Did Trauma Cause My Diabetes?

What caused killer t-cells to attack the beta cells in my pancreas, preventing them from producing insulin, making my blood sugar skyrocket and triggering my Type 1 diabetes? That was in 1962. No one has come up with a convincing explanation yet. Scientists aren’t even close to figuring out the interactions between the environment, genes, the immune system and who-knows-what-else that result in Type 1 (T1) or Type 2 (T2) diabetes. If you travel around the Internet, it appears that the entire world is one big “risk factor” for these conditions.

Suspects identified by researchers that might play a role in T1D include the smoked mutton consumed by Icelanders between Christmas and New Year’s, various viruses, respiratory infections in early childhood, early exposure to cow’s milk, psoriasis, the timing of infants’ first solid foods, low levels of Vitamin D, and many more. Risk factors for T2D, besides the well-known ones like obesity, could include not enough sleep and phthalates in soaps, lotions, plastics and toys.

But the culprit that interests me the most doesn’t get much attention in the research labs: trauma and major stress. When I was a kid, the conventional wisdom was that traumatic events — loss of a loved one, accidents — played an important role in diabetes onset. This appeared to be substantiated by a number of population studies in the ensuing decades, but the evidence hasn’t impressed major players in diabetes research. In a long summary of biochemical and environmental risk factors for T1D, the NIH barely touches upon the matter, gives it a few throwaway lines:

Although investigations of stress and IDDM [insulin dependent diabetes] have, in general, reported positive associations, most studies have been retrospective and suffered from methodological difficulties in assessing stress and measuring its frequency, intensity, and duration. Thus, prospective evaluations of the interaction among stress, the immune system, and the occurrence of autoimmune diseases are warranted.

Sorry, NIH, but I am convinced that a specific traumatic event played a major, albeit partial, role in triggering my diabetes.

In a blog post that was mainly about my mother and Sonya Sotomayor’s parents, I described the onset of the disease 51 years ago. It happened very soon after my grandfather died. In my grandmother’s apartment in Manhattan, I was so terrified by the mournful screams from my mother and grandmother when they embraced that I ran away and hid. Within two days, after an earache, sniffles, a sore throat and ravenous thirst, I was hauled to a hospital and suddenly became a kid with a scary disease.

By now, I understand that the trauma of mourning contributed to a process that was probably primed to happen anyway. Maybe my pancreas was already getting ravaged before my grandfather died and before any symptoms appeared. Maybe I would have been hospitalized at about the same time even if the women I loved hadn’t shocked me with their keening. Hard-nosed, data-driven scientists might call it a coincidence that those screams occurred just before the diagnosis. As the NIH notes, more research is needed on this one.

But was it a coincidence that after a major earthquake in California, in 1994, the Children’s Hospital of Los Angeles experienced a sudden, unusually large influx of kids with newly-diagnosed T1D? Or that after Israel’s second war with Lebanon, the post-war incidence of T1D was higher than normal in areas in northern Israel that had been attacked, and there was no change in other regions? Or that, in Denmark, the children of mothers who were bereaved during their pregnancies were more likely to develop T1D, according to one study?

Or that the British physician Thomas Wills, in the 17th century, noticed that, “Sadness, or long sorrow, as likewise convulsions, and other depressions and disorders of the animal spirits, are used to generate or foment this morbid disposition [diabetes]”?

According to one theory, psychological and/or physical stress are among the factors that cause beta cell “stress” and “accelerate the auto-immune process that leads to their own destruction,” as one researcher puts it. There is at least some evidence that infants under stress have a higher incidence of the “auto-antibodies” — cells that turn around and destroy healthy cells — that are associated with this morbid disposition.

That’s enough evidence for me. But even if you doubt that my reaction to those screams was related to the destruction of my beta cells, you cannot possibly come up with a credible argument against psychologist David Felten, who tells us:

We can no longer pretend that the patient’s perceptions don’t matter … Your mind is in every cell of your body. And your emotions are the bridge between the mental and the physical, or the physical and the mental. It’s either way. Now there is overwhelming evidence that hormones and neurotransmitters can influence the activities of the immune system, and that products of the immune system can influence the brain.

This is hardly headline news. But thinking of the bodymind as one, integrated entity has never come naturally to me. I am, at heart, a Western guy, who has stayed alive mainly by doing what conventional Western physicians have told me to do. I reflexively consider balancing diet, insulin and exercise as the regimen needed to help my diabetic body. But meditation, and doing xi kung, and telling myself not to get angry at the guy who cuts in front of me on the movie line somehow feel like they are meant to help… something else, something I can’t locate, something that is closer to my authentic self than the clanking, flawed, corroding body that is wrapped around it.

