diabetes Archives - Sanford Burnham Prebys

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Scientists and podcasters

AuthorGreg Calhoun
Date

May 27, 2025

Discovery Dialogues Episode 3 thumbnail
On May 23, 2025, the third episode of The Discovery Dialogues Podcast was released. It discusses animals that use insulin as venom and highlights an animal that can sense low blood sugar faster than a machine.

Sanford Burnham Prebys scientists bring dramatic stories of scientific achievement to life

In March 2025, Sanford Burnham Prebys scientists Ani Deshpande, PhD, and Pamela Itkin-Ansari, PhD, launched a new podcast exploring groundbreaking discoveries in science and medicine. The initial episodes have garnered rave reviews, including being hailed as “masterpieces” by upcoming podcast guest Adam Heller, PhD, the scientist and inventor who revolutionized blood sugar testing and laid the groundwork for modern continuous glucose monitoring systems.

On the first episode of The Discovery Dialogues Podcast, the hosts examined early descriptions of diabetes across ancient civilizations. Deshpande and Itkin-Ansari traced the research that led to the discovery of insulin and to life-saving treatment for diabetes.

Following its discovery as a treatment for diabetes, insulin had to be purified from millions of animal carcasses. In the follow-up episode, the podcasters discussed the race to make human insulin using genetic engineering, including interviews with Keiichi Itakura, PhD, a key member of the historic team that created the first synthetic gene to make human insulin, and Herb Boyer, PhD, the scientist who founded the first biotech company called Genentech and brought insulin to millions of patients.

Ani Deshpande, PhD, profile photo - image credit: Sanford Burnham Prebys

Ani Deshpande, PhD, is an associate professor in the Cancer Genome and Epigenetics Program at Sanford Burnham Prebys.

Pamela Itkin-Ansari, PhD, profile photo - image credit: Sanford Burnham Prebys

Pamela Itkin-Ansari, PhD, is an adjunct professor in the Center for Cardiovascular and Muscular Diseases at Sanford Burnham Prebys.

Last week, Deshpande and Itkin-Ansari released their third episode detailing animals that use insulin as venom and highlighting an animal that can sense low blood sugar faster than a machine.

We recently sat down with them to learn more about their motivations and creative process.

What is your origin story as scientists turned podcasters?

DESHPANDE: I have been very interested in communicating science for quite some time. And I think it is important for more scientists to speak in a way that all people can understand, and to embrace new ways of communicating.

I got especially excited to talk about the incredible potential of GLP-1 drugs such as Ozempic and Wegovy, but I don’t think you can properly understand them without a grasp of diabetes. I decided to tackle diabetes as the podcast’s first topic, and I reached out to Pam as a partner with complementary expertise.

ITKIN-ANSARI: I have done a lot of scientific outreach in the past as a diabetes scientist, including with the La Jolla Playhouse and Fleet Science Center, so I jumped at the opportunity. As it turns out, Ani and I are kindred spirits in terms of our desire to help people understand how biomedical research has changed the world.

What is your process for developing each episode?

DESHPANDE: We have a very elaborate process for deciding on each episode’s topic. outlining the chapters or segments and then passing drafts back and forth until we’ve refined them into a version that is both accurate and entertaining.

ITKIN-ANSARI: Getting that balance right is so important. I’m a Radiolab junkie. I have to hear every episode. The reason I keep coming back is because I get to learn something new and have a ton of fun along the way.

DESHPANDE: It is important to us that we’re not just telling stories people already know, so we take our time to find fascinating stories about the science and the personalities behind the discoveries.

How much research goes into making the podcast?

DESHPANDE: We just read and read and read and read. Then, we bounce ideas off each other to see what makes it into an episode.

ITKIN-ANSARI: The other thing is fact-checking. We feel it our job as card-carrying scientists to be as thorough as we can be to get the facts right.

While writing for the first three episodes, what information or stories surprised you?

