Medicinal herb receives a diabetes-fighting boost

                                                                                                                          

Commonly known as Paneer dodi, the herb Withania coagulans has been used in traditional Indian medicine for many years now – among other things, it is claimed to help control diabetes. A new study shows that it indeed may do so, particularly when it's ingested within special capsules.

Scientists  started by extracting plant steroid compounds from W. coagulans berries. When tested in the lab, those compounds were found to increase insulin secretion by mouse pancreatic cells in a dish.

Unfortunately, however, the berries are very bitter – this makes it quite difficult to consume a sufficiently-sized dose of an extract obtained from them. Additionally, even if someone were able to eat or drink enough of that extract, much of its medicinal content would likely be destroyed by their stomach acid.

With that in mind, the researchers encapsulated their W. coagulans steroids within nanoparticles made of chitosan, which is a natural substance derived from shellfish exoskeletons. Those particles were in turn coated in a food-based starch, making them better able to withstand acidic conditions. This was done so that they could pass through the stomach, not dissolving and releasing the steroids until reaching the small intestine.

After the nanoparticles had been fed to diabetic mice over a period of five days, the animals' blood glucose levels were found to have dropped by about 40 percent – presumably due to the rodents' increased production of insulin. A further five days after the treatment period ended, that number increased to 60 percent, suggesting the particles' gradual-release mechanism was still having an effect.

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Possible link between rotavirus vaccine and decline in type 1 diabetes

A drop in the number of young children diagnosed with type 1 diabetes could be associated with the introduction of routine rotavirus vaccination of Australian infants, according to a new study by  researchers. 

The researchers investigated the number of Australian children diagnosed with type 1 diabetes from 2000 to 2015 and found that type 1 diabetes diagnoses in children aged 0-4 years declined from 2007—the year that rotavirus vaccine was introduced as a routine infant vaccination.

This is the first time the rate of type 1 diabetes in young children in Australia has fallen since the 1980s. While not conclusively linking the rotavirus vaccine with protection against type 1 diabetes, the discovery builds on earlier research suggesting natural rotavirus infection may be a risk factor for type 1 diabetes.

Decline in type 1 diabetes
Since the 1980s, the incidence of type 1 diabetes has steadily increased in Australia and worldwide, but the reasons for this increase are poorly understood. Type 1 diabetes is a serious, lifelong autoimmune condition, in which the body's immune system destroys cells in the pancreas that produce insulin, a hormone that controls the level of glucose in the blood.

By investigating the number of Australian children diagnosed with type 1 diabetes each year since 2000, the research team observed that after 2007 the rate of type 1 diabetes decreased in children aged 0-4 years, said study lead author.

"The significant decrease in type 1 diabetes that we detected in young children after 2007 was not seen in older children aged 5-14. This suggests the young children could have been exposed to a protective factor that didn't impact older children," the Dr. said.

"We observed the decline in the rate of type 1 diabetes in children born after 2007 coincided with the introduction of the oral rotavirus vaccine onto the Australian National Immunisation Program in 2007."

The rotavirus vaccine is routinely given to Australian infants aged 2 and 4 months to protect them against a severe, potentially life-threatening form of diarrhea.

Exploring the connection
Professor , who is the study senior author, said the discovery followed on from earlier research implicating rotavirus infection in the development of type 1 diabetes.

"Twenty years ago our team revealed an association between the appearance of immune markers of type 1 diabetes in children and rotavirus infection. Subsequent studies in laboratory models suggested rotavirus infection of pancreatic cells can trigger an immune attack against the insulin-producing cells—similar to what occurs in type 1 diabetes," he said.

"While not conclusive, our latest study suggests that preventing rotavirus infection in Australian infants by vaccination may also reduce their risk of type 1 diabetes. We will be continuing this research to look more closely at the correlation, by comparing the health records of  young children with or without type 1 diabetes.

"At this stage we don't yet know whether the reduction in type 1 diabetes is a permanent effect or transient, and it may only be relevant to Australian children," the Prof. said.

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A Vaccine For Type 1 Diabetes Begins Human Trials in 2018

A prototype vaccine, decades in the making, that could prevent type 1 diabetes in children is ready to start clinical trials in 2018.

