Category: Metabolic Disorders

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Moderate Light Levels During Sleep Increases Insulin Resistance

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Even exposure to moderate light levels during nighttime sleep, compared to sleeping in a dimly lit room, harms cardiovascular function during sleep and increases insulin resistance the following morning, according to a new study published in PNAS.

“The results from this study demonstrate that just a single night of exposure to moderate room lighting during sleep can impair glucose and cardiovascular regulation, which are risk factors for heart disease, diabetes and metabolic syndrome,” said senior study author Dr Phyllis Zee at Northwestern University. “It’s important for people to avoid or minimise the amount of light exposure during sleep.”

There is evidence that daytime light exposure increases heart rate via sympathetic nervous system activation, increasing heart rate and alertness to meet the day’s challenges.

“Our results indicate that a similar effect is also present when exposure to light occurs during nighttime sleep,” Dr Zee said.

“We showed your heart rate increases when you sleep in a moderately lit room,” said Dr Daniela Grimaldi, a co-first author and research assistant professor of neurology at Northwestern. “Even though you are asleep, your autonomic nervous system is activated. That’s bad. Usually, your heart rate together with other cardiovascular parameters are lower at night and higher during the day.”

The sympathetic and parasympathetic nervous systems regulate the body physiology during the day and night. Sympathetic takes charge during the day and parasympathetic is supposed to at night, when it conveys restoration to the entire body.

The researchers found signs of insulin resistance the morning after people slept in a light room. An earlier study examined a large population of healthy people who had exposure to light during sleep, and found they were more overweight and obese, Dr Zee said.

“Now we are showing a mechanism that might be fundamental to explain why this happens. We show it’s affecting your ability to regulate glucose,” Dr Zee said.

The study participants were unaware of the biological shift in their bodies at night.

“But the brain senses it,” A/Prof Grimaldi said. “It acts like the brain of somebody whose sleep is light and fragmented. The sleep physiology is not resting the way it’s supposed to.”

Night-time exposure to artificial light is widespread in the modern world, either from light-emitting devices indoors, or from outdoor sources such as street lights. Up to 40% of people sleep with a bedside lamp on or with a light on in the bedroom and/or keep the television on.

“In addition to sleep, nutrition and exercise, light exposure during the daytime is an important factor for health, but during the night we show that even modest intensity of light can impair measures of heart and endocrine health,” said co-first author Dr Ivy Mason.

The study tested the effect of sleeping with 100 lux (moderate light) compared to 3 lux (dim light) in participants over a single night. Moderate light exposure caused the body to go into sympathetic activation. In blood vessels, sympathetic activation constricts arteries and arterioles which increases vascular resistance and decreases distal blood flow. When this occurs throughout the body, the increased vascular resistance causes arterial pressure to increase.

“These findings are important particularly for those living in modern societies where exposure to indoor and outdoor nighttime light is increasingly widespread,” Dr Zee said.

Zee’s top tips for reducing light during sleep

1) Keep lights off. If a light is necessary (eg for older people’s safety), keep it dim and close to the floor.

2) Colour is important: amber or red/orange light stimulates the brain. Avoid white or blue light.

3) Blackout shades or eye masks are good if outdoor light can’t be controlled. Move your bed so the outdoor light isn’t shining on your face

As a rule of thumb, Dr Zee said that being able to see things really well means it’s too light.

Source: Northwestern University

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Stem Cells Research Hints at Ways to Prevent Diabetic Retinopathy

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Researchers are investigating novel stem cell approaches that could lead to treatments for early retinal vascular dysfunction in diabetic patients, which could help prevent diabetic retinopathy.

Diabetic complications cause major metabolic disturbances that damage the cardiovascular, visual, peripheral nerve and renal systems through harming small and large microvessels that feed these tissues. New treatments are needed to treat the growing number of people who develop such retinal vascular dysfunction.

Research strategies include identifying and using new methods to differentiate or mature human induced pluripotent stem cells (hiPSCs) into the specific mesoderm subset of cells that display vascular reparative properties.