ITKIN-ANSARI: For me, I was amazed by the venoms of the cone snail that have already led to an FDA-approved drug for severe pain and may also revolutionize diabetes treatment.

DESHPANDE: I think it’s surprising that diabetes had been described in detail more than three millennia ago. Many of our audience members told us they were surprised by that fact as well.

What teasers can you share about future episodes?

ITKIN-ANSARI: For an upcoming episode, a legendary scientist who changed diabetes care forever after surviving the Holocaust and making his way to the U.S.

DESHPANDE: One of the most fascinating things we will cover in our future episodes and that will surprise most people is that many of the most influential drugs in the history of medicine have come from plant poisons and animal venoms. It blows my mind, and I hope our listeners will also find it to be amazing.

Listeners can find The Discovery Dialogues Podcast on Spotify, Apple Podcasts and Amazon Music. The YouTube version includes on-camera interviews and additional illustrations.

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Scientists discover an early sign of type 2 diabetes: Misfolded proinsulin

AuthorMonica May
Date

March 19, 2020

Diabetic patient is using glucometer to check glucose level

The findings could lead to tests or treatments that help prevent type 2 diabetes.

Misfolded proinsulin—a protein the body normally processes into insulin—is an early sign of type 2 diabetes, according to a study by scientists at Sanford Burnham Prebys and the University of Michigan Medical School. The discovery, published in eLife, could lead to tests or treatments that help prevent people from developing type 2 diabetes.

“Understanding the molecular events that occur as prediabetes progresses to diabetes opens new avenues for us to detect or interrupt these processes,” says Randal Kaufman, PhD, director and professor in the Degenerative Diseases Program at Sanford Burnham Prebys and co-corresponding author of the study. “With this information, we can start to find interventions that might spare millions of people from a serious, lifelong condition.”

More than one in three Americans, or approximately 88 million people, have prediabetes—which is characterized by elevated blood sugar. If left untreated, within four years nearly 40% of people with prediabetes develop type 2 diabetes, which occurs when the body doesn’t use insulin properly. In 2017, the cost of treating diabetes exceeded $327 billion, according to the American Diabetes Association. Due to increasing obesity rates, the number of people with the condition—particularly children—is on the rise.

Identifying the molecular events that occur during progression from prediabetes to full-blown diabetes remains one of the most perplexing problems in diabetes research. In the study, the scientists set out to answer this question by tracking proinsulin folding in the beta cells of humans and mice that are healthy, prediabetic and diabetic.

These studies revealed that instead of undergoing its normal folding process, proinsulin proteins were abnormally linked to each other. Levels of the abnormal proinsulin accumulated as prediabetes progressed to type 2 diabetes. Obese mice in the earliest stages of diabetes had the highest levels of abnormal proinsulin in their beta cells.

“Proinsulin misfolding is the earliest known event that may contribute to the progression from prediabetes to diabetes,” says Kaufman. “Together, these studies show that abnormally linked proinsulin holds promise as a potential measure of how close someone may be to developing type 2 diabetes.”

Now, the researchers are set to uncover more details about this process, such as the proteins that interact with the misfolded proinsulin.

“Understanding the fundamental molecular events that lead to type 2 diabetes is critical as the number of people with prediabetes continues to rise,” says Kaufman. “If we don’t find preventive measures, we will soon have a diabetes epidemic.”

The study’s first author is Anoop Arunagiri, PhD; and the study’s senior author is Peter Arvan, both of the University of Michigan Medical School.

Additional authors include Leena Haataja and Fawnnie Pamenan of the University of Michigan Medical School; Ming Liu of the University of Michigan Medical School and Tianjin Medical University in China; Anita Pottekat and Pamela Itkin-Ansari of Sanford Burnham Prebys; Soohyun Kim of Konkuk University in South Korea; Lori M. Zeltser of Columbia University; Adrienne W. Paton and James C. Paton of the University of Adelaide in Australia; and Billy Tsai of the University of Michigan.

