I was recently diagnosed with prediabetes from an A1C protein test. This test measures 3 month average blood sugar. Having blood sugar problems does explain many things, but I’m nastily surprised. I’m a white male, thin, not overweight, I get moderate to heavy exercise (although I sit most of the day), and I don’t drink sodas or eat sweets (although I have been having two bananas each morning in my shake and plenty of carbs with meals).
Update: For the past few months I’ve greatly improved my diet, exercise, and sleep habits, and yet, my fasting blood sugar has improved little. On 8/6/2014 I got tested for several things to better understand my prediabetes diagnosis. Today on 8/10/2014 I was distressed to find that I am positive for antibodies to the tyrosine phosphatase–like molecule IA-2 (islet cell antigen 512), which is an indicator of Diabetes Type 1. See latent autoimmune diabetes in adulthood (1)
“Although LADA may appear to initially respond to similar treatment (lifestyle and medications if needed) as type 2 diabetes, it will not halt or slow the progression of beta cell destruction, and people with LADA will eventually become insulin dependent.” – link
Oh Hell! This is not happening to me. My immune system is killing my pancreas? What the #$)&!? Could it be a false positive? Reversible? I don’t have GAD autoantibodies at this time.
NEGATIVE: Insulin autoAB (IAA) , Pancreatic islet cell AB (I.C.Ab) (screening), Glutamate decarboxylase 65 AB (GAD65).
… most who test positive for both GAD and ICA progress rapidly toward insulin dependency.
POSITIVE: IA-2 Ab, aka ICA-512, aka islet cell Ag 512. So, the I.C.Ab that I’m negative for above, I’m actually positive for. They did a screening that was negative (below a certain threshold), but I was positive in the actual titer, the amount measured.
Not tested yet: insulinoma-associated autoantibody, zinc transporter ZnT8.
What about the risks with just IA-2?
Individuals with no clinical symptoms, but who have autoantibodies to IA-2 and GAD, have an ∼50% risk of developing type 1 diabetes within 5 years and an even higher risk within 7–10 years. – link
As autoimmunity in type 1 diabetes progresses from initial activation to a chronic state, there is often an increase in the number of islet autoantigens targeted by T-cells and autoantibodies.[42,43] This condition is termed “epitope spreading.” There is convincing evidence that islet autoantibody responses against multiple islet autoantigens are associated with progression to overt disease. - link
How did I get this in the first place?
The best answer I’ve found so far is that I had a genetic defect (MHC haplotype / HLA genes) and when I encountered a real pathogen similar to IA-2, inherent abnormalities in my control mechanisms for the prevention of autoimmunity caused my body to generalize the attack (I have Sjogren’s SS-B antibody, and now IA-2).
An epitope is an antigenic determinant, or a site on the surface of an antigenic molecule, to which a single antibody binds. Epitope spreading (ES) refers to the development of an immune response to epitopes distinct from, and noncross-reactive with, the disease-causing epitope. … ES is a normal feature of a protective immune response … the immune system depends on diversification. – link
People with certain HLA antigens are more likely to develop certain autoimmune diseases, such as type I diabetes, ankylosing spondylitis, celiac disease, SLE (systemic lupus erythematosus), myasthenia gravis, inclusion body myositis, Sjögren syndrome, and narcolepsy.
How long do I have? What does the research say is my best hope at this time?