“Vascular diseases afflict hundreds of millions of people in the world,” said Chang-Hyun Gil, MS, PhD, a postdoctoral fellow in the Department of Surgery and co-first author of the study. “In this study, we focused on the retinal vessel in type 2 diabetes. Our results demonstrate the safe, efficient and robust derivation of hiPSC-derived specific mesoderm subset for use as a novel therapy to rescue ischemic tissues and repair blood vessels in individuals with vascular diseases. The results provide a foundation for an early phase clinical trial.”

In the study, published in Science Advances, investigators genetically reprogrammed diabetic and non-diabetic peripheral blood cells into hiPSCs and matured the cells into special blood vessel reparative cells. Upon injection into animal models with type 2 diabetic murine (T2D) retinal dysfunction, results showed significant improvement in visual acuity and electroretinograms with restoration of vascular perfusion. They hypothesised that hiPSC-derived vascular reparative cells could work as endothelial precursors that will display in vivo vessel reparative properties in these diabetic subjects.

“Unlike the use of embryonic stem cells (ESCs), genetically engineered hiPSCs do not carry the ethical challenges ESCs possess that limit their possible usage, and hiPSCs are being increasingly recognised as a viable alternative in study design and application as a cell therapy for human disorders,” Dr Gil said.

Researchers converted hiPSC into a specific mesoderm subset that was enriched to generate endothelial cells with vessel reparative properties similar to endothelial colony forming cells (ECFC).

Dr Gil said certain mesoderm subsets were better able to differentiate into ECFC and form functional blood vessels in vivo. and that mesoderm populations corrected vasodegeneration of injured retinal vessels. Tests showed enhanced function of neural retina and improved vision.

Source: Indiana University

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Bringing Back Thiazolidinediones – Without the Weight Gain

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By uncovering the subtle difference between two varieties of a protein, researchers from the Pennsylvania may have discovered how to eliminate the weight gain side effects of thiazolidinediones, which were once widely-used diabetes drugs. These findings, published in Genes & Development, could lead to more effective treatment from modified thiazolidinediones, which many likely avoid in its current form due to side effects.

“One small, undiscovered difference between the two forms of a single protein proved to be extremely significant,” said study senior author Mitchell Lazar, professor at the University of Pennsylvania. “Our findings suggest a way to improve on the mechanism of action of thiazolidinedione drugs, which holds promise for eliminating the side effect of weight gain.”

After their introduction in the 1990s, thiazolidinediones, which include rosiglitazone, soon enjoyed widespread use in diabetes. Since then, they have fallen out of favour due to their side effects. This has led some researchers to investigate whether new compounds could be developed that retain these drugs’ therapeutic effects while having fewer side effects.

In their study, Prof Lazar and his team approached this problem by studying thiazolidinediones’ target, PPARgamma (PPARγ), a protein which helps control fat cell production. The scientists examined two lines of mice: One greatly deficient in one form of the protein, PPARγ1, the other greatly deficient in PPARγ2. In the mice, the scientists showed that activating PPARγ1 or PPARγ2 with a thiazolidinedione had an anti-diabetic effect in each case, protecting mice from the metabolic harm of a high-fat diet.

However, the researchers discovered that activation of these two forms has subtly different downstream effects on gene activity. Specifically, in the PPARγ1-deficient mice (in which most of the present PPARγ takes the form of PPARγ2), the thiazolidinedione treatment caused no weight gain.

The finding therefore suggests that it may be possible to realize the benefits of thiazolidinediones without the weight gain side effect, by selectively activating PPARγ2 and not PPARγ1.

“We’re now studying in more detail how PPARγ1 and PPARγ2 work and how they differ, in the hope of finding ways to selectively activate PPARγ2,” Prof Lazar said.

Source: University of Pennsylvania

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Use of e-cigarettes Associated With Prediabetes Risk

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Analysis of a large representative database shows that e-cigarette use is associated with an increased risk of prediabetes, posing a new concern for public health.

“Our study demonstrated a clear association of prediabetes risk with the use of e-cigarettes,” explained lead researcher Shyam Biswal, PhD, at Johns Hopkins Bloomberg School of Public Health. “With both e-cigarette use and prevalence of prediabetes dramatically on the rise in the past decade, our discovery that e-cigarettes carry a similar risk to traditional cigarettes with respect to diabetes is important for understanding and treating vulnerable individuals.”

