Author: Staff Writers

There have been many advancements, when it comes to diabetes and a treatment for it. From medications to therapies, there are all kinds of ways that are effective. The latest treatment comes in the form of a tablet.

It is very possible that a capsule of insulin crystals a day can stop the development of type 1 diabetes. In an international TrialNet study that followed relatives of individuals with type 1 diabetes showed rather or not oral insulin could delay of even prevent the disease.

Type 1 diabetes is different from type 2 diabetes because it is autoimmune form; this means that patients with type 1 diabetes will produce insulin-producing beta cells that destroy their own immune system.

Åke Lernmark, Professor of Experimental Diabetes Research at Lund University in Sweden said “We know that if a person has two auto-antibodies and one of them is against insulin, there is a 50% risk that they will develop type 1 diabetes within five years. It doesn’t matter how old you are. There are indications that oral insulin may prevent or delay the clinical onset of type 1 diabetes among individuals with auto antibodies against insulin, who are thus in the risk zone.”

Lernmark is referring to a study that was presented earlier in the year by Canadian and American researchers. This study ran between 1994 and 2003 and participants with relatives who have type 1 diabetes and at least two auto-antibodies, one of those being insulin, to the oral insulin or a placebo capsule which contained an inactive substance. The results proved disappointed at first because just as many people became ill with the oral insulin as the placebo group.

Lernmark said, “However, the subsequent analyses showed something different. Among those who had high levels of insulin auto antibodies at the start of the study, the oral insulin had an effect and the development of type 1 diabetes was delayed. The delaying effect lasted for as long as the participants took the insulin.”

It is undefined at the moment on how helpful oral insulin can be in stopping type 1 diabetes. Lernmark believes that a possible explanation could be that the immune system could grow accustomed to the lower daily doses of insulin and therefore, the insulin capsules could become ineffective.

A new study from the University of Ulster reveals a possible drug that is designed to treat diabetic patients who suffer from neurodegenerative diseases such as Alzheimer’s disease.

Alzheimer’s disease has long been associated with type 2 diabetes. When insulin cannot get to the brain, it can cause damaged nerve cells, which leads to different neurodegenerative diseases. It is believed by scientists that the same drugs can also have positive benefits for keeping brain cells healthy as well.

Professor Christian Hölscher and his team from the Biomedical Sciences Research Institute on the Coleraine campus used an experimental drug called (Val8) GLP-1.

Through the drug, a protein called GLP-1 is stimulated. This helps the body control its response to blood sugar. The study scientists treated healthy mice with this drug and then studied the effects that appeared on the brain. It is typically hard for drugs to pass from the blood to the brain however the study team found that when the drugs entered the brain they appeared to have no side effects as well, in the dosage amount that was tested.

On the other hand, the drug did promote new brain cell growth in the hippocampus, which is the area of the brain that controls memory, motor/cognitive skills. In finding this, it shows that the GLP-1 may be very important for the production of new nerve cells, the mouse’s brain.

By blocking the effect of the GLP-1 in the mouse’s brain, the mice did poorly when it came to its memory and in learning. However, in booting the GLP-1, it appeared to have no effect.

“Here at the Biomedical Sciences Research Institute, we are really interested in the potential of diabetes drugs for protecting brain cells from damage and even promoting new brain cells to grow. This could have huge implications for diseases like Alzheimer’s or Parkinson’s, where brain cells are lost.” Professor Hölscher said.

“It is very encouraging that the experimental drug we tested, (Val8) GLP-1, entered the brain and our work suggests that GLP-1 could be a really important target for boosting memory. While we didn’t see benefits on learning and memory in these healthy mice, we are keen to test the drugs in mice with signs of Alzheimer’s disease, where we could see real improvements.”

“We are pleased to have supported this early stage research, suggesting that this experimental diabetes drug could also promote the growth of new brain cells. While we know losing brain cells is a key feature of Alzheimer’s, there is a long way to go before we would know whether this drug could benefit people with the disease.” Dr. Simon Ridley, Head of Research at Alzheimer’s Research UK, said.