Reading more, of late, about diabetes, the brain and behavior has helped to remind me that the physical aspects of this condition should not be placed in a category that is separate from the psychological aspects; they are part of the same condition. But the quickest way to remember that is to picture a frightened 7-year-old boy, running down a hallway in Manhattan. I am still doing my best to help him feel better, and that means dealing with everything that is churning within him, from high blood sugar to the terror that his cells have not forgotten.

Orginally published in The Insulin Chronicles and, with a different title, in Strangely Diabetic.


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Chronic stress may lead to diabetes

Dr S V Madhu, the lead researcher, said increased secretion of the stress hormone—cortisol—leads to redistribution of fat, central obesity and insulin resistance. He added, “Higher stress levels also causes activation of oxidative and inflammatory pathways resulting eventually in development of type II diabetes.”

Dr Madhu, who heads the medicine and the endocrinology and metabolism division at UCMS, said this is the first study that has used different stress scales to characterize chronic psychological stress and evaluate its role in development of diabetes.

Doctors said, among the stress scales, the ability to cope with stress was found to be the strongest independent predictor of diabetes with an odds ratio of 0.77 that translates to a 33 percent lower risk of diabetes. “This is a positive finding. It shows that de-stressing mechanisms such as yoga, listening to music, sports or travelling can reduce the risk factor,” said another senior doctor.

Simply put, diabetes is a condition in which the body has trouble turning food into energy. All bodies break down digested food into a sugar called glucose, their main source of fuel. In a healthy person, the hormone insulin helps glucose enter the cells. But in a diabetic, the pancreas fails to produce enough insulin, or the body does not properly use it. Cells starve while glucose builds up in the blood.

There are two predominant types of diabetes. In Type 1, the immune system destroys the cells in the pancreas that make insulin. In Type 2, which accounts for an estimated 90-95% of all cases, either the body’s cells are not sufficiently receptive to insulin or the pancreas makes too little of the hormone, or both.

With more than 63 million diabetic patients, India is second only to China in the number of people living with the ailment. However, awareness about the disease remains low, says Dr B M Makkar from Research Society for the Study of Diabetes in India, RSSDI.

“Studies show almost 85 percent of type II diabetics are overweight. However, only six to ten percent are aware that being overweight put them at a higher risk for diabetes,” Dr Kakkar added.

Cyborg gel implant fights diabetes with light

Light can now be used to heal diabetes in mice. By implanting a transparent gel that contains genetically modified light-sensitive cells, researchers have demonstrated a new type of implant that could one day be used to treat disease and monitor toxins in people.

“Light is a great tool to interface with biological systems, but there is a fundamental problem. It gets scattered when it hits tissue, and at depths much thinner than our skin,” says lead author Myunghwan Choi of Harvard Medical School in Boston.

Choi and his colleagues designed an implantable gel that could get around this, by guiding light under the mouse’s skin. In experiments, the team impregnated the gel with different types of genetically modified cells before implanting it.

To control diabetes, the team shone light into the mouse and at the implanted gel using a fibre optic cable attached to its head. The light triggered cells in the gel to produce a compound that stimulated the secretion of insulin and stabilised blood glucose levels. Separately, the team also showed they could monitor for cadmium poisoning using cells that fluoresced when the mouse was under stress from the toxin.

Cut the cord

Though still at the prototype stage, the ultimate idea is to reduce the need for doctors to perform repeated injections and blood tests to monitor or treat patients.

“The promise is there,” agrees Fiorenzo Omenetto, a biotechnologist at Tufts University in Medford, Massachusetts. But he adds it will have to get a little easier to live with than the current implant. “The tough thing here is the presence of a large implant and a fibre sticking out of your head. Not something I’d want if I were diabetic.”

Choi’s team plans to work on making the gel more user-friendly. For example, he says, “we are thinking of adding a micro-LED with a wireless power receiver [to the gel implant].”

“Genetically modified cells have been engineered for a variety of applications ranging from the treatment of cancer to the prevention of gout,” wrote Warren Chan of the University of Toronto, Canada, in a comment piece published alongside the work. “This suggests that the implantable hydrogel could be used for many biological and clinical applications.”