According to the Centers for Disease Control and Prevention (CDC), traditional cigarette smokers are 30% to 40% more likely than non-smokers to develop type 2 diabetes, which increases their risk for cardiovascular diseases. e-cigarettes are sometimes promoted as a healthier option for cigarette smokers, and e-cigarettes use is rising among younger demographics.

The study analysed 2016–2018 data from the Behavioral Risk Factor Surveillance System (BRFSS), the largest annual nationally representative health survey of US adults. Among the 600 046 respondents, 9% were current e-cigarette users who self-reported prediabetes diagnoses. The data also showed that e-cigarette users have a higher prevalence of high-risk lifestyle factors and worse self-related mental and physical health status than non-smokers.

In this representative sample of US adults, e-cigarette use was associated with greater odds of prediabetes compared to those who did not use e-cigarettes or traditional cigarettes – a worrying link from a public health standpoint.

“We were surprised by the findings associating prediabetes with e-cigarettes because they are touted as a safer alternative, which we now know is not the case,” commented Dr Biswal. “In the case of cigarette smoking, nicotine has a detrimental effect on insulin action, and it appears that e-cigarettes may also have the same effect.”

Prediabetes is fortunately a reversible condition, given appropriate lifestyle management. The authors make a compelling recommendation for targeting the reduction in e-cigarette use and education of young adults to reduce diabetes risk.

“Our effort for smoking cessation has led to a decrease in smoking traditional cigarettes. With this information, it is time for us to ramp up our public health efforts to promote the cessation of e-cigarettes,” cautioned Dr Biswal.

The researchers published their findings in the American Journal of Preventive Medicine.

The World Health Organization (WHO) defines prediabetes as a state of intermediate hyperglycaemia using impaired fasting glucose, defined as fasting plasma glucose of 6.1–6.9 mmol/L (110 to 125 mg/dL) and impaired glucose tolerance defined as 2h plasma glucose of 7.8–11.0mmol/L (140–200 mg/dL) after ingestion of 75g of oral glucose or a combination of the two based on a 2h oral glucose tolerance test. It is estimated that by 2030, more than 470 million people worldwide will be diagnosed with prediabetes.

Source: EurekAlert!

Categories : COVID Metabolic DisordersTags : 1 Comment

COVID Infection not Associated With Increased New-onset Diabetes Risk

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Using in vitro modelling the SARS-CoV-2 infection of human pancreatic cells, researchers have found that COVID infection is likely not associated with an increased new-onset diabetes risk. At the same time, another study has suggested that in hospitalised COVID patients, it may be a temporary form of the disease resulting from the acute stress of viral infection.

The findings, which are to appear in Cell Reports, address concerns raised over the past 18 months that infection with SARS-CoV-2 may trigger new-onset diabetes.  However, the supporting evidence for this has remained sparse, with at times conflicting evidence impeding with a proper risk assessment.

The team of researchers at the Icahn School of Medicine at Mount Sinai demonstrated that SARS-CoV-2 targets virtually all types of pancreatic cells, not just the insulin-producing beta cells, using the ACE2 receptor to gain access. However, the infection in the pancreas remained highly circumscribed, largely non-cytopathic and despite high viral burden in infected subsets, promoted only modest cellular perturbations and inflammatory responses.

Similar experimental outcomes were also observed after in vitro infection with endemic coronaviruses not previously associated with diabetes. Taken together, these findings challenge the notion that direct beta cell infection and destruction by SARS-CoV-2 can precipitate diabetes onset.

“Our provisional conclusions indicate that SARS-CoV-2 infection is likely not associated with an increased risk for new-onset diabetes,” said study leader Dirk Homann, MD, Professor of Medicine at Icahn Mount Sinai. “However, a history of SARS-CoV-2 infection may yet promote prolonged glycometabolic perturbations and even an increase in cumulative diabetes risk in vulnerable populations. Over the next few years, we need to pay careful attention to emerging observational and retrospective studies that determine diabetes incidence rates of previously SARS-CoV-2-infected individuals.”

To evaluate permissiveness of human pancreatic islet cells to in vitro SARS-CoV-2 infection, the team of researchers employed an in vitro infection model of primary human pancreatic islets with SARS-CoV-2 as well as endemic human coronaviruses. The team precisely delineated pancreatic infection patterns and associated cellular changes at the single-cell level. Altogether, they found that the extent and consequences of pancreatic SARS-CoV-2 infection, even under in vitro conditions of enhanced virus exposure, remained decidedly limited.

