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Islet transplantation requires immunosuppressive drugs be taken for the rest of a person's life, though improving the body's ability to manage glucose levels significantly lowers the risk for adverse health events. islet transportation Andrey_Popov/Shutterstock

Islet Transplantation May Correct Type 1 Diabetes, Study says

Original article written by Stephen Feller and published by United Press International on April 26, 2016. Click here to read the original article.

WASHINGTON, April 18 (UPI) — Transplants of islet cells, the cells responsible for producing insulin in the pancreas, helped people with type 1 diabetes establish near-normal control of their glucose levels, get free of hypoglycemic events and in many cases no longer need insulin therapy.

Just under 90 percent of patients receiving islet cell transplants in a National Institutes of Health-sponsored clinical trial showed significant improvement in management of their condition during the course of a year, inching researchers closer to a cure for the genetically-caused disease.

Type 1 diabetes is an autoimmune disorder, in which the immune system attacks islet cells, preventing the release of insulin, making it difficult for the body to break down sugars for use, storage or excretion.

The clinical trial, spearheaded by the Clinical Islet Transplantation Consortium, announced in September that the first patient in the study no longer needed insulin therapy.

With results from the rest of the phase 3 trial in hand, the researchers said they will look to license technology to manufacture purified human pancreatic islets for mass use, while also continuing studies on the safety and efficacy with varied groups of patients.

“For people unable to safely control type 1 diabetes, islet transplantation offers real hope for preventing severe, life-threatening hypoglycemia,” Dr. Tom Eggerman, a researcher at the National Institute of Diabetes and Digestive and Kidney Diseases, said in a press release.

For the study, published in the journal Diabetes Care, researchers recruited 48 patients at eight university medical centers around the United States.

All patients received purified islet cells from deceased human donors, with each participant given the transplant into the portal vein, which carries blood from the intestine to the liver. Each of the patients was also given immunosuppressive drugs to prevent their immune systems from rejecting the cells.

After one year, 87.5 percent of participants had no hypoglycemic events, near-normal control of glucose and better awareness of their condition. After one year, 52 percent of patients no longer needed insulin therapy.

Of patients who did not see results within 75 days — they still needed insulin treatments — 25 patients received a second transplant, and one patient received a third.

The researchers worked with the U.S. Food and Drug Administration to run the trialwith future plans for mass manufacture in mind, potentially speeding up the approval process.

“The findings suggest that for people who continue to have life-altering severe hypoglycemia despite optimal medical management, islet transplantation offers a potentially lifesaving treatment that in the majority of cases eliminates severe hypoglycemic events while conferring excellent control of blood sugar,” said Dr.Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases.

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Salk researchers Michael Downes, Ron Evans and Eiji Yoshihara. — Salk Institute

Salk Makes Step Toward Cellular Diabetes Treatment

Original article written by Bradley J. Fikes and published by The San Diego Union-Tribune on April 15, 2016. Click here to read the original article.

Salk Institute scientists say they’ve discovered a key ingredient needed to make functional insulin-producing beta cells. With that knowledge, the scientists say they can realize a dream in treating Type 1 diabetes: growing replacement beta cells from the patients themselves.

If these replacement cells can be implanted and protected, they will make insulin as the body needs, just as the original cells do. That means type 1 diabetes would, for the first time ever, be curable.

The ingredient is a protein called ERR-gamma that turns up energy production in the beta cells, said Ron Evans, a Salk researcher who co-led the study with colleague Michael Downes. These cells are made from artificial embryonic stem cells, called induced pluripotent stem cells. Typically produced from skin, these IPS cells cells are being examined for their potential to treat a variety of diseases.

The study, published Tuesday in the journal Cell Metabolism, provides more evidence that cell replacement therapy may eventually provide a cure for type 1 diabetes, caused by the destruction of beta cells through an autoimmune reaction. The study can be found atj.mp/evansbeta. The first author was Eiji Yoshihara, first author of the paper and a Salk research associate.

Type 2 diabetes is even more common than Type 1. In the United States as of 2012, about 1.25 million children and adults have type 1 diabetes, and 29.1 million had the type 2 form, according to the American Diabetes Association. In San Diego County as of 2012, about 140,600 or 6.2 percent have type 2 diabetes.

In type 2 diabetes, the body becomes resistant to insulin, and the pancreas may become disease and have trouble producing sufficient insulin. As a result, blood sugar rises beyond normal, producing all sorts of damage. This can include weight gain, heart problems, poor limb circulation leading to amputation, kidney disease and blindness. These patients may also come to require insulin.