Journal reference: Nature Photonics, DOI: 10.1038/nphoton.2013.278





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'Healthy Obese' Is Possible, But Maybe Not Forever

As many as a third of obese adults are considered metabolically healthy, meaning they have normal cholesterol and blood pressure levels and show no signs of developing diabetes. Still, they’re considered a medical mystery, but new research has shed some light on why some people can be healthy at any size, while others cannot.

It has to do with fat cells, according to a new study in the journal of Diabetologia. Compared to obese people who are healthy, those who are metabolically unhealthy have “impaired mitochondria” and a “reduced ability to generate new fat cells.”

What researchers found was that in a healthy obese person, new cells are generated to help store fat as it accumulates, whereas the cells of an unhealthy obese person “swell to their breaking point,” making their fat cells larger than any other group.

They were swollen and riddled with inflammation. The breakdown and mobilization of their fat stores was suppressed, and a closer look showed that their mitochondria were malfunctioning. Their ability to burn fuel and produce adenosine triphosphate, or ATP, the body’s energy currency, was reduced.

It leads to ectopic fat accumulation, meaning that fat gets into organs like the heart and liver. (A fatty liver is linked to Type 2 diabetes.)

However, for a healthy obese person, the fat doesn’t travel throughout the body, and remains just beneath the skin, where it doesn’t seem to cause any physical harm.

A study that appeared in the journal Diabetes Care in August found that metabolically healthy obesity is more frequently found in younger adults, but it may be a transition state, and that “some, if not many, people in this category will eventually develop the expected metabolic disturbances.”

Dr. Jussi Naukkarinen, the lead researcher in the fat cell study, said that anti-inflammatory drugs have been shown to “protect mitochondrial function and improve diabetic symptoms and glucose metabolism.” He also suggests that high glycemic foods (like sugar and white flour) play a role in spiking blood glucose and insulin levels.

But ultimately, he believes that studying healthy obese people will help those that are unhealthy.

“People haven’t really paid that much attention to metabolically healthy obesity, but I think it can teach us a lot about usual obesity,” he said. “It’s only recently that people studying depression have done happiness studies showing what goes right, and I’m thinking about the metabolically healthy obese phenomenon in the same way.”

Image via xrender/Shutterstock

The ‘Healthy Obese’ and Their Healthy Fat Cells [NYT]

Obesity and type 2 diabetes link identified | Futurity

KING’S COLLEGE LONDON (UK) — Researchers are hopeful that obesity can be “uncoupled” from insulin resistance after finding that the immune system and a key protein link the two disorders.

There are an estimated 371 million people with diabetes in the world and around 90 percent of these cases are type 2 diabetes. By 2030, there will be some 550 million with the condition based on current trends.

Cases of diabetes have more than doubled since 1980, with 70 percent of the trend due to aging populations worldwide and the other 30 percent estimated to be due to increasing prevalence of risk factors including obesity.

New research published in Cell Metabolism identifies a key mechanism in the immune system involved in the development of obesity-linked type 2 diabetes. The findings open up new possibilities for treatment and prevention of this condition, which is becoming increasingly prevalent worldwide.

The association between obesity and diabetes has long been recognized but the molecules responsible for this association are unclear.

Lead author Jane Howard and her colleagues from King’s College London studied mice genetically engineered to lack T-bet, a protein that regulates the differentiation and function of immune cells. They found that the mice had improved insulin sensitivity despite being obese.

“When T-bet was absent this altered the relationship between fat and insulin resistance; the mice had more intra-abdominal fat but were actually more sensitive to the glucose lowering effects of insulin,” says Howard. “As fat accumulation in the abdomen is typically associated with worsening insulin resistance and other features of the metabolic syndrome, the findings seen were both unusual and unexpected.”

  • Yale_freeradiacals_1
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It turned out that the intra-abdominal fat of these mice contained fewer immune cells and was less inflamed than that of normal mice. The researchers then went on to discover that by transferring immune cells lacking T-bet to young, lean mice they were able to improve insulin sensitivity. “It appears that T-bet expression in the adaptive immune system is able to influence metabolic physiology,” adds Professor Graham Lord.

Although human obesity is often associated with insulin resistance and diabetes, this is not always the case.

“Our data suggests that obesity can be uncoupled from insulin resistance, through the absence of T-bet,” says Howard. Several of the main drugs currently used to treat type 2 diabetes work by improving insulin sensitivity.

Further studies are needed to identify other molecules in the pathway of action of T-bet which could pave the way for future drug development in the treatment of type 2 diabetes. The administration of specific immune cells as immunotherapy to improve insulin resistance may also one day become a therapeutic possibility.

