Category: Metabolic Disorders

Categories : Metabolic Disorders NeurologyTags :

Liraglutide Boosts Associative Learning in People with Obesity

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Obesity leads to altered energy metabolism and reduced insulin sensitivity of cells. The so-called “anti-obesity drugs” such as liraglutide are increasingly used to treat obesity and have caused tremendous interest, especially in the USA. Researchers in Germany have now shown in people with obesity that reduced insulin sensitivity affects learning of sensory associations. The results, published in Nature Metabolism, showed that a single dose of liraglutide was able to normalise these changes and restore the underlying brain circuit function.

The brain must be able to form associations in order to control behaviour. This involves, for example, associating a neutral external stimulus with a consequence following the stimulus. In this way, the brain learns what the implication of handling of the first stimulus are. Associative learning is the basis for forming neural connections and gives stimuli their motivational force. It is essentially controlled by a brain region called the dopaminergic midbrain. This region has many receptors for the body’s signalling molecules, such as insulin, and can thus adapt behaviour to the body’s physiological needs.

But what happens when the body’s insulin sensitivity is reduced due to obesity? Does this change brain activity, ability to learn associations and thus behaviour? Researchers at the Max Planck Institute for Metabolism Research have now measured how well the learning of associations works in participants with normal body weight (high insulin sensitivity, 30 volunteers) and in participants with obesity (reduced insulin sensitivity, 24 volunteers), and if this learning process is influenced by the anti-obesity drug liraglutide.

Low insulin sensitivity reduces the brain’s ability to associate sensory stimuli.

In the evening, they injected the participants with either the drug liraglutide or a placebo in the evening. Liraglutide is a so-called GLP-1 agonist, which activates the GLP-1 receptor in the body, stimulating insulin production and producing a feeling of satiety. It is often used to treat obesity and type 2 diabetes and is given once a day. The next morning, the subjects were given a learning task that allowed the researchers to measure how well associative learning works. They found that the ability to associate sensory stimuli was less pronounced in participants with obesity than in those of normal weight, and that brain activity was reduced in the areas encoding this learning behaviour.

After just one dose of liraglutide, participants with obesity no longer showed these impairments, and no difference in brain activity was seen between participants with normal weight and obesity. In other words, the drug returned the brain activity to the state of normal-weight subjects.

“These findings are of fundamental importance. We show here that basic behaviours such as associative learning depend not only on external environmental conditions but also on the body’s metabolic state. So, whether someone has overweight or not also determines how the brain learns to associate sensory signals and what motivation is generated. The normalisation we achieved with the drug in subjects with obesity, therefore, fits with studies showing that these drugs restore a normal feeling of satiety, causing people to eat less and therefore lose weight,” says study leader Marc Tittgemeyer from the Max Planck Institute for Metabolism Research.

“While it is encouraging that available drugs have a positive effect on brain activity in obesity, it is alarming that changes in brain performance occur even in young people with obesity without other medical conditions. Obesity prevention should play a much greater role in our healthcare system in the future. Lifelong medication is the less preferred option in comparison primary prevention of obesity and associated complications,” says Ruth Hanßen, first author of the study and a physician at the University Hospital of Cologne.

Source: Max Planck Institute for Biology of Ageing

Categories : Diet and Nutrition Metabolic DisordersTags :

Most Artificial Sweeteners Linked to Abdominal and Intramuscular Fat Increases

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Source: Pixabay CC0

Artificial sweeteners have once again returned to the headlines with the WHO listing them as a possible carcinogen, Now, a long-term study on artificial sweeteners in diets published in the International Journal of Obesity has shown that, ironically, nearly all of them are linked to increased adiposity.

In the two decade long study, University of Minnesota researchers examined people’s regular dietary intake, with a focus on non-nutritive sweeteners commonly found in artificial sweeteners. They found that long-term consumption of aspartame, saccharin and diet beverages were linked to increased abdominal and intramuscular adiposity. However, the study found no significant association between the artificial sweetener sucralose and these measures of fat volume.

“This study showed that habitual, long-term intake of total and individual artificial sweetener intakes are related to greater volumes of adipose tissue, commonly known as body fat,” said Brian Steffen, PhD, MSCR, a professor in the Department of Surgery at the U of M Medical School and co-investigator on the funded grant. “This was found even after accounting for other factors, including how much a person eats or the quality of one’s diet.”

