Vitamin D Could Help Treat Diabetes

Vitamin D can help treat damaged beta cells in pancreas that produce, store and release the hormone insulin, paving the way for a new approach to treat diabetes, scientists say.

When beta cells become dysfunctional, the body can not make insulin to control blood sugar and levels of glucose can rise to dangerous levels.

Researchers accomplished their goal by using an unexpected source: vitamin D. Vitamin D in cells and mouse models proved beneficial in treating damaged beta cells.

It also provided new insights about gene regulation that could be applied to developing treatments for other diseases, including cancer.

We know that diabetes is a disease caused by inflammation. In this study, we identified the vitamin D receptor as an important modulator of both inflammation and beta cell survival.

Using beta cells created from embryonic stem cells, researchers were able to identify a compound, iBRD9, that appeared to enhance the activation of the vitamin D receptor when it was combined with vitamin D to improve the survival of beta cells.

The team accomplished this by conducting a screening test to look for compounds that improved the survival of beta cells in a dish. They then tested the combination in a mouse model of diabetes and showed that it could bring glucose back to normal levels in the animals.

A research associate  said: This study started out by looking at the role of vitamin D in beta cells. Epidemiological studies in patients have suggested a correlation between high vitamin D concentrations in the blood and a lower risk of diabetes, but the underlying mechanism was not well understood.

"It's been hard to protect beta cells with the vitamin alone. We now have some ideas about how we might be able to take advantage of this connection," he said.

The underlying process has to do with transcription – the way that genes are translated into proteins. Combining the new compound with vitamin D allowed certain protective genes to be expressed at much higher levels than they are in diseased cells.

Activating the vitamin D receptor can trigger the anti-inflammatory function of genes to help cells survive under stressed conditions.

"By using a screening system that we developed in the lab, we've been able to identify an important piece of that puzzle that allows for super-activation of the Vitamin D pathway," he said.

The discovery's implications can have far-reaching implications: It identifies a basic mechanism that can be translated into drugging many different targets in the clinic.

In this study, we looked at diabetes, but because this is an important receptor it could potentially be universal for any treatments where you need to boost the effect of vitamin D.

"For example, we are especially interested in looking at it in pancreatic cancer, which is a disease that our lab already studies," he said.

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Could vitamin D help to fight diabetes?

Currently, there are around 30 million people in the United States living with type 2 diabetes, a lifelong condition that cannot yet be cured.

Obesity, one of the major risk factors, is steadily rising, meaning that the number of people with type 2 diabetes is likely to follow suit.

The condition is caused by faulty beta cells in the pancreas. These cells manufacture and release insulin, the hormone essential for controlling glucose levels in the blood.

If beta cells produce too little insulin, or none at all, glucose can accumulate in the blood at levels that are toxic to cells and tissues.

A recent study, looked into a novel way of protecting beta cells, thereby slowing the onset of diabetes. The researchers, concentrated on a well-known compound: Vitamin D.

 Vitamin D and diabetes
Vitamin D is often referred to as the sunshine vitamin because it is created in our skin in response to direct sunlight. Previous studies have found a connection between low vitamin D levels and a higher risk of diabetes, but the mechanisms involved have been challenging to unravel.

This is due, in part, to the wide-reaching physiological functions of vitamin D; for instance, vitamin D is involved in cell growth, bone maintenance, neuromuscular activity, and the immune system. Also, importantly for this study, it has been implicated in inflammation.

 "We know that diabetes is a disease caused by inflammation. In this study, we identified the vitamin D receptor as an important modulator of both inflammation and beta cell survival."

To reach these conclusions, the researchers created beta cells using embryonic stem cells. Then, they tested a battery of compounds to investigate what effects they had on them.

Boosting vitamin D in beta cells

The researchers found that a particular compound — called iBRD9 — boosted the activity of vitamin D receptors when they were bound to vitamin D molecules. This had a protective effect on the beta cells.

They demonstrated that, in a mouse model of diabetes, iBRD9 brought glucose levels back down into the normal range.