It's not a cure, and it won't eliminate the disease altogether, but the vaccine is expected to provide immunity against a virus that has been found to trigger the body's defences into attacking itself, potentially reducing the number of new diabetes cases each year.

Over two decades of research has already provided solid evidence linking a type of virus called coxsackievirus B1 with an autoimmune reaction that causes the body to destroy cells in its own pancreas.

The type 1 form of diabetes – not to be confused with the more prevalent type 2 variety that tends to affect individuals later in life – is a decreased ability to produce the insulin used by the body's cells to absorb glucose out of the blood.

This loss of insulin is the result of pancreatic tissue called beta cells being destroyed by the body's own immune system, often within the first few years of life.

It's something of a mystery as to why the body identifies beta cells as foreign, though there could be a genetic link producing variations of human leukocyte markers, which act as the cell's 'ID tags'.

No doubt it's complex, and there are numerous ways this process can be triggered. One example established by virologist is an infection by a type of enterovirus.

Enteroviruses are nasty pieces of work; you might be most familiar with polio, but they can also cause hand, foot and mouth disease, meningitis and myocarditis. There has been suspicion of a link between this group of pathogens and diabetes for a number of years, but it took time to nail down the prime suspects.

In 2014, the team used a pair of studies on children with type 1 diabetes to show that at least one of the six viruses in the B group of coxsackieviruses was associated with the condition.

Enteroviruses are surprisingly common in newborns, with the study finding that around a quarter of the 444 known enterovirus infections in 2007 were caused by coxsackievirus B1 (CVB1).

And for some of those children, it could have been the start of a life-long, incurable condition.

"One can estimate from the generated data that less than 5 percent of CVB1-infected children go on to develop type 1 diabetes," the researchers wrote in their 2014 study.

That might not seem like a lot, but it does suggest each year hundreds of infants around the globe develop type 1 diabetes. If the other members of the CVB group also contribute to beta cell autoimmunity – which they might – the numbers could be higher.

If all goes well, this newly developed vaccine could put a stop to that.

"Already now it is known that the vaccine is effective and safe on mice," says the author.

"The developing process has now taken a significant leap forward as the next phase is to study the vaccine in humans."

Pre-clinical trials are of course just the first step. The next phase will involve testing on healthy adult humans, just to map out any complications.

As a bonus, the vaccine could help reduce other enterovirus infections.

"Additionally, the vaccine would protect from infections caused by enteroviruses such as the common cold, myocarditis, meningitis and ear infections," says the author.

It could be another eight years before we see whether the vaccine does what it's supposed to do, so we shouldn't be expecting anything revolutionary too soon.

Earlier this year, researchers identified an immature cell in the pancreas which can potentially be encouraged to take up the job of lost mature beta cells.

There will be no single cure, treatment, or prevention which will gives us a diabetes-free world.

Between 20 and 40 million people worldwide live with type 1 diabetes. A vaccine like this might not end the disease, but if it works it's certainly going to be a big step forward.
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Will these insulin-producing mini stomachs replace insulin injections for diabetes?

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Many diabetics have to be dependent on insulin injections to prevent the complications of diabetes, but scientists now have successfully developed mini-organs that will deliver insulin whenever needed and can make way for patient-specific therapy for diabetics.

In a bid to replenish insulin-producing beta cells, scientists from the University of Harvard discovered that the tissue from the lower stomach in mice has the greatest potential to be turned into beta cells. After taking samples if this tissue from mice, they grew them into mini-organs that produced insulin once transplanted back into mice. The study was published in the journal Cell Stem Cell.
 
Qiao Zhou from Harvard explained that the tissue from the pylorus region of the mice is the easiest to convert to produce beta cells, and the tissue is the best starting material. The cells in the pylorus region were most responsive to high glucose levels and produced insulin to normalise the mouse’s blood glucose. The verify the effectiveness of the tissue, the scientists destroyed the mice’s pancreatic beta cells which forced the body to rely completely on this implanted tissue to produce insulin. (Read: A diet plan diabetics can use for better blood sugar control)
For the study, there was a set of control animals did not contain reprogrammed tissue. These mice died within eight weeks.  The mice with reprogrammed cells could maintain glucose and insulin levels as long as six months.

