beta-cells

anonymous asked:

Hello! Was wondering about some good solid science to prove that eating rice, potatoes, grains don't make you fat/diabetic?

show me some good solid science that eating rice & potatoes & grains makes a person diabetic.  if that was the case all of Asia, South America & the Middle East would have the longest history of diabetes in the world.  

You have a few roads to diabetes.

Type 1 = you do something so your immune system starts attacking your insulin producing beta cells in your pancreas   We believe it is only a matter of time before it is unequivocally blamed on cow’s milk.  A recent study in Finland shows the horrific similarity between surface proteins on the pancreas and those in cow’s milk. http://www.drmirkin.com/archive/6186.html  If your immune system decides cow’s milk is an invader you could vaccinate yourself against your own cells.  It should be no surprise either.  The pancreas is a secretion glad, just like the breasts & cow’s share a common ancestor with humans so we are genetically very similar 80% overall, and if cow’s milk proteins are 80% identical to human pancreas surface proteins, then that is cannibalism & the perfect rout to auto immune disease. 

Type 2 = your body is too large for your insulin abilities or your blood is too clogged with fat for your insulin to work. 

All roads are saved by a carbohydrate focused low fat vegan diet.  Anyone telling you otherwise is a public health hazard.

The latest mini-organ…

Engineered mini-stomachs produce insulin in mice

Researchers have spent decades trying to replace the insulin-producing pancreatic cells, called beta cells, that are lost in diabetes. Now a team of researchers, reporting Feb. 18, 2016 in Cell Stem Cell, have discovered that tissue from the lower stomach has the greatest potential to be reprogrammed into a beta-cell state. The researchers took samples of this tissue from mice and grew them into “mini-organs” that produced insulin when transplanted back into the animals. The mini-organs’ stem cells also continued to replenish the insulin-producing cell population, giving the tissue a sustainable regenerative boost.

Cell Stem Cell, Ariyachet et al.: “Reprogrammed stomach tissue as a renewable source of functional beta-cells for blood glucose regulation” http://dx.doi.org/10.1016/j.stem.2016.01.003

Caption: A section of the gastric mini-organ engineered to produce insulin-secreting cells, with immunofluorescent staining.  This image shows many induced insulin-producing cells (red) present in the mini-organ. Gastric stem and progenitor cells (green) are detected at the base of the glands. Cell nuclei labeled in blue. Credit: Chaiyaboot Ariyachet

sciencealert.com
Lab-grown human beta cells have blocked diabetes in mice for good
The first lab-grown, insulin-producing pancreatic cells *ever*.
By David Nield

For the first time, researchers have converted induced pluripotent stem cells - cells capable of turning into any other type of cell - into fully functioning pancreatic beta cells, and when transplanted into diabetic mice, they blocked the disease altogether.

While the process has yet to be tested in humans, the results are exciting, because the hallmark of diabetes is a loss of functioning beta cells. If we can figure out how to transplant new, healthy beta cells into diabetes patients, we’re looking at an actual cure, not just a treatment. “This discovery will enable us to produce potentially unlimited supplies of transplantable cells derived from a patient’s own cells,” lead researcher Ronald Evans told ABC News.

Diabetes, simply put, involves the loss of functioning beta cells in the pancreas: either these cells die (type I diabetes) or they don’t do as they’re told (type II diabetes), and in both cases, it leads to a lack of insulin to regulate the glucose levels in the blood. For a long time, scientists have been trying to replace these damaged or dead beta cells with healthy ones, and it finally looks as though they might have cracked it (in mice, at least).

Diabetes Messengers

The immune system is not immune to mistakes. In type 1 diabetes, it wrongly identifies beta cells (large, green) within the pancreas as pathogens. It attacks and destroys these cells, while leaving other cells in the pancreas (small, blue) untouched. Beta cells produce a hormone, called insulin, which controls the levels of sugar in the blood. Insulin stimulates our body’s cells to absorb sugar by opening up shuttles, called transport proteins (red), on the cells’ edge. Diabetic patients can manage their sugar levels with injections of insulin, but may suffer complications. If doctors could diagnose and treat the condition earlier, they could reduce such complications and extend a patient’s life. Scientists at the MRC’s Clinical Sciences Centre have shown that when beta cells die, they release large quantities of a molecule, called microRNA 375, into the blood. A simple blood test could detect this molecule years before symptoms develop.

