Tag: diabetes

Categories : Metabolic Disorders Respiratory DiseasesTags :

Why People with Diabetes are More Vulnerable to Respiratory Infection

On By ModernMedia
Credit: Scientific Animations CC4.0

It has long been known that people with diabetes are at a substantially increased risk of developing severe lung disease if they become infected with viruses such as influenza, as well as other pathogens. When the COVID-19 pandemic started in early 2020, it became even more important to understand this mysterious phenomenon. It became clear that people with diabetes were at a significantly higher risk of coming down with severe, even fatal, lung disease after developing severe COVID, but no one understood why. In fact, some 35% of the pandemic’s COVID mortalities had diabetes.

Now, research conducted at the Weizmann Institute of Science and published in Nature has revealed how, in diabetics, high levels of blood sugar disrupt the function of key cell subsets in the lungs that regulate the immune response. It also identifies a potential strategy for reversing this susceptibility and saving lives.

Prof. Eran Elinav‘s team in his lab at Weizmann, headed by Drs. Samuel Nobs, Aleksandra Kolodziejczyk and Suhaib K. Abdeen, subjected multiple mouse models of types 1 and 2 diabetes to a variety of viral lung infections. Just as in diabetic humans, in all these models the diabetic mice developed a severe, fatal lung infection following exposure to lung pathogens such as influenza. The immune reaction, which in nondiabetics eliminates the infection and drives tissue healing, was severely impaired in the diabetic mice, leading to uncontrolled infection, lung damage and eventual death.

Next, to decode the basis of this heightened risk, the team performed an evaluation of gene expression on the level of individual cells, in more than 150 000 single lung cells of infected diabetic and nondiabetic mice. The researchers also performed an extensive array of experiments involving immune and metabolic mechanisms, as well as an in-depth assessment of immune cell gene expression in infected diabetic mice. In the diabetic mice they identified a dysfunction of certain lung dendritic cells, the immune cells that orchestrate a targeted immune response against pathogenic infection. “High blood sugar levels severely disrupt certain subsets of dendritic cells in the lung, preventing these gatekeepers from sending the molecular messages that activate the critically important immune response,” says Nobs, postdoctoral fellow and study first author. “As a result, the infection rages on, uncontrolled.”

Next, they explored ways to prevent the harmful effects of hyperglycaemia in lung dendritic cells, as a means of lowering the infection’s risk in diabetic animals. Indeed, tight control of glycaemic levels by insulin supplementation prompted the dendritic cells to regain their capacity to generate a protective immune response that could prevent the cascade of events leading to a severe, life-threatening viral lung infection. Alternatively, administration of small molecules reversing the sugar-induced regulatory impairment corrected the dendritic cells’ dysfunction and enabled them to generate a protective immune response despite the presence of hyperglycaemia.

“Correcting blood sugar levels, or using drugs to reverse the gene regulatory impairment induced by high sugar, enabled our team to get the dendritic cells’ function back to normal,” says Abdeen, a senior intern who co-supervised the study. “This was very exciting because it means that it might be possible to block diabetes-induced susceptibility to viral lung infections and their devastating consequences.”

Lung tissue of a diabetic mouse (right) contains fewer immune cells (small purple dots) than that of a non-diabetic animal (left)

With over 500 million people around the world affected by diabetes, and with diabetes incidence expected to rise over the next decades, the new research has significant, promising clinical implications.

“Our findings provide, for the first time, an explanation as to why diabetics are more susceptible to respiratory infection,” Elinav says. “Controlling sugar levels may make it possible to reduce this pronounced diabetes-associated risk. In diabetic patients whose sugar levels are not easily normalized, small molecule drugs may correct the gene alterations caused by high sugar levels, potentially alleviating or even preventing severe lung infection. Local administration of such treatments by inhalation may minimize adverse effects while enhancing effectiveness, and merits future human clinical testing.”

Source: Weizmann Institute of Science

Categories : Metabolic DisordersTags :

Scientists Identify New Cause of Diabetes – and Potential Treatment Target

On By ModernMedia
Photo by Photomix Company on Pexels

Researchers have identified an enzyme that blocks insulin produced in the body – a discovery that could provide a new target to treat diabetes. Their study, published the journal Cell, focuses on nitric oxide, which dilates blood vessels, improves memory, fights infection and stimulates the release of hormones, among other functions.

How nitric oxide performs these activities had long been a mystery.

The researchers at Case Western Reserve University and University Hospitals discovered a novel “carrier” enzyme (called SNO-CoA-assisted nitrosylase, or SCAN) that attaches nitric oxide to proteins, including the receptor for insulin action.