Disease reversal

Unlike the first kind, type 2 diabetes can be reversed, at least in some cases. Dieting and exercise leading to weight loss is key, according to recent research. A 2013 study in the journal Diabetes Care found that causing patients to burn more substantially more calories than they consume, either by diet or bariatric surgery, restores insulin sensitivity over a period of 8 weeks.

Bariatric surgery, which a portion of the gut is removed to limit food absorption, appears to reverse type 2 diabetes in nearly all patients, according to other studies.

But diets are notoriously hard to adhere to, and bariatric surgery is a drastic step many people are reluctant to take. So scientists are focusing on how type 2 diabetes arises in the first place, with the hope of finding some way of preventing it from taking place at all.

A 2014 study by UCSD researchers led by Dr. Jerrold Olefsky found that a lack of oxygen in fat cells is the trigger that starts the process that ends up causing type 2 diabetes. The study, published in the journal Cell, examined the disease in mouse models, considered a good proxy for human diabetes.

It reported that certain fatty acids, especially saturated fats, increased the need for oxygen in fat cells, causing them to fall into an oxygen-deprived state. This led to inflammation, an immune reaction and insulin resistance.

If the study results are borne out in people, it may be possible to produce a drug that would stop this process in the bud. It won’t stop obesity, but the most drastic health problems would be prevented.

For type 1 diabetes, no treatment exists to reverse the disease.

A very limited form of cell replacement therapy is already used for those with the most dangerous form of type 1 diabetes. They get transplants of islet cells or pancreases from cadavers. Those treated belong to a small subset of type 1 diabetics who get no warning signs that their blood sugar has fallen too far. They can die as a result.

Cell replacement

San Diego’s ViaCyte is already testing a replacement therapy using progenitor cells derived from human embryonic stem cells. In animal testing, these cells mature into beta and other pancreatic “islet” cells.

Another approach with induced pluripotent stem cells is being researched in the lab of Harvard University researcher Douglas Melton. He and colleagues have come up with their own formula for producing beta cells, and published studies outlining the approach.
Melton’s group reports that the cells express genetic activity very similar to adult beta cells, and regulated blood sugar when transplanted into mice whose own beta cells were destroyed.

These therapies all face difficulties, the trickiest perhaps being the patient’s own immune system, which destroyed their own islet cells in the first place.

Islet and pancreatic transplant patients are given immunosuppresive drugs. These drugs are toxic and make the patients more vulnerable to infection. Therefore, these procedures are used only on type 1 diabetics at greatest risk, said Julia L. Greenstein, vice president of discovery research at the research foundation JDRF.

ViaCyte has pioneered another approach to the problem. The islet cells are encapsulated in a semipermeable membrane that keeps out the immune system, but allows nutrients to flow in, and insulin and waste products to flow out. Moreover, the islet cells may potentially produce other blood sugar-relating hormones besides insulin.

Whether that strategy works is the point of clinical testing of ViaCyte’s product, now in a Phase 1 trial. This trial tests for safety. Participants receive easily removable implants of encapsulated cells, which are expected to mature in place and produce insulin. These implants are being removed periodically and examined to make sure the maturation process is going smoothly and that the membrane remains intact.

Presumably, other stem cell-based replacement therapies such as that the Salk scientists or Melton are developing will require an immune system-blocking barrer like ViaCyte’s, to protect the cells. Meanwhile, research continues on ways to modulate the immune system of type 1 diabetes to stop the autoimmune reaction.

Power to the cells

The Salk Institute’s Evans said applying the ERR-gamma protein promotes the growth of mitochondria, the power plants of cells. This gives the cells energy to make insulin.

“It turns on the light, it turns on the energy that flows into the cell. And that we think is the missing link,” Evans said. “It is a switch that controls mitochondrial numbers and activity. You really rev up the power of the cell. Instead of having a weak or indolent cell, you rev it up to the level that it needs to be able to release insulin in response to glucose. And that takes a lot of energy.”

In mouse models, the effect of the therapy is immediate, he said.

“The day that we implant them, the diabetes starts going away,” Evans said. “These cells, you can purify them in a dish. You can grow them exactly the way you want, to hundreds of millions of cells that all share common features. For human therapy, you need that.”

Further research may enable production of different islet cells that make other important hormones to regulate blood sugar, Evans said. And a few more years of testing and preclinical development, it should be possible to test the therapy in humans.

