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DIABE T E S


could delay a diagnosis of type 1 diabetes by two years, in people who have a very high risk of developing the condition. At this year’s event, the TrialNet team provided an update. Having now followed participants for an average of 912 days, they are continuing to see an effect. Those taking the drug were less likely to progress to a diagnosis of type 1 diabetes than a comparison group who were given a dummy (or placebo) drug.


Their latest results show that 78% of people in the placebo group were diagnosed with type 1 diabetes during the trial, compared to 50% of participants who were treated with the drug. The median (a way of measuring the average) time for people in the placebo group to develop clinical type 1 diabetes was two years, while the median time in those taking teplizumab was five years. The TrialNet team also studied what happened in the pancreas. All of the participants started off producing similar levels of their own insulin and were showing a decline in insulin production before treatment. However, just three months after receiving teplizumaub, the researchers saw a striking reversal of this loss of insulin production. For individuals in the placebo group, insulin production continued to fall, suggesting the drug had an early effect on preserving beta cell function.


Type 2 diabetes: new research In type 2 diabetes the body stops responding to insulin, beta cells stop working properly and they lose their ability to produce insulin over time. Dr. Domenico Accili, of Columbia University, considered whether there is a way to reverse this progression. Dr. Accili explained that as type 2 progresses, beta cells go through a process known as dedifferentiation. They either revert into a less mature type of beta cell, which doesn’t have the right building blocks to be able to make insulin or they turn into another type of cell found in the pancreas, called an alpha cell, which again means they cannot make


Trial investigates potential to ‘train’ immune system


Data from the allergy community shows early introduction of peanuts can reduce the risk of developing a peanut allergy. So, can a similar approach in children at high risk for type 1 diabetes prevent insulin autoimmunity? Olga Kordonouri, PhD, shared insights from the Global Platform for the Prevention of Autoimmune Diabetes (GPPAD), which has developed a randomised controlled trial with oral insulin to try to answer that question. Dr. Kordonouri, head of clinical research at Children’s Hospital Auf Der Bult, in Hannover, Germany, said GPPAD has developed an international infrastructure, which enables the screening for type 1 diabetes in newborns from the general population. Screening is used to identify infants with an elevated genetic risk of developing type 1 diabetes for participation in the Primary Oral Insulin


insulin. To establish how we could reverse this process, Dr. Accili and his team first explored what drives beta cells to lose their function. They studied transcription factors – proteins that help turn genes ‘on’ or ‘off’ and identified some that appear to play an important role. The researcher found that one protein, BAH2, could restore beta cells back to their fully mature, insulin-producing state. Another, called AFF3, helped convert alpha-like cells back to beta cells. Although further research will be required to apply this research to people with type 2 diabetes, it opens up the possibility of life-changing therapies that could one day cure the condition.


Type 2 diabetes: new treatments Results announced at the virtual conference, from the eagerly anticipated DAPA-HF trial,


Trial (POInT) and monitor them for early diagnosis of type 1 diabetes. Dr. Kordonouri said the goal is to


identify infants with genetic predisposition in order to sensitise patients to insulin to train their immune systems and induce tolerance. Participants in the trial will receive either oral insulin provided as bulk human crystals in capsules or a placebo that is identical in appearance. So far, GPPAD has screened 176,222 infants and identified more than 1,000 with 25-fold higher genetic risk for type 1 diabetes. Dr. Kordonouri said participation by parents has been well tolerated and the dropout rate has been low. The primary outcome of POInT will be the development of persistent, confirmed, multiple beta-cell autoantibodies. The trial is expected to conclude by January 2025. Visit: www.adameetingnews.org


revealed that a drug used to treat type 2 diabetes may also help to prevent the condition. DAPA-HF originally set out to investigate


if an SGLT2 inhibitor, called dapagliflozin, could benefit people with chronic heart failure. The trial involved people with and without type 2 diabetes. As a sub-study, the researchers followed those who didn’t have the condition. They wanted to know if, along with protecting against heart damage, the drug could help to prevent type 2 diabetes. Around half of the 2,600 participants without type 2 diabetes took a daily dose of dapagliflozin for 18 months. The other half received a placebo drug. The findings showed that dapagliflozin reduced new-onset type 2 diabetes by 32%. 4.9% of people in the dapagliflozin group (64 of 1,298) developed type 2 diabetes during the study, compared to 7.1% (93 of 1,307) in the placebo group.


As this drug is used to help lower blood sugar levels in people with type 2 diabetes it is possible it is merely masking the development of type 2. But the researchers do not think this is the case. HbA1c was only minimally reduced compared to the start of the study in those taking dapagliflozin and there wasn’t much of a difference in HbA1c between the treatment and placebo groups. This is the first trial to show a prevention effect from an SGLT2 inhibitor. Diabetes UK described the findings as “good news” for people with heart problems who take this drug. The charity explained that, not only does it help to reduce the risk of death from heart complications, but it could also reduce their risk of developing type 2 diabetes. CSJ


SEPTEMBER 2020 WWW.CLINICALSERVICESJOURNAL.COM l 67


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