"This study started out by looking at the role of vitamin D in beta cells," says first study author. "Epidemiological studies in patients," he reports, "have suggested a correlation between high vitamin D concentrations in the blood and a lower risk of diabetes, but the underlying mechanism was not well understood."

He continues, "It's been hard to protect beta cells with the vitamin alone. We now have some ideas about how we might be able to take advantage of this connection."

They identified a way in which vitamin D might protect beta cells. It seems to involve transcription, or how genes are decoded to produce proteins. The introduction of iBRD9 caused genes with a protective effect to be transcribed at higher rates, protecting the beta cells.

"Activating the vitamin D receptor," notes co-corresponding study author, "can trigger the anti-inflammatory function of genes to help cells survive under stressed conditions."

"By using a screening system that we developed in the lab, we've been able to identify an important piece of that puzzle that allows for super-activation of the vitamin D pathway."

While the findings have clear implications for scientists trying to design new drugs to treat diabetes, there are further-reaching possibilities.

As study co-author explains, "Because this is an important receptor, it could potentially be universal for any treatments where you need to boost the effect of vitamin D. For example, we are especially interested in looking at it in pancreatic cancer."

Of course, before any drug can be used in humans, there are many essential hoops to be jumped through. Although there were no notable side effects in mice, only time will tell if it is safe for humans, too.

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Human Stem Cells Fight Parkinson’s Disease in Monkeys

Scientists have successfully used “reprogrammed” stem cells to restore functioning brain cells in monkeys, raising hopes the technique could be used in future to help patients with Parkinson’s disease.
 

Since Parkinson’s is caused by a lack of dopamine made by brain cells, researchers have long hoped to use stem cells to restore normal production of the neurotransmitter chemical.

Now, for the first time,researchers have shown that human induced pluripotent stem cells (iPS) can be administered safely and effectively to treat primates with symptoms of the debilitating disease.

So-called iPS cells are made by removing mature cells from an individual—often from the skin—and reprogramming them to behave like embryonic stem cells. They can then be coaxed into dopamine-producing brain cells.

The scientists and a world-leader in iPS technology, said their experiment indicated that this approach could potentially be used for the clinical treatment of human patients with Parkinson’s.

In addition to boosting dopamine production, the tests showed improved movement in affected monkeys and no tumors in their brains for at least two years.

The human iPS cells used in the experiment worked whether they came from healthy individuals or Parkinson’s disease patients, the  team reported in the journal.

“This is extremely promising research demonstrating that a safe and highly effective cell therapy for Parkinson’s can be produced in the lab,” said a researcher who was not involved in the research.

The next step will be to test the treatment in a first-in-human clinical trial, which researcher told that he hoped to start by the end of 2018.

Any widespread use of the new therapy is still many years away, but the research has significantly reduced previous uncertainties about iPS-derived cell grafts.

The fact that this research uses iPS cells rather human embryonic stem cells means the treatment would be acceptable in countries such as Ireland and much of Latin America, where embryonic cells are banned.

Excitement about the promise of stem cells has led to hundreds of medical centers springing up around the world claiming to be able to repair damaged tissue in conditions such as multiple sclerosis and Parkinson’s.

While some treatments for cancer and skin grafts have been approved by regulators, many other potential therapies are only in early-stage development, prompting a warning last month by health experts about the dangers of “stem-cell tourism”.