Once implanted, the stem cells from the converted tissue replenished the insulin-producing cells increasing the sustainability of the tissue. To confirm their finding, the scientists destroyed the genes responsible for the conversion and found that the region’s stem cells replenished the insulin producing cell population. 

After isolating the tissue from the stomach, the researchers converted it to express beta cell reprogramming factors in the lab and then coaxed the cells to grow into a tiny ball of stomach that would not only produce insulin and refresh itself with stem cells. This mini stomach was then transplanted into the mice’s abdominal cavity. Out of the 22 experimental animals, five animals exhibited normal glucose levels after the destruction of their pancreatic cells.

Researchers explained that using this approach; one can biopsy from a person, grow the cells in the lab, convert them to produce insulin and then transplant them back to create a patient-specific therapy.

Insulin-producing cells grown in lab

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 Scientists have successfully converted human skin cells into functional pancreatic cells, a breakthrough that may lead to a personalised cell therapy for diabetics, ending the need for insulin jabs. The new cells produced insulin in response to changes in glucose levels, and when transplaned into mice, protected the animals from developing diabetes researchers said. The study will allow scientists to scale up pancreatic cell production and manufacture trillions of the target cells in a controlled manner.

"Our results demonstrate for the first time that human adult skin cells can be used to efficiently and rapidly generate functional pancreatic cells that behave similar to human beta cells," said Matthias Hebrok director of the Diabetes Centre at University of California "This finding opens up the opportunity for the analysis of patient-specific pancreatic beta cell properties and the optimisation of cell therapy approaches," said Hebrok.

In the study , the scientists first used pharmaceutical and genetic molecules to reprogrammed skin cells into endoderm progenitor cells -early developmental cells that have already been designated to mature into one of a number of different types of organs.

With this method, the cells do not have to be taken all the way back to a pluripotent stem cell state, meaning the scientists can turn them into pancreatic cells faster. After another four molecules were added, the endoderm cells divided rapidly , allowing more than a trillion-fold expansion. The scientists then progressed these endoderm cells two more steps, first into pancreatic precursor cells, and then into fully-functional pancreatic beta cells.

"The final step was the most unique and the most difficult, as molecules had not previously been identified that could take reprogrammed cells the final step to functional pancreatic cells in a dish," said first author Saiyong Zhu, a postdoctoral researcher at the Gladstone Institute of Cardiovascular Disease.

"This cellular reprogramming and expansion paradigm is more sustainable and scalable than previous methods," said Sheng Ding, a scientist.

Nanotherapy brings diabetes vaccine a step closer

Researchers have for the first time used nanoparticles that imitate naturally dying cells to prevent diabetes in mice, an advance that may pave the way for a human vaccine to protect against the disease.
 
Previously, researchers at The Germans Trias i Pujol Research Institute in Spain modified an individual's immune cells, known as dendritic cells, to avoid the destruction of the insulin-producing pancreatic cells (beta cells) in the body and prevent type 1 diabetes.

This requires the extraction of the subjects' dendritic cells for their subsequent manipulation and re-injection. The process is complex and costly.

In a new study with mice, the researchers said they have achieved the same effect with a much simpler process.

The researchers, in collaboration with the Catalan Institute for Nanoscience and Nanotechnology located on the Universitat Autonoma de Barcelona (UAB) Campus, created nanoparticles called liposomes in the laboratory which imitate cells in the process of natural death.

Liposomes are droplets with an external fat membrane, similar to cell membranes.

They can be made using a very specialised process, but one that is easy and safe and also easy to scale up.

In mice, liposomes arrested the destruction of the beta cells after being introduced into the body to prevent the development of diabetes.

This technique could be a much better candidate for a human vaccine, researchers said.

"After showing that liposomes prevent the onset of type 1 diabetes in mice, the next steps are to test it in human cells in vitro, to start clinical trials on human candidates for preventive vaccination and to cure the disease by combining the vaccine with regenerative therapies," researchers said.

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