“This research will help us understand the factors that keep nerve cells healthy, knowledge that could hold vital clues to tackling Alzheimer’s. With over half a million people in the UK living with the disease, learning more about how to keep our brain cells healthy is of vital importance. Funding for dementia research lags far behind that of other common diseases, but is essential if we are to realize the true potential of research like this.”

Diabetes is a common problem all around the world. In just America alone, more than 24 million people have type 2 diabetes. Diabetes can cause many different complications with different parts of the body. One recent discovery showed that those with higher blood sugar (more than the normal range) may end up with greater chance of brain shrinkage, which also occurs in aging and diseases like dementia.

Study author Nicolas Cherbuin, PhD, with Australian National University in Canberra said, “Numerous studies have shown a link between type 2 diabetes and brain shrinkage and dementia, but we haven’t known much about whether people with blood sugar on the high end of normal experience these same effects.”

This study involved 249 people who were aged 60 to 64. Each participant had a normal range of blood sugar that was defined by the World Health Organization. At the beginning of the study, each participant started with a brain scan and also had a brain scan four years later.

Participants with higher fasting blood sugar ranging from the normal range to below 6.1 mmol/l were more likely to have a loss of a brain volume in areas of the brain, the hippocampus and the amygdale. These areas control memory and cognitive skills. A fasting blood sugar that is considered impaired or pre-diabetic is a level of 6.1 mmol/l and a fasting blood sugar level of 10.0 mmol/l is considered diabetes.

The study looked to different aspects of each participant such as age, high blood pressure, smoking, alcohol used and other aspects. Researchers found that high blood sugar accounted for 6 to 10 percent of brain shrinkage.  Cherbuin said, “These findings suggest that even for people who do not have diabetes, blood sugar levels could have an impact on brain health. More research is needed, but these findings may lead us to re-evaluate the concept of normal blood sugar levels and the definition of diabetes.”

With diabetes becoming an even bigger problem around the world, more and more medical advances are being discovered to try and find a cure for the disease.

Recently, researches have designed a fresh type of biosensor which can identify small amounts of concentrations of glucose in the body’s natural fluids such as urine, tears and saliva. This new biosensor could be manufactured at a very low cost because it does not require very many procession steps in order to produce it.

Jonathan Claussen, a former Purdue University doctoral student and now a research scientist at the U.S. Naval Research Laboratory said “It’s an inherently non-invasive way to estimate glucose content in the body.”Because it can detect glucose in the saliva and tears, it’s a platform that might eventually help to eliminate or reduce the frequency of using pinpricks for diabetes testing.  We are proving its functionality.”

Leaders of the project were Claussen, Purdue doctoral student Anurag Kumar, a Purdue professor of mechanical engineering Timothy Fisher, D. Marshall Porterfield, a professor of agricultural and biological engineering and other researchers at the university’s Birck Nanotechnology Center.

“Most sensors typically measure glucose in blood. Many in the literature aren’t able to detect glucose in tears and the saliva. What’s unique is that we can sense in all four different human serums: the saliva, blood, tears and urine. And that hasn’t been shown before.” Claussen said.

There are three main parts to the sensor: the layers of nanosheets, which resemble tiny rose petals that are made from the material, graphene. Graphene is a single-atom-thick film of carbon, platinum nanoparticles and the enzyme glucose oxidase.

Within each petal are a few layers of stacked graphene. Each edge of the petals has incomplete, dangling chemical bonds which are defects where platinum nanoparticles can attach to. Electrodes are then formed by combining the nanosheet petals and platinum nanoparticles. The enzyme the convert’s glucose into peroxide which then generates a signal on the electrode.