“This is just the start,” says Howard. “The idea that the immune system can impact on metabolism is very exciting, but more research needs to be done before we can bring this work from the bench to the bedside for the benefit of patients.”

The UK Medical Research Council funded the study.

Source: King’s College London

Futurity.org – Obesity related deaths hit 1-in-5 Americans

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“Obesity has dramatically worse health consequences than some recent reports have led us to believe,” says first author Ryan Masters, who conducted the research as a Robert Wood Johnson Foundation Health Society Scholar at Columbia University’s Mailman School of Public Health.

“We expect that obesity will be responsible for an increasing share of deaths in the United States and perhaps even lead to declines in US life expectancy.”

While there have been signs that obesity is in decline for some groups of young people, rates continue to be near historic highs. For the bulk of children and adults who are already obese, the condition will likely persist, wreaking damage over the course of their lives. The study is published online in the American Journal of Public Health.

In older Americans, the rising toll of obesity is already evident. Masters and his colleagues documented its increasing effect on mortality in white men who died between the ages of 65 and 70 in the years 1986 to 2006. Grade one obesity (body mass index of 30 to less than 35) accounted for about 3.5 percent of deaths for those born between 1915 and 1919—a grouping known as a birth cohort. For those born 10 years later, it accounted for about 5 percent of deaths. Another 10 years later, it killed off upwards of 7 percent.

Straight from the Source

Read the original study

DOI: 10.2105/AJPH.2013.301379

When the obesity epidemic hit in the 1980s, it hit across all age groups, so older Americans have lived through it for a relatively short period of time. But younger age groups will be exposed to the full brunt for much longer periods.

“A 5-year-old growing up today is living in an environment where obesity is much more the norm than was the case for a 5-year-old a generation or two ago. Drink sizes are bigger, clothes are bigger, and greater numbers of a child’s peers are obese,” explains co-author Bruce Link, professor of epidemiology and sociomedical sciences at Columbia University’s Mailman School of Public Health. “And once someone is obese, it is very difficult to undo. So it stands to reason that we won’t see the worst of the epidemic until the current generation of children grows old.”

New way to look at a growing problem

This study is the first to account for differences in age, birth cohort, sex, and race in analyzing Americans’ risk for death from obesity.

“Past research in this area lumped together all Americans, but obesity prevalence and its effect on mortality differ substantially based on your race or ethnicity, how old you are, and when you were born,” says Masters. “It’s important for policy-makers to understand that different groups experience obesity in different ways.”

The researchers analyzed 19 waves of the National Health Interview Survey linked to individual mortality records in the National Death Index for the years 1986 to 2006, when the most recent data are available. They focused on ages 40 to 85 in order to exclude accidental deaths, homicides, and congenital conditions that are the leading causes of death for younger people.

The study builds on earlier research by Masters that found, contrary to conventional wisdom, that risk for death from obesity increases with age. The new study is also influenced by previous work by co-authors Eric Reither, associate professor at Utah State University, and Claire Yang, associate professor at the University of North Carolina at Chapel Hill, which showed significant cohort differences in US obesity rates.

Effects by sex and race

In the groups studied, black women had the highest risk of dying from obesity or being overweight at 27 percent, followed by White women at 21 percent. Obesity in black women is nearly twice that of white women. White men fared better at 15 percent, and the lowest risk for dying from being obese was 5 percent, for black men.

While white men and black men have similar rates of obesity, the effect of obesity on mortality is lower in black men because it is “crowded out” by other risk factors, from high rates of cigarette smoking to challenging socioeconomic conditions. There were insufficient data to make estimates for Asians, Hispanics, and other groups due to the highly stratified nature of the methodology.

In sum, by using a new, more rigorous approach, the new research shows that obesity is far more consequential than previously recognized, that the impact of the epidemic is only beginning to be felt, and that some population groups are affected much more powerfully than others.

The Robert Wood Johnson Foundation funded the study.

Source: Columbia University

Now, diabetic therapy from abdominal fats

Institute of Kidney Diseases Research Centre (IKDRC) claims to have successfully used stem-cells to bring down dependence of type-I diabetics on insulin.

The institute has claimed to be the first to discover insulin producing cells in abdominal fat and use it in stem-cell therapy to bring down patient’s dependence on insulin. A paper regarding the same was presented by the research team of IKDRC — led by its director Dr HL Trivedi at the 12th International Congress of Cell Transplantation Society at Milan, Italy.

Speaking about the discovery, Dr Trivedi said that the team experimented with fat from the abdomen.