The study’s findings raise concerns about the recommendations from the American Diabetes Association and the American Heart Association that promote the replacement of added sugars with artificial sweeteners. Based on their results, the researchers recommend considering alternative approaches, as long-term artificial sweetener consumption may have potential health consequences.

“This is an especially timely study, given the World Health Organization’s recent warning of the potential health risks of aspartame,” said Lyn Steffen, PhD, MPH, a professor in the School of Public Health and principal investigator on the study. “These findings underscore the importance of finding alternatives to artificial sweeteners in foods and beverages, especially since these added sweeteners may have negative health consequences.”

The researchers say that more studies are needed to better understand the connection between artificial sweetener intake and increased body fat. Further research is warranted to explore the underlying mechanisms and gain clearer insights into how dietary habits affect metabolic health.

Source: University of Minnesota Medical School

Categories : Metabolic DisordersTags :

Kombucha may Lower Fasting Blood Glucose in Type 2 Diabetes, Study Suggests

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People with type 2 diabetes who drank the fermented tea drink kombucha for four weeks had lower fasting blood glucose levels compared to when they consumed a similar-tasting placebo beverage, according to results reported in Frontiers in Nutrition. Though only a pilot 12-person feasibility trial, the finding suggests a dietary intervention that could help lower blood sugar levels in people with diabetes and also establishes the basis for a larger trial to confirm and expand upon these results.

Kombucha is a tea fermented with bacteria and yeasts and was consumed as early as 200BCE in China, but it has only recently become popular elsewhere. Its popularity has been bolstered by anecdotal claims of improved immunity and energy and reductions in food cravings and inflammation, but proof of these benefits has been limited. Researchers at Georgetown University’s School of Health, the University of Nebraska-Lincoln and MedStar Health conducted a clinical trial investigating its effects in diabetes.

“Some laboratory and rodent studies of kombucha have shown promise and one small study in people without diabetes showed kombucha lowered blood sugar, but to our knowledge this is the first clinical trial examining effects of kombucha in people with diabetes,” says study author Dan Merenstein, M.D., professor of Human Sciences in Georgetown’s School of Health and professor of family medicine at Georgetown University School of Medicine. “A lot more research needs to be done but this is very promising.”

Merenstein continued, “A strength of our trial was that we didn’t tell people what to eat because we used a crossover design that limited the effects of any variability in a person’s diet.”

The crossover design had one group of people drinking about eight ounces of kombucha or placebo beverage daily for four weeks and then after a two-month period to ‘wash out’ the biological effects of the beverages, the kombucha and placebo were swapped between groups with another four weeks of drinking the beverages.

Kombucha appeared to lower average fasting blood glucose levels after four weeks from 164 to 116mg/dL while the difference after four weeks with the placebo was not statistically significant. Guidelines from the American Diabetes Association recommended blood sugar levels before meals should be between 70–130mg/dL.

The researchers also looked at the makeup of fermenting micro-organisms in kombucha to determine which ingredients might be the most active. They found that the beverage was mainly comprised of lactic acid bacteria, acetic acid bacteria, and a form of yeast called Dekkera, with each microbe present in about equal measure; the finding was confirmed with RNA gene sequencing.

“Different studies of different brands of kombucha by different manufacturers reveal slightly different microbial mixtures and abundances,” says Robert Hutkins, PhD, University of Nebraska-Lincoln and the study’s senior author. “However, the major bacteria and yeasts are highly reproducible and likely to be functionally similar between brands and batches, which was reassuring for our trial.”

The researchers hope that larger studies will prove kombucha’s protective effects.

Source: Georgetown University Medical Center

Categories : Genetics Metabolic DisordersTags :

Abdominal Fat Accumulation may not be as Great a Diabetes Risk as Previously Thought

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Conventional wisdom holds that abdominal fat accumulation increases the risk for type 2 diabetes. But surprising new findings from the University of Virginia School of Medicine suggest that naturally occurring genetic variations in our genes can lead some people to store fat at the waist but also protect them from diabetes.

The unexpected discovery, which is published in eLife, provides a more nuanced view of the role of obesity in diabetes and related health conditions. It also could pave the way for more personalised medicine, such as prioritising weight loss for patients whose genes put them at increased risk but place less emphasis on it for patients with protective gene variants, the researchers say.