… The best therapeutic option in LADA patients (while waiting for trials to prevent β-cell exhaustion) is to achieve good metabolic control and prevent chronic complications. … prevention of β-cells from complete destruction should be attempted. …
glitazones have the potential to preserve endogenous insulin secretory reserve, and from many of the models studied, improvement in glucose metabolism is accompanied by a reduction in circulating insulin concentration (59). There is interesting evidence that glitazones increase insulin synthesis and the insulin content of islet cells as well as improve the secretory response of islets (60). In addition to its hypoglycemic effect, troglitazone has been shown to possess in vitro anti-inflammatory properties, as shown by the reduction of cytokines such as tumor necrosis factor-α and γ-interferon (61). The latter mechanism could explain why, in the experimental model of the NOD mouse, troglitazone protects animals from diabetes development (62). Also, another compound of the same family of drugs—rosiglitazone—has been shown to possess similar effects in reducing diabetes incidence of autoimmune diabetes (63). – link
holds promise not only for people with type 1 diabetes but also for those with LADA (latent autoimmune diabetes in adults). … At diagnosis today, she says, only an estimated 10 to 15 percent of beta-cell function remains. “It’s not a lot, but if you have to lose 85 to 90 percent of your beta cells to develop the symptoms of diabetes, it might mean that if you can preserve 20 to 25 percent, it might be enough” to keep from becoming insulin-dependent. Dr. Raz sees DiaPep277 being used as a preventive method in the future, noting that results of the Diabetes Prevention Trial 1 in the United States showed that type 1 diabetes can sometimes be predicted several years in advance. “The best time to treat would be when you still have a large reserve of beta cells—several years before the clinical diagnosis of diabetes,” he explains. For now, however, Dr. Elias is quick to point out that DiaPep277 is not a cure for type 1 diabetes and will not prevent the disease. – link
DiaPep277® is a synthetic peptide of 24 amino acids derived from the sequence of the human heat shock protein 60 (Hsp60). The peptide modulates the immune response that leads to autoimmune diabetes by diminishing or blocking the immunological destruction of beta cells. – link
There is also the work at Viacyte to produce an implant that works as an artificial pancreas:
By acting essentially as a replacement endocrine pancreas, the source of insulin and other regulatory hormones produced in our bodies, ViaCyte’s VC-01 combination product has the potential to be a virtual cure for type 1 diabetes
What is IA-2 (also known as ICA512)?
IA-2 is a major autoantigen in type 1 diabetes. Autoantibodies to IA-2 appear years before the development of clinical disease and are being widely used as predictive markers to identify individuals at risk for developing type 1 diabetes. IA-2 is an enzymatically inactive member of the transmembrane protein tyrosine phosphatase family and is an integral component of secretory granules in neuroendocrine cells. Its role in islet function is unclear. – link
Meanwhile, are my T-Cells constantly killing my pancreas cells? Does something bring on the attack? How much of my pancreas is still working? Does the physical pain in my pancreas mean something? Did my recent high C-Reactive Protein test (a general marker for inflammation) result from my eating gluten that day or not getting enough sleep? How many of the things below for Type 2 pre-diabetes help for LADA?
There is no established management strategy for people diagnosed with LADA. – link
Do Beta Cells regenerate?
Yes. The “insulin-secreting beta cells of the pancreas, which are either killed or become dysfunctional in the two main forms of diabetes, have the capacity to regenerate. … vascular endothelial growth factor A (VEGF-A) is important for development of the islets’ blood supply and for beta-cell proliferation.” – link
“In 2009, researchers in Pittsburgh led by Dr. Andrew Stewart found that, in humans, the proteins cdk-6 and cyclin D1 caused beta cells to regenerate after they had been destroyed by diabetes. Cdk-6 is not easily measurable in rodents (where most of the research is done), so it had not been previously studied. ” – link
Keep the sugar/carbs down:
A study done in Seattle found that beta cells subjected to high glucose levels (about 288 mg/dl in a test tube) lost function rapidly. But when switched to a low-glucose environment (about 15 mg/dl), most of them recovered normal insulin production.
The following is a collection of what most people interested in optimum health should consider.
What is prediabetes?
Insulin hormone normally triggers your body to remove glucose from your blood by shuttling it into your cells to burn as energy. This action keeps your blood sugar reading within a healthy range. Prediabetes is a condition where your fasting blood glucose is over a concentration of 100 mg/dl because either your cells have developed a resistance to insulin (Type 2 diabetes, most commonly) or your pancreas is not producing the insulin required (Type 1 diabetes)… or both. Type 1 diabetes is an autoimmune disorder where T cells mediate the destruction of the insulin-producing beta cells in your pancreas. Type 2 diabetes is a metabolic disorder of insulin resistance in many cells and it can progress to stress-induced (we think) death of the beta cells.