“We found three genes that were identical to the genes that produce insulin in pancreas. What were the genes doing in the abdominal fat was a question. But more important was that we managed to use them in stem-cell therapy to reduce diabetics dependence on insulin,” said Dr Trivedi.

He, however, clarified that so far the use of stem-cell has only helped reduced the dependence of diabetics on insulin and not in eliminating it. “In future we may be able to achieve that too,” said Dr Trivedi.

Associate professor in regenerative medicine and stem-cell therapy Dr Umang Thakkar, who presented the paper on use of stem-cell in type-I diabetes, said 20 patients were taken for the study.

“Ten of them had stem cells from abdominal fat of a donor while the remaining used cells from their own body fat. The latter group showed better response because your body tends to accept its own cells rather than from a donor. 45% reduction in insulin dependence was registered in the group that used its own body fat while it was 35% for the other group. The mean age of the group was 20 years,” said Dr Thakkar.

He said another encouraging factor was that in the group that used stem-cells from its own body fat there were no instances of ketoacidosis — a condition common among diabetics in which there is sudden spurt in blood sugar level accompanied by breathlessness. All the patients in the study group were type-I diabetics.

'Reverse vaccine' for Type 1 diabetes seems to pass human test

The therapy is designed to protect cells in the pancreas that make insulin, a hormone the body needs to convert sugars and starches into energy. In people with Type 1 diabetes, the immune system goes haywire and attacks those crucial insulin-producing cells for reasons that medical researchers don’t understand.

Researchers dubbed the treatment a reverse vaccine because it suppresses the immune system instead of stimulating it. As hoped, the experimental vaccine reduced the number of immune system “killer” cells that went on the attack.

“We’re trying to turn off one specific immune response,” said Dr. Lawrence Steinman, an immunologist at Stanford University and senior author of the study published Wednesday in Science Translational Medicine.

About 1.25 million Americans have Type 1 diabetes. For nearly 100 years, the standard treatment has been insulin replacement therapy, in which insulin is injected in amounts that correspond with blood-sugar levels.

Attempts at new treatments and cures have focused on suppressing large portions of the immune system — sometimes using powerful drugs developed for other conditions, such as the blood cancer lymphoma. Steinman called this the “big hammer” approach.

“We’re trying to do something different,” he said. “We want to eliminate just the immune cells that attack the insulin-producing cells in the pancreas.”

Steinman and his team designed a molecule that contained the gene for making proinsulin, the precursor to insulin. The molecule also included instructions for triggering the killer cells’ response and then shutting it down.

If everything went as planned, the DNA molecule would suppress the killer cells and allow the pancreatic cells to function properly, producing insulin.

After successful trials with diabetic mice, the team prepared to test its vaccine on humans. They selected 80 volunteers ages 18 to 40 who had been diagnosed with Type 1 diabetes within the last five years. After that time, many Type 1 sufferers have already lost all of their insulin-producing cells, Steinman said. (Although many people with Type 1 diabetes are diagnosed as children, the researchers avoided testing their reverse vaccine on kids because of safety concerns.)

Two-thirds of the study volunteers received the reverse vaccine in one of four doses ranging from 0.3 to 6.0 milligrams. The rest of the volunteers got a placebo. Injections were made once a week for 12 weeks.

Throughout the study, both the experimental and placebo groups also received insulin replacement therapy. All subjects were monitored for up to two years after the initial treatment to watch for any side effects.

To see whether the vaccine was working, the team measured two key components of the volunteers’ blood: killer cells and C-peptide, a protein involved with making insulin.

Compared with patients who got the placebo, those who received the vaccine in 1.0 and 3.0 mg doses saw beneficial improvements in their levels of C-peptide during and after treatment. But three months after the treatment stopped, C-peptide levels declined, indicating the vaccine had worn off, the team wrote.

Patients in the vaccine group, no matter the dosage, saw the number of killer cells fall and the amount of proinsulin rise over 15 weeks without affecting the rest of their immune system cells. The changes were much more modest in patients who got the placebo.

No significant side effects or safety concerns arose during the study, the team reported.

Dr. Hertzel Gerstein, an endocrinologist at McMaster University in Ontario who treats Type 1 diabetes patients, called the research encouraging, and said he was looking forward to further studies with many more patients.

“It’s a small study with preliminary findings,” he said. “It could or could not translate into anything clinically relevant. But certainly this holds some promise.”

Dr. Peter Butler, director of the Larry L. Hillblom Islet Research Center at UCLA, said a reverse vaccine was a promising approach, but he was concerned that the benefits lasted only a few weeks. It might be impractical to keep the killer cells at bay with such a narrowly targeted vaccine, he said.