They found that the SCAN enzyme was essential for normal insulin action, but also discovered heightened SCAN activity in diabetic patients and mice with diabetes.

Mouse models without the SCAN enzyme appeared to be shielded from diabetes, suggesting that too much nitric oxide on proteins may be a cause of such diseases.

“We show that blocking this enzyme protects from diabetes, but the implications extend to many diseases likely caused by novel enzymes that add nitric oxide,” said the study’s lead researcher Jonathan Stamler, professor at the Case Western Reserve School of Medicine.

“Blocking this enzyme may offer a new treatment.”

Given the discovery, next steps could be to develop medications against the enzyme, he said.

Many human diseases, including Alzheimer’s, cancer, heart failure and diabetes, are thought to be caused or accelerated by nitric oxide binding excessively to key proteins.

With this discovery, Stamler said, enzymes that attach the nitric oxide become a focus.

With diabetes, the body often stops responding normally to insulin.

The resulting increased blood sugar stays in the bloodstream and, over time, can cause serious health problems.

Individuals with diabetes, the Centers for Disease Control reports, are more likely to suffer such conditions as heart disease, vision loss and kidney disease.

But the reason that insulin stops working isn’t well understood.

Excessive nitric oxide has been implicated in many diseases, but the ability to treat has been limited because the molecule is reactive and can’t be targeted specifically, Stamler said.

“This paper shows that dedicated enzymes mediate the many effects of nitric oxide,” he said. “Here, we discover an enzyme that puts nitric oxide on the insulin receptor to control insulin. Too much enzyme activity causes diabetes. But a case is made for many enzymes putting nitric oxide on many proteins, and, thus, new treatments for many diseases.”

Source: Case Western Reserve University

Categories : Metabolic Disorders Obstetrics & GynaecologyTags :

Macrophages ‘Eat’ Pancreatic β Cells to Regulate Insulin Post Partum

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

Scientists have long known that pancreatic β cells increase during pregnancy and promptly return to their original number following birth. But the underlying mechanisms that cause the cells to go back to their original number are still not well understood.

In a significant breakthrough, a research group using mouse models, has discovered that macrophages ‘eat’ (phagocytose) the pancreatic β cells, thereby revealing the process behind their return to previous levels after pregnancy.

The research group, which was led by Associate Professor Junta Imai, Assistant Professor Akira Endo, and Professor Hideki Katagiri from Tohoku University’s Graduate School of Medicine, published the results in the journal Development Cell.

Initially, the group examined the number of pancreatic β cells in the islets of Langerhans in a mouse model of pregnancy.

They confirmed the cell number was double at the end of the pregnancy when compared to non-pregnant mice, but that it then gradually decreased, returning to the original amount after delivery.

“After we observed the islets of Langerhans before and after delivery, we noticed an increase in macrophages, which protect the body from infections by engulfing bacteria, foreign substances and dead cells, after delivery,” says Imai.

“When we applied treatment to inhibit this process, the blood glucose levels became too low (hypoglycaemia).”

Additional microscopic observation of the islets of Langerhans after birth revealed β cells to be phagocytosed by macrophages.

This mechanism appeared to keep the mother’s blood glucose levels from decreasing excessively after delivery by rapidly reducing pancreatic β cells to their normal pre-pregnancy number.

Next, the group identified the protein responsible for attracting the macrophages into the islets of Langerhans: cytokine CXCL10.

Accordingly, the inhibition of CXCL10 function suppressed the decrease in pancreatic β cells after birth.

“We hope our results will contribute to clarifying the means by which normal blood glucose levels are maintained as well as the development of methods to prevent and treat diabetes,” adds Imai.

Source: Tohoku University

Categories : Cardiovascular Disease Metabolic DisordersTags :

Collaboration Key to Address SA’s Fatal, Diabetes-linked Cardiovascular Disease Burden

On By ModernMedia
Photo by Hush Naidoo on Unsplash

Only concerted multi-disciplinary collaboration and research will stem the tide of diabetes and diabetes-linked cardiovascular disease (CVD), the latter currently the leading cause of death locally and worldwide, claiming 17.9 million lives annually1.

This was the consensus among some of the world’s leading cardiologists and researchers gathered at the SA Heart Association’s annual congress aptly themed: ‘The Cardiac Collaboration,’ which took place at the Sandton Convention Centre in Johannesburg from 26-29 October this year.