The study’s DOI is 10.7554/eLife.44532.

This work was supported by the National Institutes of Health (R01DK111174, R24DK110973 and R01DK48280) and the Juvenile Diabetes Research Foundation International (2-SRA-2018-539-A-B).

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A new approach to restore insulin production in diabetes

AuthorSusan Gammon
Date

May 23, 2018

diabetes

If you have diabetes, there is a strong chance you are either on insulin therapy now, or will be in the future. This holds true for people with Type 1 and Type 2 diabetes; both types lead to elevated blood glucose levels.

Insulin therapy maintains blood glucose at healthy levels to prevent the complications that come with diabetes, such as vision problems, kidney disease, neuropathy, heart disease—and the list goes on.

Insulin is usually administered under the skin using a syringe, insulin pen or insulin pump. But scientists are working to change that.

Fred Levine, MD, PhD, a scientist at SBP, has been working on methods to restore pancreatic beta cells—the cells that live in pancreatic islets and store and secrete insulin.

In Type 1 diabetes—an autoimmune disease—beta cells are destroyed by the immune system. In Type 2 diabetes, beta cells gradually lose their ability to produce insulin. “Regenerating insulin-producing beta cells could potentially free millions of patients from daily doses of insulin,” says Levine.

Levine’s initial work, published in two papers in Stem Cells and Cell Death and Disease, began with an observation that injuring the pancreas of diabetic mice causes alpha cells to convert to convert to insulin-producing beta cells. Alpha cells are also located in pancreatic islets but don’t normally produce insulin.

“There was a signal coming from the injured pancreas driving the conversion of alpha cells to beta cells—a process known as transdifferentiation—and we wanted to know what that signal was,” says Levine.

Levine’s next study found that the activation of PAR2, a receptor on alpha cells, was driving the transition to insulin-producing beta cells. That research was published in a later paper Cell Death and Disease.

“This was a good step toward understanding how to restore beta cells, and there are good drug candidates that can activate PAR2, so it could work in humans,” says Levine. “But there was still hurdle. The transdifferentiation process only occurs in the setting of profound beta cell deficiency—there had to be practically zero functional beta cells for alpha cells to convert.”

Most people with Type 2 diabetes and a smaller percentage with Type 1 have some, but not enough, functional beta cells. For these patients, activating PAR2 alone wouldn’t be a sufficient to treat diabetes. Levine’s group hypothesized that there must be an inhibitory signal coming from beta cells preventing the process.

In the latest study, published in Islets, Levine’s research team found that insulin is the inhibitory signal that prevents transdifferentiation.

“It makes sense that insulin inhibits transdifferentiation, because why would your body generate beta cells if you already had a significant number of cells producing insulin,” says Levine. “But biology isn’t perfect, hence the need for insulin therapy.”

“We were able to work around these obstacles and generate insulin-producing beta cells by using a combination of drugs, one that activates PAR2 (2fLI), and two that inhibit insulin secretion and action (diazoxide and S961). It’s a two element process—one which is positively acting on alpha cells and the other repressive of beta cells,” explains Levine.

“Our research offers the prospect of a straightforward pharmacological approach to regenerate insulin-producing cells to treat diabetes,” says Levine. “For Type 2 diabetes, we could potentially drive transdifferentiation in vivo by activating PAR2 and inhibiting insulin for a short term. It could result in restoration of long-term beta cell function.

“For Type 1 diabetes, we would still need to address the autoimmune aspect of the disorder, because new beta cells would continue to be attacked by the immune system,” adds Levine. “But as our understanding and ability to rein in the autoimmune system improves, the approach could be a much needed breakthrough for the disease.”