Steinman said his team was planning further tests with longer treatment periods.

“This is only a first step,” he said. “But there is potential for protecting people from the ravages of this disease in the long run.”

The study was funded by Bayhill Therapeutics, a start-up founded by Steinman and three of the study’s co-authors. The company, now known as Tolerion Inc., aims to bring the vaccine to market.

brad.balukjian@latimes.com

New technique clears hurdle to diabetes transplants

Scientists at Washington University School of Medicine in St Louis have developed a new technique to trigger reproduction in the laboratory of clusters of human cells that make insulin, potentially removing a significant obstacle to transplanting the cells as treatment for patients with type 1 diabetes.

Efforts to make this treatment possible have been limited by a dearth of insulin-producing beta cells that can be removed from donors after death, and by the stubborn refusal of human beta cells to proliferate in the laboratory after harvesting.

The new technique by researchers uses a cell conditioning solution originally developed to trigger reproduction of cells from the lining of the intestine.

“Until now, there didn’t seem to be a way to reliably make the limited supply of human beta cells proliferate in the laboratory and remain functional”, said Michael McDaniel, Professor of Pathology and Immunology.

“We have not only found a technique to make the cells willing to multiply, we’ve done it in a way that preserves their ability to make insulin”, Dr. McDaniel said.

The current method for harvesting human islets, which are comprised primarily of the insulin-producing beta cells, makes it necessary to find two or three donors to extract enough cells and produce an adequate supply of insulin to treat a single patient with diabetes.

Lead author Haytham Aly, a postdoctoral research scholar, reported on his work with beta cells and was approached by Thaddeus Stappenbeck, Associate Professor of Pathology and Immunology, who studies autoimmune problems in the gut.

Dr. Stappenbeck had developed a medium that causes cells from the intestine’s lining to proliferate in test tubes.

“He said, why don’t you try it, and he gave us some samples. We put the solution in our freezer for a month or so, and when we finally gave it a try, we were amazed at the results: human beta cells in Dr. Stappenbeck’s solution reproduced at a rate that was 20 times higher than beta cells in a solution that contained the sugar glucose”, Dr. Aly said.

The advantage of Dr. Stappenbeck’s solution may be that it is designed to activate multiple growth signalling pathways in cells, according to the researchers. Earlier attempts to make beta cells proliferate focused on one or two growth pathways. The solution also activates genes that help prevent beta cells from dying.

Potential diabetes cure

RESEARCHERS at the Harvard Stem Cell Institute (HSCI) have discovered a hormone that holds promise for a dramatically more effective treatment of type 2 diabetes. The researchers believe that the hormone might also have a role in treating type 1, or juvenile, diabetes. The work was published on April 24 by the on-line version of the journal Cell.

The hormone, called betatrophin, causes mice to produce insulin-secreting pancreatic beta cells at up to 30 times the normal rate. The new beta cells only produce insulin when called for by the body, offering the potential for the natural regulation of insulin and a great reduction in the complications associated with diabetes. HSCI co-director Doug Melton and postdoctoral fellow Peng Yi, who made the discovery, caution that much work remains to be done before it can be used as a treatment in humans. But their work has already drawn the attention of drug manufacturers.

“If this could be used in people,” said Melton, Harvard’s Xander University Professor and co-chair of the University’s Department of Stem Cell and Regenerative Biology, “it could eventually mean that instead of taking insulin injections three times a day, you might take an injection of this hormone once a week or once a month, or in the best case maybe even once a year.” “Our idea here is relatively simple,” he said. “We would provide this hormone, type 2 diabetics will make more of their own insulin-producing cells, and this will slow down, if not stop, the progression of their diabetes. I’ve never seen any treatment that causes such an enormous leap in beta cell replication.”

According to Melton, betatrophin could be in human clinical trials within three to five years. Most of Melton’s work has involved using stem cells but stem cells played no direct role in the discovery of betatrophin. “We were just wondering what happens when an animal doesn’t have enough insulin. We were lucky to find this new gene that had largely gone unnoticed before.

“Another hint came from studying something that people know about but don’t think much about, which is: What happens during pregnancy?” he said, “When a woman gets pregnant, her carbohydrate load, her call for insulin, can increase an enormous amount because of the weight and nutrition needs of the foetus… and it turns out that this hormone goes up during pregnancy. We looked in pregnant mice and found that this hormone is turned on to make more beta cells.”