“There is a growing body of evidence for metabolically healthy obesity. In this condition, people who would normally be at risk for cardiovascular diseases and diabetes because they are obese are actually protected from adverse effects of their obesity. In our study, we found a genetic link that may explain how this occurs in certain individuals,” said researcher Mete Civelek, PhD, of UVA’s Center for Public Health Genomics. “Understanding various forms of obesity is important to tailor treatments for individuals who are at high risk for adverse effects of obesity.”

As medicine grows more sophisticated, understanding the role of naturally occurring gene variations will play an important role in ensuring patients get the best, most tailored treatments. The new work by Civelek and his team, for example, indicates that variants can simultaneously predispose some people to store fat at the abdomen, thought to put them at increased risk for metabolic syndrome, while also protecting them from type 2 diabetes. (Metabolic syndrome raises the risk for diabetes, stroke and other serious health issues.)

One of the metrics doctors use to determine if a patient has metabolic syndrome is abdominal obesity. This is often calculated by comparing the patient’s waist and hip measurements. But Civelek’s research suggest that, for at least some patients, it may not be that simple, with doctors using genetic testing to guide patients to good health.

“We found that among the hundreds of regions in our genomes which increase our propensity to accumulate excess fat in our abdomens, there are five which have an unexpected role,” said Yonathan Aberra, the lead author of the study and a PhD candidate at UVA’s Department of Biomedical Engineering, a joint program of the School of Medicine and School of Engineering. “To our surprise, these five regions decrease an individual’s risk for type 2 diabetes.”

In addition to producing surprising findings, Civelek’s research provides important new tools for his fellow researchers seeking to understand the complexities of gene variations. The sophisticated approach Civelek and his collaborators developed to identify the relevant variants and their potential effects will be useful for future research into metabolic syndrome and other conditions.

The tools could also prove invaluable in the development of new and better treatments for metabolic syndrome, the scientists say.

“We now need to expand our studies in more women and people from different genetic ancestries to identify even more genes that underlie the metabolically health obesity phenomenon,” Civelek said. “We plan to build on our findings to perform more experiments to potentially identify a therapeutic target.”

Source: University of Virginia Health System

Categories : Ageing Metabolic DisordersTags :

Metformin Also Seems to Protect Against Muscle Atrophy and Fibrosis

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Diabetes and muscle function might seem like they don’t have much to do with each other. But University of Utah Health researchers have discovered that metformin can also prevent muscle atrophy and muscular fibrosis – which can help the elderly bounce back faster from injury or illness. Their findings were published in the journal Aging Cell.

Metformin, the researchers found, actually has surprising applications on a cellular level. It can target senescent cells which impact muscle function. Senescent cells secrete factors associated with inflammation that may underlie fibrotic tissue, a hardening or scarring of tissues. They also discovered that metformin also reduces muscle atrophy.

“We’re interested in clinical application of this research,” says Micah Drummond, PhD, senior author of the study and professor of physical therapy and athletic training at the College of Health. “For example, knee surgeries in the elderly are notoriously hard to recover from. If we give a metformin-type agent during the recovery period, could we help the muscles get back to normal faster?”

Reinvigorating muscle recovery

Ageing comes with the risks of falls, hospitalisation, or developing chronic disease, which are more likely with muscle disuse. The research team wanted to find a therapeutic solution that could properly target both disuse atrophy and muscle recovery.

There’s an optimal level of senescent cells that are beneficial, no matter your age. In younger, healthier people, short-term senescence is required for a proper recovery from injury, and completely blocking the senescent effect impedes the body’s efforts to heal. Typically, a younger person can bounce back more easily after muscle disuse without the use of an intervention such as Metformin.

“In the case of aging, we know that there’s immune dysfunction,” says Drummond. “As you get older, it becomes harder for your body to clear senescent cells and they accumulate. That’s one reason recovery is much slower for the elderly after periods of disuse.”

Metformin’s anti-senescent properties have been demonstrated through pre-clinical studies. To test the intervention in humans, the team recruited 20 healthy male and female older adults for a multi-week study. They had participants undergo a muscle biopsy and MRI before the intervention, which involved five days of bed rest. One group of 10 received metformin and the other 10 received placebo pills during a two-week run-in period, then each group continued the placebo or metformin treatment during bed rest.

After the bed rest, participants received another muscle biopsy and MRI, then ceased treatments. All patients completed a seven-day re-ambulation period followed by a final muscle biopsy.

“We saw two things in our study,” Drummond says. “When participants took Metformin during a bed rest, they had less muscle atrophy. During the recovery period, their muscles also had less fibrosis or excessive collagen. That build-up can make it harder for the muscle to properly function.”