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SBP welcomes Congresswoman Susan Davis

AuthorSusan Gammon
Date

May 4, 2018

Kristiina Vuroi

Susan Davis, U.S. Representative for California’s 53rd congressional district (D-San Diego), visited our Institute in April and met with several members of the faculty and SBP President Kristiina Vuori, MD, PhD  Davis, a strong advocate for increasing the NIH budget to advance scientific discoveries, has a long history of supporting initiatives on diabetes and cardiovascular health.

Davis was following up on an invitation for a tour of our campus from Chris Larson, PhD, vice president, drug discovery at SBP. Larson sits on the Board of Directors for the Southern California Chapter of the American Diabetes Association and meets regularly with Davis regarding issues related to diabetes care and research.

Pamela Itkin-Ansari, PhD, adjunct professor at SBP met with Davis and shared her research on implanting small encapsulation devices that contain pancreatic islet cells as an approach to treat type 1 (juvenile) diabetes. The work has now progressed to international clinical trials, which impressed Rep. Davis.

As a teenager, Davis worked as a counselor at a camp for diabetic children—most of whom have type 1 diabetes.  The experience led to a lifelong interest in improving the health and welfare of diabetic patients, both type 1 and type 2.

“Congresswoman Davis’ visit went really well,” says Larson, who organized a tour of the Prebys Center, showcasing the high-throughput drug discovery capabilities of the facility. “She was especially keen to learn how our automated technology can screen hundreds of thousands of chemical compounds to find future drugs.

“It was an honor to host Congresswoman Davis, and she and her staff are most welcome to visit anytime,” says Larson.

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Exciting diabetes and obesity research highlights from Medical City

AuthorDeborah Robison
Date

May 22, 2017

diabetes wordcloud

Center for Metabolic Origins of Disease

With more than one-third of adults in the U.S. considered obese, scientists are searching for new ways to treat obesity and associated health problems such as type 2 diabetes. Four researchers from Sanford Burnham Prebys Medical Discovery Institute (SBP) at Lake Nona have been invited to present new perspectives and insights at the American Diabetes Association’s 77th Scientific Sessions, to be held June 9-13, 2017, in San Diego. The conference is the world’s largest gathering of research experts and clinicians focused on diabetes research, prevention and care. The presentations will inform new treatment strategies for the nearly 30 million people diagnosed with diabetes.

Potential early therapeutic target for diabetes prevention
Obesity often leads to accumulation of fat in muscle and faulty machinery involved in taking up glucose from a meal to use it for energy, leading to type 2 diabetes. A recent advance from the laboratory of Daniel P. Kelly, MD, scientific director of SBP at Lake Nona, may lead to a way to stop this pre-diabetic state from advancing. Dr. Kelly will present findings on a recently discovered cellular glucose sensor in muscle that serves as a key connection between insulin resistance and accumulation of fat in muscle, which occurs in obesity-related diabetes. When the protein is inhibited in skeletal muscle cells, regulatory genes that influence glucose uptake and insulin signaling are enhanced. The team is now validating the pathway as a therapeutic target to prevent type 2 diabetes.

Fatty liver and type 2 diabetes
Peter Crawford, MD, PhD, director of SBP’s Cardiovascular Metabolism Program, is studying the root causes of nonalcoholic fatty liver disease (NAFLD), a condition that affects nearly 80 percent of people with type 2 diabetes. About 5 percent of NAFLD cases advance to liver cirrhosis – a disease characterized by scarring and fibrosis that could require liver transplant. Dr. Crawford is an expert on how the liver processes energy derived from food. At the ADA meeting, he will discuss how the interruption of normal fat metabolism can lead to enhanced scarring. Through ongoing research, he hopes to be able to specifically identify which diabetes patients are at risk of developing advanced liver disease and to develop therapies that protect against disease progression.