“Concerns surrounding the possibility that infection with SARS-CoV-2, the etiological agent of COVID, may cause new-onset diabetes persist amidst an evolving research landscape,” said Verena van der Heide, MD, PhD, co-first author of the study and postdoctoral research fellow at the Icahn School of Medicine at Mount Sinai. “Our findings stand in notable contrast to three recent reports that also based their speculation about the diabetogenic potential of SARS-CoV-2 on in vitro infection of human islets. As detailed in our manuscript, however, we believe that our careful experimental design and comprehensive analysis strategy make a compelling case for the considerable limits of pancreatic SARS-CoV-2 infection.”

“There are strong epidemiological associations between COVID infection in humans and diabetes, but whether the SARS-CoV-2 virus actually infects and damages the insulin-producing cells in the human pancreas, the so-called ‘beta cells,’ has been highly controversial,” said Andrew Stewart, MD, Director of the Diabetes, Obesity and Metabolism Institute at Icahn Mount Sinai. “This study by Dr. Homann and his collaborators in Mount Sinai’s Precision Immunology Institute and the Department of Microbiology provides strong evidence that SARS-CoV-2 causes little or no damage to beta cells, making it unlikely that COVID infection can predispose to development of Type 1 diabetes.”    

The conclusions they came to are in line with a 2020 report by Dr Homann and his team, showing that ACE2 receptors and other entry factors are lacking among islet endocrine cells but readily detected in microvascular and ductal structures of the pancreas.

Meanwhile, a second, separate study of 594 individuals who exhibited signs of diabetes mellitus during the early pandemic showed that half of the 79 patients without a diabetes diagnosis reverted to normal blood sugar levels by one year.

“We believe that the inflammatory stress caused by COVID may be a leading contributor to ‘new-onset’ or newly diagnosed diabetes,” said Sara Cromer, MD, lead author of the second study. “Instead of directly causing diabetes, COVID may push patients with pre-existing but undiagnosed diabetes to see a physician for the first time, where their blood sugar disorder can be clinically diagnosed. Our study showed these individuals had higher inflammatory markers and more frequently required admission to hospital ICUs than COVID patients with pre-existing diabetes.”

The second study was published in the Journal of Diabetes and its Complications.

Source: Mount Sinai Medical Center

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Getting Adequate Sleep Results in Reduced Calorie Intake

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Getting adequate sleep could be key to fighting growing rates of obesity around the world, according to a study published in JAMA Internal Medicine, which focused solely on improving sleep duration in overweight individuals.

Understanding the underlying causes of obesity and how to prevent it is the best way to fight obesity, according to first author Dr Esra Tasali. “The current obesity epidemic, according to experts, is mostly explained by an increase in caloric intake, rather than lack of exercise,” she said.

In a randomised clinical trial with 80 adults, published in JAMA Internal Medicine, researchers found that young, overweight adults who habitually slept fewer than 6.5 hours a night were able to sleep for 1.2 hours longer after a personalised sleep hygiene counselling session. The sleep intervention was intended to extend time in bed duration to 8.5 hours and, compared to controls, the increased sleep duration also reduced participants’ overall caloric intake by an average of 270 kcal (calories) per day.

“Over the years, we and others have shown that sleep restriction has an effect on appetite regulation that leads to increased food intake, and thus puts you at risk for weight gain over time,” said Tasali. “More recently, the question that everyone was asking was, ‘Well, if this is what happens with sleep loss, can we extend sleep and reverse some of these adverse outcomes?”

The study examines the effects of sleep extension on caloric intake but also does so in a real-world setting, with no influence on participants’ diets. Participants slept in their own beds, tracked their sleep with wearable devices, and otherwise followed their normal lifestyle without any instructions on diet or exercise.

“Most other studies on this topic in labs are short-lived, for a couple of days, and food intake is measured by how much participants consume from an offered diet,” said Tasali. “In our study, we only manipulated sleep, and had the participants eat whatever they wanted, with no food logging or anything else to track their nutrition by themselves.”