Tying these results to senescence, the research team examined muscle biopsies from study participants. They found that the participants who took Metformin had fewer markers of cellular senescence.

“This is the first paper that has made the direct connection between a therapy targeting cellular senescence and improved muscle recovery following disuse in aging,” says lead author Jonathan Petrocelli, PhD He explains that metformin helps muscle cells better remodel and repair tissue during periods of recovery after inactivity.

“Our real goal is to have patients maintain their muscle mass and function as they age, because atrophy and weakness are some of the strongest predictors of disease development and death,” he says.

Drummond’s team is following up on these findings by examining combining the drug with leucine, an amino acid that promotes growth and could accelerate recovery even further. They’ve already demonstrated the potency of this combination in preclinical animal studies.

“Metformin is cheap, effective and quite safe, so it’s exciting to see that we can use it to accelerate recovery for older individuals,” adds Drummond.

Source: University of Utah Health

Categories : Cardiovascular Disease Metabolic DisordersTags :

SGLT-2 Inhibitors Reduce HF Hospitalisation Risk in Type 2 Diabetes

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A study published in Annals of Internal Medicine has suggested that the new sodium-glucose co-transporter 2 inhibitors (SGLT-2i) may be viable as a first-line treatment in patients with type 2 diabetes (T2D), with reduced odds of hospitalisation for heart failure compared to those receiving metformin.

In cardiovascular outcome trials among adults with T2D, SGLT-2i have shown therapeutic promise, including reduced risk of hospitalisation for heart failure compared to placebo. However, SGLT-2i have mainly been evaluated as a second-line treatment, as metformin is generally given as a first-line, antidiabetic treatment.

In a new study, researchers from the Brigham compared cardiovascular outcomes among adults with T2D who initiated first-line treatment with either metformin or SGLT-2i. For the study, 8613 patients treated with SGLT-2i were matched to 17 226 patients treated with metformin. The authors found that patients receiving SGLT-2i showed a similar risk for myocardial infarction, stroke, and all-cause mortality, and a lower risk for hospitalization for heart failure compared with patients who received metformin. The risk for adverse events was similar except for an increased risk for genital infections compared with those receiving metformin.

“Our results suggest that SGLT-2i may be considered as first-line treatment for patients with T2D and cardiovascular disease or who are at increased risk for cardiovascular events,” said lead author HoJin Shin, BPharm, PhD, of the Division of Pharmacoepidemiology and Pharmacoeconomics. “However, more evidence from randomised clinical trials or observational studies will help us to identify patients who would benefit most from using SGLT-2i as first-line type 2 diabetes treatment.”

Source: EurekAlert!

Categories : Metabolic Disorders PaediatricsTags :

Childhood TV Watching Linked to Metabolic Syndrome in Adulthood

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A new study has added to the evidence that excessive TV watching as a child can lead to poor health in adulthood. The research, published this week in the journal Pediatrics, found that children who watched more television were more likely to develop metabolic syndrome as an adult.

Metabolic syndrome is a cluster of conditions including hypertension, hyperglycaemia, excess body fat, and abnormal cholesterol levels that lead to an increased risk of heart disease, diabetes and stroke.

Using data from 879 participants of the Dunedin study, researchers found those who watched more television between the ages of 5 and 15 were more likely to have these conditions at age 45.

Television viewing times were asked at ages 5, 7, 9, 11, 13 and 15. On average, they watched just over two hours per weekday.

“Those who watched the most had a higher risk of metabolic syndrome in adulthood,” says Professor Bob Hancox, who led the study.

“More childhood television viewing time was also associated with a higher risk of overweight and obesity and lower physical fitness.”

Boys watched slightly more television than girls and metabolic syndrome was more common in men, than women (34% and 20% respectively). The link between childhood television viewing time and adult metabolic syndrome was seen in both sexes however, and may even be stronger in women.

There was little evidence that watching less television as an adult reduced the association between childhood television viewing and adult health.

“While, like any observational study, researchers cannot prove that the association between television viewing at a young age directly causes adult metabolic syndrome, there are several plausible mechanisms by which longer television viewing times could lead to poorer long-term health.

“Television viewing has low energy expenditure and could displace physical activity and reduce sleep quality,” he says.

“Screentime may also promote higher energy intake, with children consuming more sugar-sweetened beverages and high-fat dietary products with fewer fruit and vegetables. These habits may persist into adulthood.”