Brain nutrient sensors help maintain energy balance
Diabetes researcher Julio Ayala, PhD wants to understand how specialized regions in the brain control food intake, energy expenditure and body weight. His ADA presentation will focus on how nutrient-sensors that control the balance between energy-consuming and energy-producing processes in almost every cell in our bodies also play a very specific role in the brain. His research shows that hormones, such as glucagon-like peptide-1 (GLP-1) regulate the activities of these brain nutrient sensors to influence hunger, satiety and ultimately body weight. Defective sensors are implicated in obesity and could be a target for new therapeutic treatments.

Glucose Sensor in Macrophages
Insulin resistance is a key feature of type 2 diabetes. When present, the impairment prevents insulin from getting glucose into muscle where it’s used for energy, and instead causes blood sugars to become elevated. The events that drive the development and progression of insulin resistance are not known. Laszlo Nagy, MD, PhD, director of SBP’s Genomic Control of Metabolism Program, will present new research that suggests that the inflammatory process—and specifically a type of white blood cells called macrophages—are involved. He will present a novel hypothesis on the role of macrophages, defined in Greek as “big eaters”, and identify molecules involved in muscle growth and glucose metabolism. His research aims to reveal cellular interactions that could become new therapeutic targets to treat type 2 diabetes.

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Drug reverses type 2 diabetes in mice

AuthorJessica Moore
Date

March 30, 2017

insulin syringes

Type 2 diabetes is a massive public health challenge. About eight percent of the world’s adult population has it, and the complications are serious—increased risk of heart attack and stroke, kidney problems, hearing and vision loss and painful nerve damage. Managing blood sugar with diet, routine monitoring and insulin helps prevent these issues, but that takes more time and effort than many patients have.

A new experimental drug developed with the help of scientists at Sanford Burnham Prebys Medical Discovery Institute (SBP) may spell the end of insulin reliance. A study published in Nature Chemical Biology shows that the compound, which can be given as a pill, restores blood sugar control in a mouse model of diet-induced diabetes.

“By targeting an enzyme that controls insulin receptor signaling, we found a way to recover cells’ ability to respond to insulin,” says Anthony Pinkerton, PhD, director of medicinal chemistry at SBP’s Conrad Prebys Center for Chemical Genomics and a contributor to the research. “This could lead to a new treatment approach for type 2 diabetes.”

The candidate drug blocks an enzyme called low molecular weight protein tyrosine phosphatase (LMPTP), which regulates the insulin receptor. Human genetic studies suggested that individuals with lower LMPTP activity were protected from type 2 diabetes, but the mechanism of protection remained unclear.

The new investigation, led by Nunzio Bottini, MD, PhD, professor at UC San Diego, found that LMPTP has direct actions on the insulin receptor that reduce its signaling activity, making cells less sensitive to insulin. Turning off the LMPTP gene prevented mice from becoming diabetic when they were fed a high-fat diet, so the research team screened compounds to identify LMPTP inhibitors. Chemical improvements to the best compound gave a potent, orally available drug that improved glucose control in mice with type 2 diabetes.

“This is still a few steps away from clinical trials,” says Robert Liddington, PhD, professor at SBP who also collaborated on the study. “No adverse events were noted in mice who received the drug for a month, and the compound is highly selective for LMPTP, but considerably more optimization and testing has to be done to show that it’s safe when taken long-term and is likely to work in humans.”

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Are artificial sweeteners bad for your health?

AuthorJessica Moore
Date

October 25, 2016

artificial sweetener packets

These days, we’re fighting a war on sugar, and it might seem like we’re winning. Low-calorie, artificial sweeteners are added to 15% of the volume of foods and beverages purchased in the United States.1 And they’re in all sorts of products labeled “light” or “no added sugar,” from soda to yogurt to protein bars. By replacing sugar, they’re meant to help consumers take in fewer calories. But epidemiological data suggest they may do the opposite, elevating the risk of health problems like type 2 diabetes and cardiovascular disease. 