Instead, to objectively track participants’ caloric intake, investigators relied on the “doubly labelled water” method to track change in energy stores, which uses isotopes of hydrogen and oxygen in drinking water. “This is considered the gold standard for objectively measuring daily energy expenditure in a non-laboratory, real-world setting and it has changed the way human obesity is studied,” said Professor Dale A. Schoeller, senior study author and pioneer of the method.

Overall, individuals who increased their sleep duration were able to reduce their caloric intake by an average of 270 kcal per day – which would translate to roughly 12 kg of weight loss over three years if the effects were maintained over a long term.

Perhaps the most surprising aspect of the study was the intervention’s simplicity. “We saw that after just a single sleep counselling session, participants could change their bedtime habits enough to lead to an increase in sleep duration,” said Dr Tasali. “We simply coached each individual on good sleep hygiene, and discussed their own personal sleep environments, providing tailored advice on changes they could make to improve their sleep duration. Importantly, to blind participants to sleep intervention, recruitment materials did not mention sleep intervention, allowing us to capture true habitual sleep patterns at baseline.”

Even though the study did not systematically assess factors that may have influenced sleep behaviour, “limiting the use of electronic devices before bedtime appeared as a key intervention,” said Dr Tasali.

Following just a single counselling session, participants increased their average sleep duration by over an hour a night. Despite prescribing no other lifestyle changes, most participants had a large decrease in how much they ate, with some participants’ intake reduced by 500kcal per day.

The subjects were only involved in the study for a total of four weeks, with two weeks for gathering baseline information about sleep and caloric intake, followed by two weeks to monitor the effects of the sleep intervention.

“This was not a weight-loss study,” said Dr Tasali. “But even within just two weeks, we have quantified evidence showing a decrease in caloric intake and a negative energy balance – caloric intake is less than calories burned. If healthy sleep habits are maintained over longer duration, this would lead to clinically important weight loss over time. Many people are working hard to find ways to decrease their caloric intake to lose weight – well, just by sleeping more, you may be able to reduce it substantially.”

Source: University of Chicago Medicine

Categories : Cardiovascular Disease Metabolic DisordersTags :

GLP-1: The Missing Link of Diabetes and Hypertension

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An international team of researchers has finally cracked the puzzle of why so many patients with hypertension also have diabetes. Their discovery has shown that glucagon-like peptide-1 (GLP-1) couples the body’s control of blood glucose and blood pressure.

Senior Author Professor Julian Paton at the University of Auckland, said: “We’ve known for a long time that hypertension and diabetes are inextricably linked and have finally discovered the reason, which will now inform new treatment strategies.”

The study is published online in Circulation Research.

It has long been known that GLP-1 is released from the wall of the gut after eating and acts to stimulate insulin from the pancreas to control blood sugar levels.  However, the researchers found that GLP-1 also stimulates the carotid body, a chemoreceptor located in the neck.

Researchers used RNA sequencing to read all the messages of the expressed genes in the carotid body in rats with and without high blood pressure. This led to the finding that the receptor that senses GLP-1 is located in the carotid body, but less so in hypertensive rats.

David Murphy, Professor of Experimental Medicine from Bristol Medical School: Translational Health Sciences (THS) and senior author, explained: “Locating the link required genetic profiling and multiple steps of validation.  We never expected to see GLP-1 come up on the radar, so this is very exciting and opens many new opportunities.”

Professor Paton added: “The carotid body is the convergent point where GLP-1 acts to control both blood sugar and blood pressure simultaneously; this is coordinated by the nervous system which is instructed by the carotid body.”

Even when on medication, many patients with hypertension and/or diabetes are at high risk of life-threatening cardiovascular disease. This is because most medications only treat symptoms and not causes of high blood pressure and high sugar.

Professor Rod Jackson, an epidemiologist from the University of Auckland, said: “We’ve known that blood pressure is notoriously difficult to control in patients with high blood sugar, so these findings are really important because by giving GLP-1 we might be able to reduce both sugar and pressure together, and these two factors are major contributors to cardiovascular risk.”

Lead author Audrys Pauža, PhD student in the Bristol Medical School, added: “The prevalence of diabetes and hypertension is increasing throughout the world, and there is an urgent need to address this.