Find out more about this study, and the Clinical Sciences Centre’s research on pancreatic cells.

Written by Deborah Oakley

Image produced from work by Mathieu Latreille The MRC’s Clinical Sciences Centre Copyright held by original author Research published in Journal of Molecular Medicine, May 2015 You can also follow BPoD on Twitter and Facebook

Diabetes in a Dish
With NIH grant, UC San Diego researchers hope to build bits of miniature pancreas

Although type 1 diabetes can be controlled with insulin injections and lifestyle modifications, major advances in treating the disease have not been made in more than two decades and there remain fundamental gaps in what is understood about its causes and how to halt its progression.

With a 5-year, $4-million grant from the National Institutes of Health, researchers at University of California, San Diego School of Medicine and bioengineers at UC San Diego Jacobs School of Engineering, with colleagues at UC Irvine and Washington University in St. Louis hope to change this.

The team’s goal is to bioengineer a miniature pancreas in a dish, not the whole pancreas but the organ’s irregularly shaped patches – called Islets of Langerhans – that regulate the body’s blood sugar levels.

“The bottleneck to new cures for type 1 diabetes is that we don’t have a way to study human beta cells outside of the human body,” said Maike Sander, MD, professor in  the departments of Pediatrics and Cellular and Molecular Medicine and director of the Pediatric Diabetes Research Center at UC San Diego and Rady Children’s Hospital-San Diego. “If we are successful, we will for the first time be able to study the events that trigger beta cell destruction.”

Beta cells in islets secrete the hormone insulin. In patients with type 1 diabetes, the beta cells are destroyed and the body loses its ability to regulate blood sugar levels. Researchers, however, are unsure of the mechanism by which beta cells are lost. Some researchers believe that the disease may be triggered by beta cell apoptosis (self-destruction); others believe that the body’s immune system initiates attacks on these cells.

To actually bioengineer the pancreas’ endocrine system, researchers plan to induce human stem cells to develop into beta cells and alpha cells, as well as other cells in the islet that produce hormones important for controlling blood sugar levels. These cells will then be co-mingled with cells that make blood vessels and the cellular mass will be placed within a collagen matrix mimicking the pancreas. The matrix was developed by Karen Christman, PhD, associate professor of bioengineering at the Jacobs School of Engineering.

“Our previous work with heart disease has shown that organ-specific matrices help to create more mature heart cells in a dish,” Christman said. “I am really excited to apply the technology to diabetes research.”

If the pancreatic islets can be successfully bioengineered, researchers could conduct mechanistic studies of beta cell maturation, replication, reprogramming, failure and survival. They say new drug therapies could be tested in the 3D culture. It would also be possible to compare beta cells from people with and without the disease to better understand the disease’s genetic component. Such work might eventually lead to treatments for protecting or replacing beta cells in patients.

If there are any diabetic biology nerds out there like me (or if you know any) i found these cute little plushies that are actually the best things in the world

an insulin producing beta cell! (disclaimer: doesn’t actually produce insulin, bummer i know)

and a pancreas plush pillow!

the first site has a variety of different cells, microbes, and other little critters to choose from, and the second site a a huge list of organs to choose from, and has more than just plushes (pins, stickers, magnets, ect.) 

seriously go check them out!!!! i need like all of them now

30 November 2013

Plan Beta

For Type 1 diabetes sufferers, eating a chocolate bar can be deadly. This is because they lack a protein called insulin, which removes sugar from the blood preventing dangerously high concentrations occurring. The irreversible destruction of the pancreas’ beta cells that produce insulin is to blame, and often means enduring a lifetime of injections to keep sugar levels in check. However, switching off one particular gene can transform different cells into these vital insulin factories. With this gene inactivated, new beta cells (here coloured green) have begun to re-emerge, only four days after they were completely eliminated from this mouse pancreas. In the midst of a global diabetes epidemic that has seen the number of sufferers rise seven-fold over the last 20 years, this new avenue of exploration for potential treatment methods is most welcome.

Written by Jan Piotrowski

Image by Monica Courtney and others
University of Nice-Sophia Antipolis, France
Originally published under a creative commons attribution licence
Research published in PLOS Genetics, October 2013

health.ucsd.edu
Stem Cell-Derived Beta Cells Under Skin Replace Insulin

Scientists at University of California, San Diego School of Medicine and Sanford-Burnham Medical Research Institute have shown that by encapsulating immature pancreatic cells derived from human embryonic stem cells (hESC), and implanting them under the skin of diabetic mouse models, sufficient insulin is produced to maintain glucose levels without unwanted potential trade-offs of the technology.