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Insulin diagram - Beta Cells

Beta Cells From Love Handles

Original article written by Eth Zurich and published by EurekAlert! American Association for the Advancement of Science (AAAS) on April 11, 2016. Click here to read the original article.

Researchers led by Martin Fussenegger, Professor of Biotechnology and Bioengineering at ETH Zurich’s Department of Biosystems Science and Engineering in Basel, have performed a feat that many specialists had until now held to be impossible: they have extracted stem cells from a 50-year-old test subject’s fatty tissue and applied genetic reprogramming to make them mature into functional beta cells.

In the presence of glucose, the beta cells generated using this “genetic software” produce the hormone insulin – just like natural beta cells, which are found in the pancreas. The researchers reported this in the journal Nature Communications.

The diagram shows the dynamics of the most important growth factors during differentiation of human induced pluripotent stem cell to beta-like cells. CREDIT: Eth Zurich

Maturation dynamic reproduced

The Basel-based researchers took the stem cells and added a highly complex synthetic network of genes – the genetic software. They designed this network to precisely recreate the key growth factors involved in this maturation process.

Central to the process are the growth factors Ngn3, Pdx1 and MafA. Concentrations of these factors change during the differentiation process. For instance, MafA is not present at the start of maturation. Only on day four, in the final maturation step, does it appear, its concentration rising steeply and then remaining at a high level. The changes in concentration of Ngn3 and Pdx1, however, are very complex: while the concentration of Ngn3 rises and then falls again, the level of Pdx1 rises at the beginning and towards the end of maturation.

Fussenegger stresses that it is essential to reproduce these natural processes as closely as possible in order to produce functioning beta cells: “The timing and the quantities of these growth factors are extremely important.”

New beta cells respond to glucose

In Fussenegger’s opinion, it is a real breakthrough that a synthetic gene network has been successfully used to achieve genetic reprogramming that delivers beta cells. Until now, scientists have controlled such stem cell differentiation processes by adding various chemicals and proteins using pipettes.

“It’s not only really hard to add just the right quantities of these components at just the right time, it’s also inefficient and impossible to scale up,” Fussenegger says. In contrast, the new process can successfully transform three out of four adipose stem cells into beta cells.

These beta cells not only look very similar to their natural counterparts – both kinds contain dark spots known as granules, which store insulin. The artificial beta cells also function in a very similar way. “At the present time, the quantities of insulin they secrete are not as great as with natural beta cells,” he admits.

But the key point is that the researchers have for the first time succeeded in reproducing the entire natural process chain, from stem cell to differentiated beta cell.

Implants of endogenous cells

In future, the Basel-based ETH researchers’ new technique might make it possible to implant new functional beta cells in diabetes sufferers that are made from their own adipose tissue.

While beta cells have been transplanted in the past, this has always required subsequent suppression of the recipient’s immune system – as with any transplant of donor organs or tissue. “With our beta cells, there would likely be no need for this action, since we can make them using endogenous cell material taken from the patient’s own body,” Fussenegger says, adding: “This is why our work is of such interest in the treatment of diabetes.”

Complete maturation in the petri dish

To date, the ETH researchers have merely cultured their beta cells; they have yet to implant them in a diabetes sufferer. This is because they first wanted to test whether stem cells could be fully differentiated from start to finish using genetic programming.

Fussenegger is convinced that this new method could also be used to produce other cells. Stem cells taken from adipose tissue could be differentiated into various cell types, he says – “And most people have an overabundance of fat from which these stem cells can be harvested.”


Saxena P, Heng BC, Bai P, Folcher M, Zulewski H, Fussenegger, M. A programmable synthetic lineage-control network that differentiates human IPSCs into glucose-sensitive insulin-secreting beta-like cells. Nature Communications, published online April 11th 2016. DOI: 10.1038/NCOMMS11247


Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

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Diabetes Supplies - Bottles

Consequences and Burdens of Type 1 Diabetes in Low-Income and Middle-Income Countries

Diabetes is a global epidemic. Just consider the following from the World Health Organization’s fact sheet on diabetes:

-In 2014 the global prevalence of diabetes was estimated to be 9% among adults aged 18+ years
-In 2012, an estimated 1.5 million deaths were directly caused by diabetes
-More than 80% of diabetes deaths occur in low- and middle-income countries
-WHO projects that diabetes will be the 7th leading cause of death in 2030

Most everyone in the U.S. has likely felt the burden of diabetes in one way or the other, but in low and middle income, the burden of diabetes is felt even more strongly, as poor access to health services is coupled with a lack of primary health care education.