“Drugs targeting the GLP-1 receptor are already approved for use in humans and widely used to treat diabetes. Besides helping to lower blood sugar these drugs also reduce blood pressure, however, the mechanism of this effect wasn’t well understood.

“This research revealed that these drugs may actually work on the carotid bodies to enact their anti-hypertensive effect. Leading from this work, we are already planning translational studies in humans to bring this discovery into practice so that patients most at risk can receive the best treatment available.”

The research has also revealed many novel targets for ongoing functional studies that the team hope will lead to studies in human hypertensive and diabetic patients.

Source: University of Bristol

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Simple Dietary Supplement in Type 1 Diabetes Calms Immune System

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Gut microbiome. Credit: Darryl Leja, NIH

A clinical trial performed by Australian scientists showed that a simple dietary supplement that targeted gut microbiota could improve gut health and strengthen the immune system in individuals with type 1 diabetes.

The supplement is a type 2–resistant starch consisting of a high-amylose (70%) maize starch that has been modified by bonding the acetate and butyrate. The supplement is resistant to digestion in the upper gastrointestinal tract and delivers a very high yield of short-chain fatty acids (SCFAs) in the colon. This makes it a useful tool to measure the effect of SCFAs on intestinal biology.

According to senior author and lead investigator Dr Eliana Marino, the study tested 21 adults with type 1 diabetes who incorporated the supplement into their daily diet for six weeks. Increased production of metabolites by the gut microbiota was observed, specifically SCFAs. This has an important role in preventing type 1 diabetes.

“People with 1 diabetes have shown altered gut microbiota and reduced production of short-chain fatty acids in stools and blood. We previously have demonstrated that the supplement used in this human study protected mice from diabetes,” said Dr Marino.

Published in Microbiome, the clinical trial showed that participants’ blood immune cells developed a more regulatory phenotype post-intervention.

“We were very excited to find that blood immune cells had become more regulated. Because type 1 diabetes is caused when the immune system becomes too activated and attacks the insulin-producing cells in the pancreas,” said co-lead researcher Associate Professor Hamilton-Williams.

“Type 1 diabetes is a lifelong autoimmune disease that is on the rise with no cure. Individuals living with type 1 diabetes depend on insulin treatment. As a consequence, they can develop late life-threatening inflammatory complications, such as kidney failure, neurological and cardiovascular diseases,” said co-lead researcher Associate Professor Sonia Saad

“While glucose control and insulin requirements didn’t change overall, the participants with the highest short-chain fatty acid concentrations showed the best glucose control after the supplementation,” said co-lead researcher Dr Kirstine Bell.

“Using this supplement for longer and starting it earlier in the disease could potentially stop the immune attack, preserving insulin-producing cells and improving glucose regulation,” said Dr Marino.

“This dietary supplementation represents a safe and accessible alternative therapy for many children with type 1 diabetes or other autoimmune diseases. Also, it could decrease the risk of subsequent inflammatory complications such as cardiovascular disease as clinical trials are underway,” said Dr Marino.

Source: Monash University

Categories : Medical Research & Technology Metabolic DisordersTags :

New Diabetes Management Device Combines Testing and Injection

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By combining blood glucose measurement with insulin administration in a single device, the complicated process of blood sugar management could be made easier for people with diabetes.

Patients with diabetes often use two types of insulin to control their blood sugar levels: long-acting insulin, which helps control glucose levels over a 24-hour period, and short-acting insulin, which is injected at mealtimes. Patients first measure their blood glucose levels with a glucose meter with a finger prick. They must also estimate how many carbohydrates are in their meal and combine this information with their blood glucose levels to calculate and inject the proper insulin dose.

Existing technologies such as continuous blood glucose monitors and insulin pumps can help with some parts of this process. However, these devices are not widely available, so most patients must rely on finger pricks and syringes. To this end, MIT researchers have developed devices to simplify the process, which they describe in the Journal of Controlled Release.

“Every day, many patients need to do this complicated procedure at least three times,” explained MIT postdoc Hen-Wi Huang. “The main goal of this project is to try to facilitate all of these complex procedures and also to eliminate the requirement for multiple devices. We also used a smartphone camera and deep learning to create an app that identifies and quantifies food content, which can aid in carbohydrate counting.”