“Artificial sweeteners were approved for consumption by the U.S. Food and Drug Administration because they’re non-toxic and don’t cause cancer at the recommended daily intake,” said George Kyriazis, PhD, assistant professor in the Integrative Metabolism Program, who recently presented evidence of their possible health risks during a public lecture at the University of Central Florida. “But we’re only now figuring out whether and how they may affect metabolism.”

The potential impact of artificial sweeteners, including sucralose, aspartame, saccharin and acesulfame potassium, on American health could be huge. In large studies following the same group of people over 10-20 years, those who drank at least one artificially sweetened beverage every day were 40% to 60% more likely to develop type 2 diabetes or suffer a heart attack or stroke as those who didn’t.2 The jump in relative risk is roughly the same as that with one or more regular sugary sodas.

Why is consumption of low-calorie sweeteners associated with all these problems if they’re not metabolized by our cells? Kyriazis thinks a potential mechanism lies in their ability to activate sweet taste receptors, the focus of his research. Sweet taste receptors, despite their name, are actually found in many organs, including the intestine and pancreas, where they regulate sugar uptake and secretion of sugar-regulating hormones, respectively.

Kyriazis has shown that sweet taste receptors are essential for artificial sweeteners to wreak havoc on metabolism. For example, adding saccharin to the water of normal mice for a few months causes them to become pre-diabetic, but mice lacking sweet taste receptors are protected from this condition. Whether this is also true in humans is unknown, but Kyriazis is leading a proof-of-concept clinical study at the Translational Research Institute for Metabolism and Diabetes at Florida Hospital that will begin recruiting soon.

“We will give healthy participants an FDA-approved food additive that inhibits sweet taste receptors and see if it can prevent any of the anticipated negative metabolic effects of saccharin consumption,” Kyriazis explained. “These studies could further our understanding of the role of sweet taste receptors in metabolic disease, which will help determine their validity as a target for future drug development.”

 

References:

  1. Ng SW, Slining MM, Popkin BM. Use of caloric and noncaloric sweeteners in US consumer packaged foods, 2005–2009. J Acad Nutr Diet 2012.
  2. Swithers SE. Artificial sweeteners produce the counterintuitive effect of inducing metabolic derangements. Trends Endocrinol Metab 2013. Table 1, refs 25, 26, 30.
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SBP scientists reflect on progress in diabetes research

AuthorDeborah Robison
Date

June 23, 2016

ADA

“The most significant advances in diabetes treatment, which were underscored at the ADA meeting, is the clinical evidence that two newer classes of anti-diabetic drugs significantly improve cardiovascular outcomes and overall mortality. These drug families are insulin secretion enhancers such as liraglutide (LEADER trial) and drugs that promote glucose elimination in the urine, such as canagliflozin and empagliflozin (EMPA-REG OUTCOME trial). This has major impact because reducing the risk of heart disease is always the end goal in treating diabetes—the association with heart disease is what makes type 2 diabetes so serious. These trials also present a remarkable opportunity for basic researchers—many of us, including several here in Lake Nona, study how drugs in these classes affect metabolism. The answers to those questions should lead to new drug targets that are even more specific and precision-oriented.”

Peter Crawford, MD, PhD
Associate Professor and Director
Cardiovascular Metabolism Program

“From the sessions that I saw, there was a significant emphasis on combination treatments—either combining two or more already approved drugs that have related functions or generating fusions of multiple protein drugs. An example of the former is the combination of basal insulin and glucagon-like peptide-1 receptor agonists to control fasting and post-meal glucose levels, respectively. With regards to fusion proteins, there were many posters and presentations highlighting efforts to generate dual and triple combinations that would lower glucose and aid weight loss. These approaches may reduce the need for patients to take multiple drugs and therefore improve efficacy and patient adherence.”

