Dr Beverley Shields, at the University of Exeter Medical School, who led the research, said: "This finding is really exciting. It suggests that a person with Type 1 diabetes will keep any working beta-cells they still have seven years after diagnosis. We are not sure why this is; it may well be that there is a small group of "resilient" beta-cells resistant to immune attack and these are left after all the "susceptible" beta-cells are destroyed. Understanding what is special about these "resilient" beta-cells may open new pathways to treatment for Type 1 diabetes."
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During digestion, pancreatic beta cells release not only insulin, but in a much smaller amount, the hormone amylin, which helps mediate sharp rises in blood glucose levels following meals. Pramlintide (Symlin) is a new, synthetic form of amylin that may help improve blood glucose control for some type 1 and type 2 diabetic people who use insulin. Pramlintide has few side effects (nausea is the main one) but it adds another set of injections to a diabetic person's daily pharmaceutical routine, as it cannot be mixed in the same syringe with insulin.
Karen Addington, UK Chief Executive of the type 1 diabetes charity JDRF, said: "These results provide further evidence that the immune system's assault on insulin-producing beta cells is not as complete as we once believed -- and may change over time. This further opens the door to identifying ways to preserve insulin production in people diagnosed with or living with type 1 diabetes."
"What is interesting is that some patients retain beta cell function for over 50 years," he said. "And, it seems if you retain some, that's a lot better." So, for Darkes to still have some functioning beta cells would not be impossible, but it wouldn't eliminate the disease, Von Herrath said. "Depending on how many beta cells he has, maybe his form of type 1 diabetes was not very severe."

Acarbose (Precose) and miglitol (Glyset) are alpha-glucosidase inhibitors. These drugs help the body to lower blood glucose levels by blocking the breakdown of starches, such as bread, potatoes, and pasta in the intestine. They also slow the breakdown of some sugars, such as table sugar. Their action slows the rise in blood glucose levels after a meal. They should be taken with the first bite of a meal. These drugs may have side effects, including gas and diarrhea.
In type 1 diabetes, the body produces none of the insulin that regulates our blood sugar levels. Very high glucose levels can damage the body's organs. Patients with type 2 diabetes, however, do produce insulin - just not enough to keep their glucose levels normal. Because I was fit and not overweight (obesity is a major risk factor in type 2 diabetes; however, a number of non-obese people, particularly members of south Asian communities, are also prone to it), my doctor told me I could control my condition with diet alone.
Evidence linking hepatic insulin sensitivity to intraorgan triglyceride content has been steadily accumulating. In insulin-treated type 2 diabetes, insulin dose correlates with the extent of fatty liver (35), and in turn, this is associated with insulin sensitivity to suppression of hepatic glucose production (36). Decreasing the fat content of liver is associated with improvement in insulin suppression of glucose production and, thereby, with improvement in fasting plasma glucose (20,23).
This 2013 paper http://www.ncbi.nlm.nih.gov/pmc/... on page 5 reported that after the 8 weeks on that 600 kcal diet 10 out of the 11 participants, so not all, of the Counterpoint study, as the study is now known, regained normal glucose metabolism, 3 months after resuming a normal diet 4 out of the 10 still had a normal glucose metabolism, 3 had an impaired glucose tolerance, 3 had better controlled diabetes, no more recent figures published in spite of the first publication had been published in Octobre 2011, which doesn't bode well for the long term outcome I'd say, I'd have expected them would to have reported the longer term results by now were they positive.
In 1991, the National Institutes of Health issued a consensus statement, cautiously recommending surgery as a treatment for people living with morbid obesity, meaning they have a body mass index, or BMI, over 40. For people who have health complications connected to obesity, such as type 2 diabetes, the limit goes down to a BMI of 35. Relying on these guidelines, insurance companies and public payers like Medicaid and Medicare typically only cover surgery for people living with diabetes who fall into that category.
Clearly separate from the characteristic lack of acute insulin secretion in response to increase in glucose supply is the matter of total mass of β-cells. The former determines the immediate metabolic response to eating, whereas the latter places a long-term limitation on total possible insulin response. Histological studies of the pancreas in type 2 diabetes consistently show an ∼50% reduction in number of β-cells compared with normal subjects (66). β-Cell loss appears to increase as duration of diabetes increases (67). The process is likely to be regulated by apoptosis, a mechanism known to be increased by chronic exposure to increased fatty acid metabolites (68). Ceramides, which are synthesized directly from fatty acids, are likely mediators of the lipid effects on apoptosis (10,69). In light of new knowledge about β-cell apoptosis and rates of turnover during adult life, it is conceivable that removal of adverse factors could result in restoration of normal β-cell number, even late in the disease (66,70). Plasticity of lineage and transdifferentiation of human adult β-cells could also be relevant, and the evidence for this has recently been reviewed (71). β-Cell number following reversal of type 2 diabetes remains to be examined, but overall, it is clear that at least a critical mass of β-cells is not permanently damaged but merely metabolically inhibited.
Who is at risk of developing prediabetes? A well-known paper published in the Lancet in 2010 recommends screening for type 2 diabetes (which would also screen for prediabetes) every 3-5 years in all adults over the age of 45, regardless of other risk factors. Overweight and obese adults (a BMI >25 kg/m2) are also at significantly greater risk for developing prediabetes, as well as people with a family history of type 2 diabetes.
You should have no more than three of these “feeding times” per day. The reason limiting the number and duration of your meal times is so important has to do with staying out of the vicious cycle of increasing insulin resistance. To get smart on insulin resistance — the cause of both type 2 diabetes and obesity — read Dr. Jason Fung’s book, The Obesity Code: Unlocking the Secrets of Weight Loss, or watch his free lecture on YouTube.
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