Globally, CVD takes more lives than TB, HIV and malaria combined, while 215 South Africans are killed by CVD every day – with 80% of CVD and strokes being preventable.1,2 The prevalence of diabetes has also increased in South Africa, from 4.5% in 2010 to 12.7% in 2019. Of the 4.58 million people aged 20-79 years who were estimated to have diabetes in 2019, 52.4% were undiagnosed.3

With diabetes being a key driver of CVD – especially in Africa (with limited access to novel drugs and the prevalence of sugar-rich, poverty-driven lifestyles), the mutual consensus at this year’s congress was that collaboration is key.

Dr Zaheer Bayat, Chairperson of the Society for Endocrinology, Metabolism and Diabetes of South Africa (SEMDSA), told delegates that endocrinologists and cardiologists would have to work together to improve outcomes for diabetic patients, 30% of whom suffered cardiovascular events. He warned that a 134% increase of people living with diabetes was predicted over the next two decades, translating into a dramatic surge in chronic kidney disease, cardiovascular disease, blindness, and amputations.

Dr Bayat said he intends appealing for mass diabetes screening to find the 52% of people whom researchers estimate are undiagnosed. Ideally, this should be followed by access to cheaply acquired, effective new glucose-lowering drugs.

“The reality is that this country cannot afford all the new treatments for everyone – not private funders, not government. So, drugs are not really a solution – the best solution is to change lifestyle and prevent disease in the first place,” said Dr Bayat.

“We’re here to fight for our patients, not our pockets. Can we afford to have 52% of our patients not knowing they’re diabetic? People who should be contributing to our economy are living with diabetes and eventually dying,” he asserted.

Dr Bayat also said that globally, First World countries such as the USA and Sweden are reducing myocardial infarctions, strokes, and amputations, because they’re doing all the right things together. This included adopting a healthy lifestyle, effective management of sugar, blood pressure and cholesterol and smoking cessation.

“However, here in South Africa with private healthcare representing 15% of healthcare delivery but consuming 50% of the spend and the public sector representing 85% of the population and consuming the other half – we’re not doing nearly as well. With only 200 cardiologists in the country (one per 190 000 population), and even less nephrologists, we need to join together and change the trajectory of diabetes. We must work together to reduce morbidity and mortality,” said Dr Bayat.

According to the SA Heart Association, this graphically illustrates the importance of a multi-disciplinary approach, the very reason why the conference was called ‘The Cardiac Collaboration.’

The SA Heart Association has already begun forging formal ties with other academic societies and next year, it hopes to join and host joint sessions with collaborative meetings to connect a multidisciplinary team in order to achieve a well-rounded balance of care.

References:

  1. https://www.heartfoundation.co.za/wp-content/uploads/2017/10/CVD-Stats-Reference-Document-2016-FOR-MEDIA-1.pdf.
  2. https://world-heart-federation.org/what-we-do/prevention/#:~:text=An%20estimated%2080%25%20of%20cardiovascular,and%20%E2%80%9Cknowing%20your%20numbers%E2%80%9D.
  3. International Diabetes Federation. IDF Diabetes Atlas.10th ed. International Diabetes Federation; Brussels, Belgium: 2021. [Google Scholar] (primary). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10218408/#:~:text=The%20prevalence%20of%20diabetes%20mellitus,%25%20were%20undiagnosed%20%5B5%5D. (secondary).
Categories : Cancer Metabolic DisordersTags :

Diabetes Worsens Colorectal Cancer Survival Odds by 41%

On By ModernMedia
Photo by Nataliya Vaitkevich on Pexels

In an analysis of information on adults with colorectal cancer, patients who also had diabetes, particularly those with diabetic complications, faced a higher risk of early death. The results are published in CANCER, a peer-reviewed journal of the American Cancer Society.

For the study, Kuo‐Liong Chien, MD, PhD, of National Taiwan University, and his colleagues examined data registered between 2007 and 2015 in the Taiwan Cancer Registry Database, which is linked to health insurance and death records. Their analysis included 59 202 individuals with stage I–III colorectal cancer who underwent potentially curative surgery to remove their tumours. Among these patients, 9448 experienced a cancer recurrence and 21 031 died from any cause during the study period.

Compared with individuals without diabetes, those with uncomplicated diabetes were at a minimally or insignificantly higher risk of all‐cause and cancer‐specific death, whereas those with complicated diabetes had 85% higher odds of death from any cause and 41% higher odds of death from cancer. These associations were more pronounced in women and in patients with early‐stage colorectal cancer.

Also, compared to patients without diabetes, patients with uncomplicated or complicated diabetes had a 10–11% higher risk of colorectal cancer recurrence.