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Scientists create eggs that could allow infertile women to have children

Scientists have created working mammalian eggs from scratch and used them to produce healthy offspring. The new study marks the first time that eggs have been completely made without help from an animal. Although the research was conducted in mice and only on eggs, it shows it may be possible to use the same techniques for humans and for sperm - potentially meaning it will be possible to make new humans entirely in the lab.
Once it is done for one animal, then "developing similar culture systems in other species should be only a matter of technicality", said Dr Dusko Ilic, reader in stem cell science at King's College London. If that happens then we might be able to rewind the process of "mammalian extinction" - not only helping infertile humans but bringing back other extinct animals too. However, it is likely to be many years before the technique is reliable and safe enough for humans. And scientists and policymakers will have to overcome the various ethical challenges that are presented by the possibility of making children without human adults fertilising or carrying them.
In the experiments, the Japanese team - led by Professor Katsuhiko Hayashi, from Kyushu University - used stem cells both obtained from embryos and generated from mature cells taken from the tips of mouse tails. The latter were used to create induced pluripotent stem (iPS) cells which have the properties of embryonic stem cells, including the ability to transform into a multitude of different tissues. Both kinds of stem cell were exposed to specific cocktails of chemicals and biological signals to coax them to develop into eggs.
A key part of the process was mingling the stem cells with "gonadal somatic cells" taken from 12-day-old mouse embryos. These play an important supporting role in egg development. Writing in the online edition of Nature journal, the scientists describe how follicles formed spontaneously and surrounded the early stage eggs. The sac-like structures house maturing eggs in the ovaries. A number of the eggs were eventually fertilised using a standard IVF technique and the resulting embryos produced healthy, fertile offspring.
The success rate was low - just 11 out of 316 two-cell embryos ended up delivering live births. Nevertheless, British scientists working in the same field praised the Japanese achievement. Professor Richard Anderson, from the University of Edinburgh, said: "This is the first report of anyone being able to develop fully mature and fertilisable eggs in a laboratory setting right through from the earliest stages of oocyte (egg) development.. 

 Although we are a long way from making artificial eggs for women at the moment, this study also provides us with a basis for experimental models to explore how eggs develop from other species, including in women. This is extremely challenging at the moment due to the difficulties of getting eggs to study."


He added: "One day, this approach might be useful for women who have lost their fertility at an early age, as well as for improvements in more conventional infertility treatments. But the very careful analyses in this paper show the complexity of the process and how it is a long way from being optimised."

Professor Robin Lovell-Badge, from the Francis Crick Institute in London, said the work "should be considered as a beginning, albeit a very promising one, and not an end". He added: "Clearly, if applied to humans, being able to get functional eggs via reprogramming skin cells to iPS cells, would have importance in overcoming female infertility, e.g. due to cancer treatment as a child, but it also opens up many other uses in research, in regenerative medicine, and potentially in avoiding genetic disease."

But he pointed out that there were "still many practical and ethical challenges to be resolved". Martin Johnson, professor of reproductive sciences at Cambridge University, who described the research as "remarkable", said: "The data are primarily of interest to scientists, although potentially of clinical interest to those patients who lack eggs of their own." 
 

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Stem cells may help treat spinal cord injuries

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 Scientists have successfully used stem cells for the first time to promote regeneration after injury to a specialised band of spinal chord nerve fibres that are important for motor function.
Researchers from Hokkaido University in Japan together with an international team of scientists implanted specialised embryonic stem cells into the severed spinal cords of rats.
The stem cells, called neural progenitor cells, were taken from rat embryos and directed to develop as spinal cord tissue.
The implants, or "grafts," promoted extensive regeneration of the severed nerve fibres, with the rats showing improvement in their ability to move their forelimbs.
The team also used grafts of human neural stem cells in injured rats with similar results, demonstrating the potential of the success of this method across species.

 The corticospinal tract (CST) is a band of nerve fibres that travels from the brain, through the brain stem and into the spinal cord.

This structure is very important for motor function in humans. Injuries to the CST can result in paralysis. Much research has been done, with some progress, on using stem cells to regenerate other bands of nerve fibres in the spinal cord.

But these have involved small gaps between the severed nerves in the presence of bands of bridging tissue. Lesions to nerve fibres located in the CST, however, and those involving large gaps and no bands of bridging tissue have proven largely resistant to regeneration.

The success of the current trial, reported in the journal Nature Medicine, is promising for the future treatment of humans with severe spinal cord injuries, researchers said.

But much work remains to be done before it can be translated into clinical treatments, they said.