknown. Therefore, in this DRC funded study, we propose to study the ISR in the beta cells to determine its role in propagating T1D.
Wearable Skin Fluorescence Imaging Patch for the Detection of Blood Glucose Level on an Engineered Skin Platform
A Potential Second Cure for T1D by Re-Educating the Patient’s Immune System
L Ferreira
Validating the Hypothesis to Cure T1D by Eliminating the Rejection of Cells From Another Person by Farming Beta Cells From a Patient’s Own Stem Cells
Han Zhu
Taming a Particularly Lethal Category of Cells May Reduce/Eliminate the Onset of T1D
JRDwyer 2022 Lab 1
Can the Inhibition of One Specific Body Gene Prevent Type 1 Diabetes?
Is Cholesterol Exacerbating T1D by Reducing the Functionality and Regeneration Ability of Residual Beta Cells?
Regeneration Ability of Residual Beta Cells
A Call to Question… Is T1D Caused by Dysfunctionality of Two Pancreatic Cells (β and α)?
Xin Tong
Novel therapy initiative with potential path to preventing T1D by targeting TWO components of T1D development (autoimmune response and beta-cell survival)
flavia pecanha