The mechanisms behind the relationship between diabetic severity and poor colorectal cancer prognosis could involve various pathways and responses triggered by high insulin and glucose levels in the blood, as well as elevated inflammatory states, which are characteristic of type 2 diabetes.

“While a higher diabetes prevalence was noted in patients with colorectal cancer, the study suggests that coordinated medical care involving multiple specialists can help prevent diabetes complications, potentially improving long-term colorectal cancer oncological outcomes, particularly in women and patients with early-stage cancer,” said Dr Chien.

Source: Wiley

Categories : Metabolic DisordersTags :

Don’t Overlook Latent Autoimmune Diabetes in Adults, Researchers Caution

On By ModernMedia
Photo by Photomix Company on Pexels

To reduce the risk of complications, it is important to measure antibodies those with adult onset diabetes, while also considering the levels of these antibodies.

In a study published in the journal Diabetes Care, researchers demonstrate that individuals with Latent Autoimmune Diabetes in Adults (LADA) have an equally high risk of developing cardiovascular disease as people with type 2 diabetes, but a higher risk of developing retinopathy and poorer glucose control. Many also lack adequate treatment.

LADA is a common but relatively unknown form of diabetes. Similar to type 1 diabetes, it is an autoimmune disease characterised by antibodies against insulin-producing cells. It develops in adulthood, and the autoimmune process progresses more slowly than in type 1 diabetes. LADA also shares features with type 2 diabetes, which means those affected risk getting the wrong diagnosis if antibodies are not measured. Incorrect diagnosis can result in inadequate treatment. Previous studies suggest that between five and ten percent of all individuals initially diagnosed with type 2 diabetes actually have LADA. Researchers at Karolinska Institutet, and the Universities of Lund and Helsinki set out to examine the risk of complications in LADA.

Our results emphasise the importance of diagnosing LADA correctly and careful monitoring of glucose control in these individuals, so that treatment can be intensified if needed, thereby reducing the risk of complications.

Yuxia Wei, PhD-student and Sofia Carlsson, senior lecturer, Institute of Environmental Medicine, Karolinska Institutet

According to the study LADA was characterised by fewer metabolic risk factors than type 2 diabetes, such as high blood pressure and high blood lipids. However, a lower proportion of individuals with LADA achieved good glucose control. The lack of glucose control was most evident in LADA patients with high levels of the antibody GADA (glutamic acid decarboxylase antibody). A significant portion of individuals with LADA lacked any glucose-lowering treatment.

The results of the new study are based on the ESTRID study, where researchers followed over 4000 individuals with diabetes, of whom 550 had LADA, for up to 12 years after diagnosis. According to the researchers, it is the most comprehensive study to date regarding the risk of complications in LADA.

Source: Karolinska Institutet

Categories : Medical Research & Technology Metabolic DisordersTags :

‘We Will Rock You’: The Special Cells that Secrete Insulin to Music

On By ModernMedia
Freddie Mercury performing with Queen in 1977. Source: Wikimedia Commons

Music has often been touted as a soothing treatment to aid healing. Now, researchers at ETH Zurich in Basel have come up with another medical approach. They have developed a novel method to get music to make specially designed cells secrete insulin. They found that this works especially well with the bass rhythm “We Will Rock You,” a global hit by British rock band, Queen.

Diabetics depend on an external supply of insulin via injection or pump. Researchers led by Martin Fussenegger from the Department of Biosystems Science and Engineering at ETH Zurich in Basel want to make the lives of these people easier and are looking for solutions to produce and administer insulin directly in the body. Any alternatives must be able to release insulin in controlled quantities on command.

One such solution the scientists are pursuing is enclosing insulin-producing designer cells in capsules that can be implanted in the body. To be able to control from the outside when and how much insulin the cells release into the blood, researchers have studied and applied different triggers in recent years: light, temperature and electric fields.

Equipping cells to receive sound waves

To make the insulin-producing cells receptive to sound waves, the researchers used a protein from the bacterium E. coli. Such proteins respond to mechanical stimuli and are common in animals and bacteria. The protein is located in the membrane of the bacterium and regulates the influx of calcium ions into the cell interior. The researchers incorporated the blueprint of this bacterial ion channel into human insulin-producing cells, letting these cells create the ion channel themselves and embed it in their membrane.

As the scientists have been able to show, the channel in these cells opens in response to sound, allowing positively charged calcium ions to flow into the cell. This leads to a charge reversal in the cell membrane, which in turn causes the tiny insulin-filled vesicles inside the cell to fuse with the cell membrane and release the insulin to the outside.