Kumar said, “Typically, when you want to make a nanostructure biosensor you have to use a lot of processing steps before you reach the final biosensor product. That involves lithography, chemical processing, etching and other steps. The good thing about these petals is that they can be grown on just about any surface, and we don’t need to use any of these steps, so it could be ideal for commercialization.”

“Because we used the enzyme glucose oxidase in this work, it’s geared for diabetes. But we could just swap out that enzyme with, for example, glutamate oxidase, to measure the neurotransmitter glutamate to test for Parkinson’s and Alzheimer’s, or ethanol oxidase to monitor alcohol levels for a breathalyzer. It’s very versatile, fast and portable.” Claussen said.

The biosensor is also being used with a variety of chemical compounds to test for other medical conditions as well, other than diabetes.

A trial led by Carla Greenbaum, MD, Diabetes Research Program director at Benaroya Research Institute (BRI) at Virginia Mason and sponsored by the Immune Tolerance Network (ITN) and funded by the National Institutes of Health shows a new break in reversing autoimmunity in Type 1 diabetes.

The trial involved a two-pronged approach; two drugs were administered as a combination. The first drug in the combination interferes with the immune response that ultimately causes type 1 diabetes. The second drug boosts the part of the immune response that regulates overactive immune cells.

There are over one million people in the United States that have type 1 diabetes and that number is growing every year. With type 1 diabetes, the body’s immune system begins to attack and destroy insulin-producing cells that are in the pancreas which are referred to beta cells. When diagnosed with type 1 diabetes there are still a number of beta cells that are active in the body. Because these beta cells are natural insulin producers and can decrease over the long-term effects of diabetes, there are many therapies that are needed for the cure of diabetes.

The two drugs Proleukin (IL-2) and Rapamune (sirolimus) were administered to patients to find out whether or not the drugs would affect the immune system and halt the autoimmune destruction of the remaining beta cells. The researchers of a study describe a flourishing boost of regulatory components of the immune system also were prolonged that were not expected. Due to the temporary impairment of the beta cell function that was lead by the researchers, they concluded that the drug combination was not having a desired effect. Monitoring of the insulin production in the nine subjects indicated that the beta cell preservation goal was therefore not achieved and the study was then halted.

Dr. Greenbaum said, “This study result has been extremely important to scientists looking for ways to stop the immune attack. Our aim would be to harness the good effects of this therapy while preventing the bad effects.” Participants who haven’t yet completed the study will continue to be followed.”

Gerald Nepom, MD, PhD, Director of ITN said, “The clinical and mechanistic findings from this study can help guide future treatments that boost good immunity. This was an important clinical trial that will improve the design of subsequent trials to rescue beta cells in Type 1 diabetes.”

Diabetes affects more than 24 million people in the United States. New technology and medical advances surface everyday that get us one step closer to find the cure.

New technology that delivers a sustained release of therapeutics for up to six months could also be used to help with routine injections for health conditions like HIV/AIDS, various forms of cancer and diabetes.

Researchers from the University of Cambridge have created reformable, injectable and spreadable hydrogels that can be loaded with proteins and various other therapeutics. These hydrogels contain 99.7 percent of water by weight with the remaining percent being made up of cellulose polymers that are held together by cucurbiturils, which are barrel-shaped molecules that can act as a miniature pair of handcuffs.

Leader of the research and the Department of Chemistry, Dr Oren Scherman said, “The hydrogels protect the proteins so that they remain bio-active for long periods, and allow the proteins to remain in their native state. Importantly, all the components can be incorporated at room temperature, which is key when dealing with proteins which denature when exposed to high heat.”

Scherman, DrXian Jun Loh and PhD student Eric Appel, who developed that hydrogels, says that “they are capable of delivering a sustained release of the proteins that they contain for up to six months, compared with the current maximum of three months”. The rate of release can be controlled due to the ratio of materials that are in the hydrogel.

Hydrogels double the window of content release and use less non-water material than the current technology does. An extra material serves as scaffolding of sorts that holds the hydrogel together. However, the performance can be affected, so the lesser structure formation material that is contained in the hydrogel can help it to perform more effectively.