The researchers came up with two all-in-one devices, both of which incorporate the new smartphone app. Using a photo, the app estimates the volume of food and carbohydrate content.

The first device that consolidates many of the existing tools that patients use now, including a lancet for drawing blood and glucose test strips. The device conveys blood glucose information to the smartphone app via Bluetooth, and the app works out the correct insulin dose, delivered via a needle in the same device.

“What our device is doing is automating the procedures to prick the skin, collect the blood, calculate the glucose level, and do the computation and insulin injection,” Dr Huang says. “The patient no longer needs a separate lancing device, glucose meter, and insulin pen.”

Many of the components included in this device are already FDA-approved, but the device has not been tested in human patients yet. Tests in pigs showed that the system could accurately measure glucose levels and dispense insulin.

For their second device, the researchers wanted to come up with a system that would require just one needle prick. To achieve that, they designed a novel glucose sensor that could be incorporated into the same needle that is used for insulin injection.

The researchers designed a flexible electronic sensor that can be attached to the needle and measure glucose levels in the interstitial fluid, just below the surface of the skin. Once the needle penetrates the skin, it takes between five and 10 seconds to measure the glucose levels. This information is transmitted to the smartphone app, which calculates the insulin dose and delivers it through the inserted needle.

In tests in the pigs, the researchers showed that they could accurately measure glucose levels with this system, and that glucose levels dropped after insulin injection.

Because this device uses a novel type of glucose sensor, the researchers expect that it will require further development to get to a point where it could be tested in patients.

Source: MIT

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Newly Discovered Hormone Implicated in Development of Diabetes

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A newly discovered hormone named fabkin helps regulate metabolism and may play an important role in the development of both type 1 and type 2 diabetes, according to a new study published in Nature.

Fabkin levels were abnormally high in mice and human patients with either type 1 or type 2 diabetes, and blocking the activity of fabkin prevented the development of both forms of diabetes in the animals. Fabkin likely plays a similar role in humans and the hormone complex could be a promising therapeutic target, according to the researchers.

“For many decades, we have been searching for the signal that communicates the status of energy reserves in adipocytes to generate appropriate endocrine responses, such as the insulin production from pancreatic beta cells,” said senior author Gökhan S. Hotamisligil. “We now have identified fabkin as a novel hormone that controls this critical function through a very unusual molecular mechanism.”

Many hormones are involved in the regulation of metabolism, such as insulin and leptin. Fabkin is different from traditional hormones in that it is not a single molecule with a single defined receptor. Instead, fabkin is composed of a functional protein complex consisting of multiple proteins, including fatty acid binding protein 4 (FABP4), adenosine kinase (ADK) and nucleoside diphosphate kinase (NDPK). Through a series of experiments, the researchers determined that fabkin regulates energy signals outside of cells. These signals then act through a family of receptors to control target cell function. In the case of diabetes, fabkin controls the function of beta cells in the pancreas that are responsible for insulin production.

Hotamisligil and colleagues previously discovered that a protein known as FABP4 is secreted from fat cells during lipolysis, the process in which lipids stored within fat cells are broken down, typically in response to starvation. Since then, many studies showed links between circulating FABP4 and metabolic diseases including obesity, diabetes, cardiovascular disease, and cancer. However, the mechanism of action was unknown.

In the new study, the researchers showed that when FABP4 is secreted from fat cells and enters the bloodstream, it binds with the enzymes NDPK and ADK to form the protein complex now identified as fabkin. In this protein complex, FABP4 modifies the activity of NDPK and ADK to regulate levels of molecules known as ATP and ADP, which are the essential units of energy in biology. The researchers discovered that surface receptors on nearby cells sense the changing ratio of ATP to ADP, triggering the cells to respond to the changing energy status. As such, fabkin is able to regulate the function of these target cells.

The pancreas’ beta cells are a target of fabkin and the hormone is a driving force behind the development of diabetes, the researchers showed. When fabkin in mice was neutralised with an antibody, the animals did not develop diabetes. When the antibody was given to obese, diabetic mice, they reverted to a healthy state.

“The discovery of fabkin required us to take a step back and reconsider our fundamental understanding of how hormones work.” said lead author Kacey Prentice. “I am extremely excited to find a new hormone, but even more so about seeing the long-term implications of this discovery.”

Source: Harvard University