The results are important because screen times have increased in recent years with new technologies.

“Children today have far more access to screen-based entertainment and spend much more time being sedentary. It is likely that this will have even more detrimental effects for adult health.

“These findings lend support to the World Health Organization recommendation that children and young teenagers should limit their recreational screen time.”

Source: University of Oregon

Categories : Metabolic DisordersTags :

T Cell Monitoring may Help Prevent Type 1 Diabetes

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A 3D map of the islet density routes throughout the healthy human pancreas. Source: Wikimedia CC0

Scripps Research scientists have shown that people at risk of developing type 1 diabetes could be identified by analysis of the T cells which drive the disease. The new approach, if validated in further studies, could be used to select suitable patients for a newly FDA-approved treatment that stops the autoimmune process, thereby making type 1 diabetes a preventable condition.

In the study, which appears in Science Translational Medicine, the researchers isolated T cells from mouse and human blood samples. By analysing the T cells that can cause type 1 diabetes, they were able to distinguish the at-risk patients who had active autoimmunity from those who had no significant autoimmunity – with 100% accuracy in a small sample.

“These findings represent a big step forward because they offer the possibility of catching this autoimmune process while there is still time to prevent or greatly delay diabetes,” says study senior author Luc Teyton, MD, PhD, professor in the Department of Immunology and Microbiology at Scripps Research.

The study’s first authors were graduate student Siddhartha Sharma and research assistants Josh Boyer and Xuqian Tan, all of the Teyton lab at the time of the study.

Type 1 diabetes usually occurs in childhood or early adulthood, in an autoimmune process that destroys the pancreas’s insulin-producing islet cells. The process can last years, with multiple starts and stops. Exactly how the process begins is not well understood, though it is known to involve genetic factors and may be triggered by routine viral infections.

In 2022, the US Food & Drug Administration approved an immune-suppressing therapy that can protect islet cells and at least delay diabetes onset by months to years if given in the early stages of autoimmunity. However, doctors have not had a good method for identifying people who could benefit from such treatment. They have traditionally examined levels of anti-islet antibodies in patient blood samples, but this antibody response has not been a very accurate measure of autoimmune progression.

“Anti-islet antibody levels are poorly predictive at the individual level, and type 1 diabetes is fundamentally a T cell-driven disease,” Teyton says.

In the study, Teyton and his team constructed protein complexes to mimic the mix of immune proteins and insulin fragments that CD4 T cells normally would recognise to initiate the autoimmune reaction. They used these constructs as bait to capture anti-insulin CD4 T cells in blood samples. They then analysed the gene activity within the captured T cells, and expression of proteins on the cells, to gauge their state of activation.

In this way, they were able to develop a classification algorithm that correctly identified which at-risk patients, in a set of nine, had ongoing anti-islet autoimmunity.

Teyton now hopes to validate the CD4 T cell-based approach with a long-term study in a larger cohort of participants, comparing this approach to the traditional approach of quantifying anti-islet antibodies.

Teyton and his colleagues also are working to make the process of isolating and analysing anti-islet T cells in blood samples more affordable and convenient, so that it can be used more easily in a clinical setting.

“If we can develop this into a useful method for identifying at-risk patients and tracking their autoimmunity status, we not only would have a way of getting the right people into treatment, but also would be able to monitor their disease progress and evaluate potential new preventive therapies,” Teyton says.

Source: Scripps Research Institute

Categories : Metabolic DisordersTags :

Earlier Breakfast Time Linked to Reduced Risk of Developing Diabetes

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According to the findings of a study published in the International Journal of Epedmiology, eating breakfast after 9am increases the risk of developing type 2 diabetes by 59% compared to people who eat breakfast before 8am. This is the main conclusion of a study which followed more than 100 000 participants in a French cohort. The results show that people can reduce the risk of diabetes not only by changing what their diet, but also their mealtimes.

Type 2 diabetes is associated with modifiable risk factors, such as an unhealthy diet, physical inactivity and smoking. But another factor may be important: timing of meals. “We know that meal timing plays a key role in regulating circadian rhythms and glucose and lipid control, but few studies have investigated the relationship between meal timing or fasting and type 2 diabetes,” says Anna Palomar-Cros, ISGlobal researcher and first author of the study.