Drug therapy is moving further away from small molecule drugs and more toward protein-based therapy. Applications of insulin treatment, wound healing and hormone therapy are all ideal candidates for hydrogels.

More than a quarter of the 2.9 million individuals within the UK who have been diagnosed with diabetes have to inject themselves daily with insulin so that they can control their blood sugar levels. By using the insulin that is injected with the hydrogel the number of daily injections could be reduced to just two a year.

Appel said, “There’s been a lot of research that shows patients who need to take a pill each day for the rest of their lives, especially HIV patients in Africa who do not show any obvious symptoms, will take the pills for a maximum of six months before they stop, negating the point of taking the medication in the first place. If patients only have to take one shot which will give them six month’s worth of medication, we’ll have a much greater chance of affecting an entire population and slowing or stopping the progression of a disease.”

The research team is working with other researchers at the Brain Repair Center in the Department of Clinical Medicine. They are hoping to find out how the technology can be used to treat brain cancer.

New findings suggest that a group of hormone-producing cells in the brain can actually control blood sugar levels. This new finding could result in both a diabetes treatment and a weight loss drug.

Typically, in fruit flies both starvation and reduced diet will lead to hyperactivity. When a fly is hungry, they buzz around with intense aggravation, trying to find more food. This happens due to enzyme, which is called AMP-activated kinase. This enzyme stimulates the secretion of the adipokinetic hormone, which is similar to glucagon. This hormone acts differently than insulin, it acts like an opposite. It tells the body when to release sugar or food that is needed for hyperactivity. The body will use up its energy stores until it finds food.

Associate professor of biology Erik Johnson and his research team at Wake Forest University turned off the AMP-activated kinase, the cells the decreased the sugar release and the hyperactivity response stopped nearly completely. Even when the fruit flies where facing starvation.

Johnson said, “Since fruit flies and humans share 30 percent of the same genes and our brains are essentially wired the same way, it suggests that this discovery could inform metabolic research in general and diabetes research specifically. The basic biophysical, biochemical makeup is the same. The difference in complexity is in the number of cells. Why flies are so simple is that they have approximately 100,000 neurons versus the approximately 11 billion in humans.”

Due to the findings of this investigation, neat future medical advances could take place.

One of those medical advances is in diabetes research. The adipokinetic hormone in an insect is similar to the hormone glucagon found in humans. Glucagon raises the blood sugar levels and insulin reduces them. In humans, it is very hard to study the glucagon system because the pancreatic cells are hard to pull apart. By studying the fruit flies remarkable similar hormone, a cure for diabetes could be just around the corner.

Another medical advancement is in weight loss.

Johnson said, “Exercise stimulates AMP-activated kinase, so manipulation of this molecule may lead to getting the benefits of exercise without exercising. When you turn off AMP-activated kinase, you get fruit flies that eat a lot more than normal flies, move around a lot less, and end up fatter.”

A new chemical could be the answer to treating metabolic disorders such as type 2 diabetes suggests biologists at the UC San Diego.

Diabetes is a huge concern across the United States, particularly due to obesity. However, there are many other reasons why a person might develop type 2 diabetes.

The chemical does not directly control the glucose production in the liver, it affects the activity of a key protein that regulars the internal mechanisms of our daily night and day lives, out biological clock.

It has been suspected for years that obesity and diabetes walk hand in hand and that they could both be linked to issues with the biological clock. Using this theory, lab mice were used, their biological clocks altered and dealing with issues of obesity and diabetes.

A couple of years ago, a team led by the dean of the Division of Biological Sciences at UC San Diego Steve Kay, made a discovery. The team discovered the first biochemical link between the biological clock and diabetes. Cryptochrome, a key protein that regulates the biological clocks of mammals, insects and plants and it also regulates the glucose production in the liver. They also discovered that in altering the levels of the protein, they could improve the health of the diabetic mice.