A Lack of Money to Treat Diabetes

Though insulin was discovered 95 years ago, children and young people across the world still suffer or die from preventable complications because of a lack of insulin. This is due to limited access to insulin globally, particularly in many parts of the developing world. What’s more, even when insulin is available, many families struggle with the cost of insulin and test strips because the cost is so disproportionate to their average monthly income. As of 2012, 12.7% of people across the world live on less than $2 a day. With an income this limited, many of those afflicted with type 1 diabetes simply can’t afford the medicine they need every day. With around 78,000 children under 15 being diagnosed with type 1 diabetes each year, the demand for insulin is only increasing.

A Lack of Type 1 Diabetes Education

In addition to poor access to medical supplies in low-income and middle-income countries, education on living with diabetes is severely lacking in developing countries. Without adequate diabetes education and support, living a full, productive and healthy life with diabetes can be nearly impossible. Even with access to insulin, not knowing how to properly manage your diabetes has severe health repercussions.
What’s more, myths about diabetes abound in many developing nations. A study in India, which has the largest number of patients with diabetes and is known as the “Diabetes capital of the world,” found that nearly half of adult patients surveyed believed that diabetes can be cured by herbal treatment and that bitter foods reduce the elevated blood sugar levels. Misconceptions and myths such as these result from insufficient education and awareness about type 1 diabetes, and only serve to increase the economic and public health burdens of diabetes in low-income and middle-income countries.

The Cyclical Challenges of Diabetes

To make matters worse, the problems of diabetes globally aren’t solely a lack of medication and healthcare. Rather, it becomes cyclical, creating a challenge to not just thrive, but survive.

Consider the child who has diabetes but has inadequate access to insulin and test strips, leading to recurring bouts of diabetic ketoacidosis. Because of this, he can’t attend school regularly. By the time he reaches adulthood, his education is severely lacking. This affects his ability to get a job that pays enough to cover the cost of supplies to manage his diabetes in adulthood. In addition to not being able to afford the medical supplies he needs, his lower level of education means that he’s statistically more likely to believe common myths and misconceptions regarding diabetes, making it even harder to manage.

Ultimately, living with diabetes presents unique challenges no matter where you live, but living with type 1 diabetes in low-income and middle-income countries can significantly exacerbate these challenges. This is why the Diabetes Research Connection has made it our mission to support innovative scientific inquiry until diabetes is eliminated across the globe.

To get involved in the global fight against type 1 diabetes, support one of our diabetes research projects.

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Type 1 Diabetes Researchers

How to Get Involved in the Global Fight Against Diabetes

The Diabetes Research Connection’s mission is to connect donors with early-career scientists, enabling them to perform peer-reviewed, novel research designed to prevent and cure type 1 diabetes, minimize its complications and improve the quality of life for those living with the disease.

April 7 is World Health Day 2016, and this year’s theme is “beat diabetes”. In recognition of this, we invite you to join us in the global fight against diabetes. Read on to learn about a few ways you can get involved.

Support early-career scientists’ research.

We’ve made it easy for donors and strong proponents of type 1 diabetes research to help fund young scientists with exciting and inventive research project ideas. Currently, we’re raising money to fund two projects. Joseph Lancman, Ph.D., of Sanford Burnham Prebys Medical Discovery Institute, is researching ways to replace insulin producing beta-cells, allowing recipients to live a life free of daily insulin injections, while Sangeeta Dhawan, Ph.D., of UCLA’s School of Medicine, is researching how to create better insulin producing cells with cell regeneration. When you support one or more of these projects, 100% of your contribution goes directly to the scientists.

Submit research project ideas or refer early-career scientists to the Diabetes Research Connection.

Have an innovative idea for a type 1 diabetes research project? We can help you get it funded by facilitating the connection between donors and scientists.

Graduate students, post-docs, instructors and nontenured junior faculty whose work is focused on type 1 diabetes are invited to apply. Grants are up to $50,000 for one year, and scientists receive 100% of what they raise.

Serve on a peer-review committee.

If you’d like to get more deeply involved in the fight to beat type 1 diabetes, consider serving on one of our committees. Our Scientific Review Committee consists of more than 80 diabetes experts from across the country who volunteer their time and expertise to vet each research project we work with for novelty and scientific merit. Our Layperson Review Committees help scientists translate complex and jargon-heavy descriptions into simple and engaging website presentations that donors are likely to fund.

Learn more about serving on a committee here.