Turn up the bass

In cell cultures, the researchers first determined which frequencies and volume levels activated the ion channels most strongly. They found that volume levels around 60 decibels (dB) and bass frequencies of 50 hertz were the most effective in triggering the ion channels. To trigger maximum insulin release, the sound or the music had to continue for a minimum of three seconds and pause for a maximum of five seconds. If the intervals were too far apart, substantially less insulin was released.

Finally, the researchers looked into which music genres caused the strongest insulin response at a volume of 85dB. Rock music with booming bass like the song “We Will Rock You,” from Queen, came out on top, followed by the soundtrack to the action movie The Avengers. The insulin response to classical music and guitar music was rather weak by comparison.

“We Will Rock You” triggered roughly 70% of the insulin response within five minutes, and all of it within 15 minutes. This is comparable to the natural glucose-induced insulin response of healthy individuals, Fussenegger says.

Sound source must be directly above the implant

To test the system as a whole, the researchers implanted the insulin-producing cells into mice and placed the animals so that their bellies were directly on the loudspeaker. This was the only way the researchers could observe an insulin response. If, however, the animals were able to move freely in a “mouse disco,” the music failed to trigger insulin release.

“Our designer cells release insulin only when the sound source with the right sound is played directly on the skin above the implant,” Fussenegger explains. The release of the hormone was not triggered by ambient noise such as aircraft noise, lawnmowers, fire brigade sirens or conversations.

Ambient noise won’t do

As far as he can tell from tests on cell cultures and mice, Fussenegger sees little risk that the implanted cells in humans would release insulin constantly and at the slightest noise.

Another safety buffer is that insulin depots need four hours to fully replenish after they have been depleted. So even if the cells were exposed to sound at hourly intervals, they would not be able to release a full load of insulin each time and thereby cause life-threatening hypoglycaemia. “It could, however, cover the typical needs of a diabetes patient who eats three meals a day,” Fussenegger says. He explains that insulin remains in the vesicles for a long time, even if a person doesn’t eat for more than four hours. “There’s no depletion or unintentional discharge taking place.”

As a proof of concept only, clinical application is a long way off, but it shows that genetic networks can be controlled by mechanical stimuli such as sound waves. Whether this principle will ever be put to practical use depends on whether a pharmaceutical company is interested in doing so. It could, after all, be applied broadly: the system works not only with insulin, but with any protein that lends itself to therapeutic use.

Source: ETH Zurich

Categories : Ageing Metabolic DisordersTags :

Metformin Also Seems to Protect Against Muscle Atrophy and Fibrosis

On By ModernMedia
Photo by Barbara Olsen on Pexels

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 : Medical Research & Technology Metabolic DisordersTags :

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

On By ModernMedia
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

Categories : Metabolic DisordersTags :

Even Modest Alcohol Intake Does not Reduce Diabetes, Obesity Risk

On By ModernMedia
Photo by Pavel Danilyuk on Pexels

Having only one or two alcoholic drinks per day does not protect against endocrine conditions such as obesity and type 2 diabetes, according to a new study published in the Journal of Clinical Endocrinology & Metabolism.

It is widely accepted that excessive alcohol consumption causes a wide range of health issues and is thus a major public health concern. Whether modest alcohol consumption has beneficial health effects remains controversial, however, due to the limited power of observational studies.

The researchers used mendelian randomisation (MR), which can help to mitigate biases due to confounding and reverse causation in observational studies, and evaluate the potential causal role of alcohol consumption.

“Some research has indicated that moderate drinkers may be less likely to develop obesity or diabetes compared to non-drinkers and heavy drinkers. However, our study shows that even light-to-moderate alcohol consumption (no more than one standard drink per day) does not protect against obesity and type 2 diabetes in the general population,” said Tianyuan Lu, PhD, from McGill University in Québec, Canada. “We confirmed that heavy drinking could lead to increased measures of obesity (body mass index, waist-to-hip ratio, fat mass, etc) as well as increased risk of type 2 diabetes.”

The researchers assessed self-reported alcohol intake data from 408 540 participants in the U.K. Biobank and found people who had more than 14 drinks per week had higher fat mass and a higher risk of obesity and type 2 diabetes. An extra drink per week was associated with an increased of 8% for diabetes risk and 10% for obesity risk.

These associations were stronger in women than in men. No data supported the association between moderate drinking and improved health outcomes in people drinking less than or equal to seven alcoholic beverages per week.

Source: The Endocrine Society