The bionic pancreas is another project from Boston University and Massachusetts General Hospital in a joint effort to create a bionic pancreas, a type of artificial pancreas which not only includes insulin but also glucagon to raise blood sugar. The system is intended to use an algorithm that checks every 5 minutes to calculate the amount of insulin or glucagon needed. The project has recently formed into a public benefit corporation called Beta Bionics. This newer structure allows it to serve not just shareholders, but also the public good. Beta Bionics also became the first American company to raise over a $1 million from small investors under new public investing rules!
In type 2 diabetes, even though insulin resistance is what leads to the condition, injections of insulin are not the first resort. Instead, other drugs are used to help boost insulin production and the body’s regulation of it. Insulin resistance occurs when the body’s cells don’t respond properly to insulin, which is a hormone made in the pancreas that’s responsible for ferrying glucose to cells for energy.

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In a study that looked at the anti-hyperglycemic and lipid-lowering properties of Emblica officinalis Gaertn. (Amla) fruit in normal and diabetic human volunteers, the results showed a significant decrease in fasting and 2-h post-prandial blood glucose levels on the 21st day in both normal and diabetic subjects receiving 1, 2 or 3 grams of Amla powder per day as compared with their baseline values.
By day eight, I was being called the "disappearing man", and began to feel a bit detached from my colleagues. While my energy levels were fine and glucose levels were 4.3mmol/L, constipation had set in, as a result of not drinking enough water. Thankfully, laxatives cured this. Taylor emailed to say my progress was so good, I  could come off the liquid diet and go back to normal foods.
Steve Vincent, 58, from Southampton, England, was diagnosed with type 2 in December 2010. He was told there was no known cure and he had an increased risk of heart attack, stroke, blindness and limb loss. He had a BMI of 29, weighed 93kg and showed an HbA1c of 10.7%. In summer 2011 he read the reversal story and went on a daily 600 calories green vegetable diet and three litres of water, for two months. At the end he was and remains diabetes-free. In December 2012 he told me: "All my blood test levels are within the normal range, and my cholesterol and blood pressure levels are now normal." When he came off the diet he weighed just 72kg, although he has put on weight since then as he admits he has not been eating as healthily as he might, but his BMI remains at a healthy 24, and his HbA1c level is 5.5%.
However, the observation that normalization of glucose in type 2 diabetes occurred within days after bariatric surgery, before substantial weight loss (15), led to the widespread belief that surgery itself brought about specific changes mediated through incretin hormone secretion (16,17). This reasoning overlooked the major change that follows bariatric surgery: an acute, profound decrease in calorie intake. Typically, those undergoing bariatric surgery have a mean body weight of ∼150 kg (15) and would therefore require a daily calorie intake of ∼13.4 MJ/day (3,200 kcal/day) for weight maintenance (18). This intake decreases precipitously at the time of surgery. The sudden reversal of traffic into fat stores brings about a profound change in intracellular concentration of fat metabolites. It is known that under hypocaloric conditions, fat is mobilized first from the liver and other ectopic sites rather than from visceral or subcutaneous fat stores (19). This process has been studied in detail during more moderate calorie restriction in type 2 diabetes over 8 weeks (20). Fasting plasma glucose was shown to be improved because of an 81% decrease in liver fat content and normalization of hepatic insulin sensitivity with no change in the insulin resistance of muscle.
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.
In a study that looked at the anti-hyperglycemic and lipid-lowering properties of Emblica officinalis Gaertn. (Amla) fruit in normal and diabetic human volunteers, the results showed a significant decrease in fasting and 2-h post-prandial blood glucose levels on the 21st day in both normal and diabetic subjects receiving 1, 2 or 3 grams of Amla powder per day as compared with their baseline values.

Q. I have Type 2 diabetes, and I currently take 1,000 milligrams (mg) of metformin twice a day, 5 mg of Onglyza (saxagliptin) once a day, and 5 mg of glipizide once a day. Does it matter when I take the Onglyza and the glipizide? I used to take them both at breakfast, but I thought I might get better blood-glucose-lowering coverage if I took one of them with lunch and one with dinner.
Another non-insulin injection for people with diabetes is exenatide (Byetta). This medication, originally derived from a compound found in the saliva of the Gila monster, triggers insulin release from the pancreas when blood glucose levels rise. Exenatide is meant to be used along with oral diabetes drugs. It is dosed twice daily and should be injected within an hour of the morning and evening meals. Recently, the FDA warned that exenatide may increase the risk of severe even fatal pancreatitis (inflammation of the pancreas) and that the drug should be discontinued and not restarted if signs and symptoms of pancreatitis develop (severe abdominal pain, for example). It is not for use in people with type 1 diabetes.
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Initial clinical trial results, published in a 2012 PLOS One paper, reported that two doses of BCG spaced four weeks apart led to reductions in autoreactive T cells, an increase in Tregs and what turned out to be a transient increase in insulin production. But by the end of that short, 20-week trial, there was no reduction in HbA1c, the established measure of blood sugar levels over time. An extension and expansion of that trial with long term follow-up, the current results are based on data from 282 human study participants – 52 with type 1 diabetes who participated in the BCG clinical trials and 230 who contributed blood samples for mechanistic studies.

If you google “diabetes cure” you are directed to websites like WebMD and the Mayo Clinic where you find information on diet, exercise, medication, and insulin therapy, but nothing about the cure. This lack of information may have to do with the fact that Americans spend $322 billion a year to treat diabetes, $60 billion a year on weight-loss programs, and $124 billion a year on snack foods. This is about 3% of the US economy! Because so many peoples’ livelihoods are supported by diabetes and its main cause, obesity, the viral effect of people getting cured and telling others is greatly diminished.
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