Engage online with social media.

Help raise awareness of the research currently being done to cure type 1 diabetes by joining us online. Follow us on Facebook, Twitter, LinkedIn and Instagram, and help us reach even more people by liking and sharing our posts.

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The Bionic Pancreas Is Getting Closer To Reality

Original article published in TIME HEALTH by Alexandra Sifferlin on April 1, 2016. To view the original article Click Here.

The invention could seriously change the management of type-1 diabetes

The race is on for what may be the biggest innovation in decades for Type 1 diabetes management—the bionic pancreas—and on Friday, one of the lead researchers in the field announced at the Endocrine Society’s annual meeting that he’s launched a company to bring that invention to market.

unknown1Ed Damiano, a professor of biomedical engineering at Boston University who is developing a bionic pancreas (also referred to as the artificial pancreas), has spun his academic research into a company called Beta Bionics. Recently, Beta Bionics secured $5 million from the pharmaceutical company Eli Lilly, which manufactures the insulin used in the device. “My goal is to bring this technology in a responsible and expeditious manner to as many people with diabetes as possible,” says Damiano.

As TIME previously reported, Damiano was inspired to make the device when his son David was diagnosed with diabetes as an infant. He wants the device on the market by the time David, now 16, goes off to college.

People with diabetes are constantly tracking and adjusting their blood sugar with insulin or food. A bionic pancreas would automate that process. Damiano’s device, called the iLet, takes blood sugar readings every five minutes, and depending on blood-sugar levels, releases insulin to bring the sugar down or another hormone called glucagon to bring it back up, keeping blood sugar steady throughout the day.

Damiano incorporated Beta Bionics as a benefit corporation. A benefit corporation allows companies to have a protected public-benefit mission. “It’s a for-profit organization but you are allowed to make management decisions that are in the interest of your mission that may or may not maximize return of equity to shareholders,” explains Damiano.

Beta Bionics is not without competition. Other research groups are developing similar technology. The medical device company Medtronic is in the game, and researchers at the University of Virginia and Harvard University announced in January that they will soon test their artificial pancreas in 240 people. One of the differences between Beta Bionic’s device and others is that instead of offering automated insulin delivery only, Beta Bionic’s also releases glucagon, which allows people to bring up their blood sugar without eating a snack. Damiano says they will likely have an insulin only version of the iLet approved in 2018 with the full system approved soon after that. Beta Bionics plans to begin its final pivotal clinical trial of the device in the middle of 2017.

I’m still very hopeful about the bionic pancreas and we’re getting closer,” says Fred Cunha, whose daughter Elise, 8, was one of the youngest people to try the bionic pancreas in a trial.Even though my wife and I can see her blood sugar on our Apple watches these days, it’s still a twenty-four-seven deal.”

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See our approved research projects and campaigns.

Role of the integrated stress response in type 1 diabetes pathogenesis
In individuals with type 1 diabetes (T1D), the insulin-producing beta cells are spontaneously destroyed by their own immune system. The trigger that provokes the immune system to destroy the beta cells is unknown. However, accumulating evidence suggest that signals are perhaps first sent out by the stressed beta cells that eventually attracts the immune cells. Stressed cells adapt different stress mitigation systems as an adaptive response. However, when these adaptive responses go awry, it results in cell death. One of the stress response mechanisms, namely the integrated stress response (ISR) is activated under a variety of stressful stimuli to promote cell survival. However, when ISR is chronically activated, it can be damaging to the cells and can lead to cell death. The role of the ISR in the context of T1D is unknown. Therefore, in this DRC funded study, we propose to study the ISR in the beta cells to determine its role in propagating T1D.
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A Potential Second Cure for T1D by Re-Educating the Patient’s Immune System
L Ferreira
Validating the Hypothesis to Cure T1D by Eliminating the Rejection of Cells From Another Person by Farming Beta Cells From a Patient’s Own Stem Cells
Han Zhu
Taming a Particularly Lethal Category of Cells May Reduce/Eliminate the Onset of T1D
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Can the Inhibition of One Specific Body Gene Prevent Type 1 Diabetes?
Is Cholesterol Exacerbating T1D by Reducing the Functionality and Regeneration Ability of Residual Beta Cells?
Regeneration Ability of Residual Beta Cells
A Call to Question… Is T1D Caused by Dysfunctionality of Two Pancreatic Cells (β and α)?
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Novel therapy initiative with potential path to preventing T1D by targeting TWO components of T1D development (autoimmune response and beta-cell survival)
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