Kay and his team discovered a small molecule, one that can be created into a drug, can control the detailed molecular cogs and timekeeping mechanisms of cryptochrome so that it can be repressed by the production of glucose by the liver. Humans, much like mice and other animals have evolved biochemical mechanisms so that a steady supply of glucose can flow to the brain, when we are not active or eating.

“We found that if we increased cryptochrome levels genetically in the liver we could inhibit the production of glucose by the liver,” said Kay.

Kay said. “At the end of the night, our hormones signal that we’re in a fasting state. And during the day, when we’re active, our biological clock shuts down those fasting signals that tell our liver to make more glucose because that’s when we’re eating.”

The cause of diabetes comes from an accumulation of glucose in the blood that can lead to health issues such as blindness, kidney failure, strokes and heart disease. There are two types of diabetes; type 2 diabetes is most common in Americans and type 1 is typically caused by the destruction of insulin producing cells in the pancreas results in the high blood sugar.

Joslin Diabetes Center scientists have recently indentified biological mechanisms through glucagon-like peptide-1 (GLP-1), which is known as a gut hormone that protects against kidney disease also has the same mechanisms that slow down the same actions in diabetes. These findings will possibly lead to new therapeutic agents which can help to prevent hyperglycemia on renal endothelial cells.

Diabetic complications come in many different forms but one of those is through renal complications known as diabetic nephropathy. Diabetic nephropathy is one of the most life threatening complications from diabetes that most often leads to end-stage renal disease (ESRD). About 44 percent of people who have been diagnosed with diabetes in the United States have ESRD, which requires either a kidney transplant or dialysis.

George King, M.D., lead author of the study and chief scientific officer, head of the Dianne Nunnally Hoppes Laboratory for Diabetes Complications and a professor of medicine at Harvard Medical School said, “We are very eager to develop new treatments for diabetic kidney disease.”

GLP-1 is an incretion hormone that is produced in the intestine upon the intake of food. It increases the insulin within the pancreas and slows down the absorption of glucose from the gut which reduces the action of glucagon. This all has a huge impact on lowering glucose levels in the blood. It also reduces appetite as well.

Different studies have shown that GLP-1 also improves renal endothelial cells. These cells regulate blood clotting, blood vessel activity and immune response and other issues that are damaged through insulin resistance. GLP-1 receptors are abundant in the intestine and can also be found in the kidneys and endothelium as well.

Through the Joslin study, the effects of GLP-1 in non-diabetic and diabetic mice were investigated. These mice has and over expression of the enzyme PKCB (protein kinase C-beta). This is produced in excess when the glucose in the blood is high. Excessive amounts of PKCB can lead to diabetic complications, which includes kidney disease. Through PKCB, Ang II, a peptide hormone that affects renal filtration and blood flow and regulates blood pressure, increases and accelerates the progression of kidney disease.

Dr. King says, “We’ve been interested in diabetic kidney disease for a long time, particularly the role of PKCβ and Ang II in promoting kidney damage. We were interested in investigating how GLP-1 could protect against the effects of hyperglycemia on renal function.”

“Two major findings were discovered through the Joslin study, mechanisms were identified by which GLP-1 can induce protective actions on the glomerular (renal) endothelial cells by inhibiting the signaling pathway of Ang II and its pro-inflammatory effect and also demonstrated a dual signaling mechanism by which hyperglycemia through PKCB activation can increase the Ang II action and inhibit GLP-1’s protective effects by reducing the expression with diabetes are more sensitive to Ang II; our data suggests one reason why,” says Dr. King.

“We now know that increased PKCβ decreases GLP-1R which makes the kidney less responsive to treatment with GLP-1-based drugs. Possible new treatments could combine PKCβ inhibitors with higher doses of GLP-1 agonists. GLP-1 is one potential pharmaceutical that could both lower glucose and minimize the toxic effects of Ang II to lower the risk of kidney diseases,” says Dr. King.