The research, published online in Stem Cell Research, suggests that encapsulated hESC-derived insulin-producing cells may be an effective and safe cell replacement therapy for insulin dependent-diabetes.

“Our study critically evaluates some of the potential pitfalls of using stem cells to treat insulin dependent-diabetes,” said Pamela Itkin-Ansari, PhD, assistant project scientist in the UC San Diego Department of Pediatrics and adjunct assistant professor in Development, Aging and Regenerative program at Sanford-Burnham.

“We have shown that encapsulated hESC-derived insulin-producing cells are able to produce insulin in response to elevated glucose without an increase in the mass or their escape from the capsule,” said Itkin-Ansari. “These results are important because it means that the encapsulated cells are both fully functional and retrievable.”

Previous attempts to replace insulin producing cells, called beta cells, have met with significant challenges. For example, researchers have tried treating diabetics with mature beta cells, but because these cells are fragile and scarce, the method is fraught with problems. Moreover, since the cells come from organ donors, they may be recognized as foreign by the recipient’s immune system – requiring patients to take immunosuppressive drugs to prevent their immune system from attacking the donor’s cells, ultimately leaving patients vulnerable to infections, tumors and other adverse events.

Encapsulation technology was developed to protect donor cells from exposure to the immune system – and has proven extremely successful in preclinical studies.

Itkin-Ansari and her research team previously made an important contribution to the encapsulation approach by showing that pancreatic islet progenitor cells are an optimal cell type for encapsulation. They found that progenitor cells were more robust than mature beta cells to encapsulate, and while encapsulated, they matured into insulin-producing cells that secreted insulin only when needed.

In the study, Itkin-Ansari and her team used bioluminescent imaging to determine if encapsulated cells stay in the capsule after implantation.

“We were thrilled to see that the cells remained fully encapsulated for up to 150 days, the longest period tested,” said Itkin-Ansari. “Equally important is that we show that the progenitor cells develop glucose-responsiveness without a significant change in mass – meaning they don’t outgrow their capsule.”

Next steps for the development of the approach will be to figure out the size of the capsule required to house the number of progenitor beta cells needed to respond to glucose in humans.

“And of course we want to learn how long a capsule will function once implanted,” said Itkin-Ansari. “Given these goals and continued successful results, I expect to see the technology become a treatment option for patients with insulin dependent-diabetes.”

Patching into diabetes could start changing lives

Managing diabetes can be a challenge at the best of times. Monitoring blood sugar levels, taking insulin injections at just the right time. That may be about to change thanks to a tiny patch.

The group of Dr. Zhen Gu at the University of North Carolina have developed a patch that not only senses changes in blood sugar levels, but administers insulin and blood-glucose sensing enzymes to track levels and stop spikes in blood sugar levels.

Source: University of North Carolina

The patch, made from biocompatible materials, has 100 tiny needles and imitates Beta cells, which generate and store insulin. The patch acts as a proxy to these cells and takes over the monitoring of blood sugar and insulin levels.

The patch could be a game-changer for the more than 387 million people worldwide living with diabetes.

Hope for Type 1 Diabetics

Some good news for those with Type 1 Diabetes (insulin-dependent).  This form of Diabetes, which usually gets diagnosed during childhood and is dependent on life-long injections of insulin, occurs when the immune system destroys pancreatic beta cells and the body stops producing its own insulin. 

Insulin production

New technology has enabled researchers to detect far lower levels of insulin and have found that 73% of diabetics tested had working beta cells producing low levels of insulin regardless of how long they’ve had the disease.  Possible reasons include:

  • Some cells being immune to attack
  • New cells regenerating

This opens up the possibility to focus on regeneration of beta cells in future medical research, or even the link between nutrition/environment and auto-immune disease.

Genetic markers

German researchers found 2 genetic markers that predicts whether children will develop Type 1 Diabetes - DR3/DR4-DQ8.  I would like to emphasize that this doesn’t mean you WILL develop Type 1 Diabetes.  It just makes it more likely if all the right triggers are present.  In future this could make it easier for healthcare practitioners to identify those at risk and develop a lifestyle plan to avoid triggers.

Read more:

Most Type 1’s still producing Insulin

Blood Test to predict Type 1 Diabetes