In this study, a team from ISGlobal joined at team from INSERM in France to investigate the association between meal frequency and timing and the incidence of type 2 diabetes among 103 312 adults (79% women) from the French NutriNet-Santé cohort. Participants filled in online dietary records of what they ate and drank over a 24-hour period on 3 non-consecutive days, as well as the timing of their meals. The research team averaged the dietary records for the first two years of follow-up and assessed the participants’ health over the following years (an average of seven years).

Early breakfast, early dinner

There were 963 new cases of type 2 diabetes during the study. The risk of developing the disease was significantly higher in the group of people who regularly ate breakfast after 9am, compared to those who ate breakfast before 8 am. “Biologically, this makes sense, as skipping breakfast is known to affect glucose and lipid control, as well as insulin levels,” explains Palomar-Cros. “This is consistent with two meta-analyses that conclude that skipping breakfast increases the risk of type 2 diabetes,” she adds.

The research team also found that a late dinner (after 10 pm) seemed to increase the risk, while eating more frequently (about five times a day) was associated with a lower disease incidence. In contrast, prolonged fasting is only beneficial if it is done by having an early breakfast (before 8am) and an early dinner.

“Our results suggest that a first meal before 8am and a last meal before 7pm may help reduce the incidence of type 2 diabetes,” concludes Manolis Kogevinas, ISGlobal researcher and co-author of the study. In fact, the same ISGlobal team had already provided evidence on the association between an early dinner and a lower risk of breast or prostate cancer.

Taken together, these results consolidate the use of chrononutrition (ie the association between diet, circadian rhythms and health) to prevent type 2 diabetes and other chronic diseases.

Source: Barcelona Institute for Global Health (ISGlobal)

Categories : Medical Research & Technology Metabolic DisordersTags :

This Open-source Autoinjector Could Be Made for a Tenth of the Price of Commercial Ones

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Research team led by Joshua Pearce has developed a new 3-D printed, completely open-source autoinjector for a tenth of the cost of a commercially purchased product. (Photo by Anjutha Selvaraj)

A new study published in PLOS One describes the development of a spring-driven autoinjector for the delivery of insulin and other medications. This device, made from a combination of 3D-printed and commercially available parts, could cost less than $7 to make while a store-bought version is closer to $70.

Sir Frederick Banting was an inspiration for a new open source self-administering drug delivery device. Long before open source was an option or even a concept, the now-celebrated former University of Western Ontario lecturer refused to patent insulin because he wanted it to be inexpensive and widely available for the betterment of all.

A century after Banting won the Nobel Prize for his discovery, Western researchers led by engineering and Ivey Business School professor Joshua Pearce has developed a new 3D printed, completely open-source autoinjector – a device designed to deliver a single dose of medicine – for a tenth of the cost of a commercially purchased product.

“I think of this device, like so much of what we’re doing here at Western, very much as following the golden rule: do unto others as you would have them do unto you,” said Pearce. “It makes the world slightly better to have an open-source version of an autoinjector, especially for people who don’t have access or the financial means to purchase a proprietary one.”

Autoinjectors are used all over the world by health care practitioners, patients and parents (for children under 12) to inject insulin into people with diabetes. Other chronic conditions such as psoriasis, multiple sclerosis and rheumatoid arthritis can also be treated using an autoinjector. The device is also essential during emergency conditions for migraine, anaphylaxis and status epilepticus patients, as well.

Pearce, along with research assistant Anjutha Selvaraj and post-doctoral associate Apoorv Kulkarni, have created the new open-source autoinjector to make the device – considered more reliable and easier to operate than a simple syringe for self-administering medications into the body – an equitable alternative to the more expensive options.

Studies show self-administration of medications by patients improves compliance and comfort and empowers patients as they are actively involved in their personal care. It also allows patients to avoid time-consuming and costly visits to the hospital, which is a bonus for overburdened health care systems.

And, as with all open-source hardware, there is money to be made as the digitally replicable device enables low-cost distributed manufacturing. All materials, designs and assembly instructions are also detailed in the new study, and the effectiveness of the autoinjector is tested against the current standard (ISO 11608-1:2022) for needle-based injection systems. It is released with an open source hardware license. Companies wishing to commercialise the device will still need to meet their own local regulatory requirements.

“Does this design make it possible for other people to commercialise it anywhere in the world? Yes, it does,” said Pearce. “But more importantly, it means we can really target isolated communities, whether they’re in northern Canada, Africa or anywhere in else in the world, and improve health care access for everyone.”

Source: University of Western Ontario