Julio Ayala, PhD
Associate Professor
Integrative Metabolism Program
ADA Thomas R. Lee Career Development Award Recipient ’14

“During the ADA meeting two symposia and numerous other presentations examined evidence implicating gut microbiota in the development of type 1 and type 2 diabetes. I am personally enthusiastic about the potential of novel therapeutic strategies that either prevent harmful changes in gut microbiota or even directly transplant “therapeutic” microbial species. Nevertheless, our current understanding of the potential mechanisms is very limited due to the complex factors affecting the microbiome such as the host’s genetics and the environment (diet, antibiotic use, history of infections etc.).”

George Kyriazis, PhD
Assistant Professor
Integrative Metabolism Program

“Of particular interest to me were the symposia on experimental strategies for understanding how the brain controls metabolism. Specifically, optogenetics and magnetogenetics are emerging as two powerful research tools for this purpose, and involve genetically modifying neurons to express either light- or magnetic field-sensitive proteins so that their activity can be controlled with fiber optic light or magnets, respectively. These sophisticated techniques will help investigators delineate which regions in the brain play a critical role in regulating blood glucose, which could lead to more effective therapies for diabetes and obesity.”

Melissa Burmeister, PhD
Staff Scientist
Dr. Julio Ayala Lab

 

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The science of crowdfunding

Authorkcusato
Date

March 3, 2016

Header image

He doesn’t need money to produce an album. He’s not raising funds to start a new business in his hometown. And he’s not asking for cash because he’s a famous rapper who suddenly finds himself “bankrupt.” He is a young scientist who needs money to conduct research aimed to save lives, so he is turning to crowdfunding.

Joseph Lancman, PhD, is a scientist in the organogenesis lab of Duc Dong, PhD, at Sanford Burnham Prebys Medical Discovery Institute (SBP) in La Jolla. Lancman’s crowdfunding site just went live on Diabetes Research Connection (DRC), a San Diego-based company that created a platform to connect donors directly with early-career scientists. In the next 90 days, Lancman hopes to generate $50,000 for his research project that may provide the scientific breakthrough needed to find a cure for type 1 diabetes. Watch his video here.

“We recently discovered a way to reprogram cells and change their identity without removing them from the body,” Lancman said. “We believe this breakthrough will have great implications for people with degenerative diseases, like diabetes.”

As many as three million Americans have type 1 diabetes.  Millions of children and adults struggle with this disease, yet funding has decreased dramatically for research. In fact, the head of the National Institutes of Health (NIH)  said last year that young scientists in this country now face the worst funding in 50 years.

So, if you are a young scientist with a great idea, where do you go? Alberto Hayek, MD, co-founder and president of the DRC and world-renowned diabetes expert, says some go away. “Due to the limited funding available, scientists just starting out in their career are forced to leave the field of diabetes and go to fields that have more funding. We are giving scientists the funding needed to test and validate research that departs from conventional thinking,” Hayek said.

Dong says his lab heard about DRC from others in the field. “The DRC is committed to funding innovative projects that may not be considered mainstream approaches. The crowdfunding model itself is highly innovative, by making sure that 100% of donations will go directly into specific labs and projects chosen by the individual donors,” Dong said.

And it works. Since DRC launched its platform in 2014, six research projects from all over the country have been 100% funded. Every dollar of the money raised goes directly to the scientist. The power to fund projects has been given to the people.

Lancman has a total of 90 days to make it happen. He needs 5,000 people to donate $10 each in order to reach his goal. He’s excited to be able to continue to work towards a cure for diabetes, and allow people to live full lives without painful daily insulin injections.

Come on, social media.

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New links between heart hormones, obesity, and diabetes

AuthorGuest Blogger
Date

February 17, 2016

Header image

New research from SBP’s Sheila Collins, PhD, and Richard Pratley, MD, has revealed an important relationship between proteins secreted by the heart and obesity, glucose intolerance, and insulin resistance. The findings, published in Obesity, offer a new approach to treating metabolic disorders, including type 2 diabetes, by targeting the pathway that controls the proteins’ concentration in the blood. Continue reading “New links between heart hormones, obesity, and diabetes”