How can I tell if my pancreas is producing enough insulin?
The C-peptide level may be measured to see if any insulin is still being produced by the body. It may also be measured in cases of hypoglycemia (low blood sugar) to see if the person’s body is producing too much insulin.
Results: The standard range is 0.5 – 6.3 ng/mL. My fasting result was 1.5 ng/mL.
“Anything below the normal range of 0.5 to 3.0 ng/ml of blood means that insulin production has slowed down abnormally, and generally indicates type 1 diabetes. Type 2s, on the other hand, will often yield C-peptide results in the normal range, meaning their fluctuating blood sugars must be due to insulin resistance, rather than decreased production.”
Glad to be still making insulin, now to get my fasting blood sugar under control…
Why is it prediabetes dangerous?
Untreated, it will progress to full diabetes which kills one person every six seconds. Even if you never become diabetic, having a high fasting blood sugar is correlated with a shorter life, brain shrinkage, dementia and coronary artery disease.
What caused my prediabetes?
My car accident? One site says, “an automobile accident with injury can negatively affect glucose metabolism and result in blood levels far above 100 mg/dL, even during fasting.” How long does that last? I still have back pain from time to time from being rear ended in a car accident a few years ago.
I eat late, work out late (sporadically), don’t sleep enough, and by the morning when breakfast rolls around, I still have high blood sugar. My body is constantly producing insulin and it is now resistant, probably, unless I have rare adult-onset Type 1 diabetes where my beta-cells are not producing enough insulin.
Either way, resistance or lack of insulin production means I can’t get the glucose out of my blood, so I’m not storing enough for use when needed. Insulin resistance also leads to dangerous fluctuations in blood sugar and that can cause panic feelings, mental fog, forgetfulness, and other serious issues such as damage to the heart and other organs.
Diabetes kills one person every six seconds and afflicts 382 million people worldwide, according to the International Diabetes Federation, which has been canvassing the help of people ranging from celebrity chef Jamie Oliver to Bob Marley’s nephew to raise awareness about the problem.
The number of diabetes cases has climbed 4.4 percent over the past two years and is more than 5 percent of the world’s population, according to new figures the Brussels-based federation released today. The number of people affected by the disease is expected to climb 55 percent to 592 million by 2035 as factors including poor diet, a more sedentary lifestyle, increases in obesity and life expectancy fuel an epidemic, it said. There were only 285 million sufferers worldwide in 2009.
Pre-diabetes and diabetes are linked to a rapid loss of brain function, far more than would be expected from normal ageing, found the two-year Sydney Memory and Ageing Study
What is Insulin Resistance (IR)?
The liver and muscles are your two most important organs that respond to insulin. A healthy liver responds to insulin by not producing glucose. A healthy muscle responds by using glucose. An insulin resistant liver, however, produces unwanted glucose (and more fat), and insulin resistant muscle cells cannot absorb glucose from the bloodstream, leading to high levels in the blood. Blood vessels become resistant, too. Insulin-resistant blood vessels don’t open up as well and don’t prevent the buildup of fatty plaques that can cause arteries to harden. It makes sense, therefore, that IR is correlated with stroke, even in non-diabetics.
What to Do?
Get a Blood Sugar Monitor and Start a Log
I’ve started a log of what I eat, how much I sleep, exercise and my blood sugar every morning. With this data, I’ve been plotting correlations to see what effects my blood sugar the most. Fasting blood glucose level seems to be an overall health indicator. Stable lower blood sugar levels correlate with long life and a healthy brain. Things that lower your insulin resistance (and put you in a healthy fasting glucose range) are generally good for your overall health.
Your Meter May Be Wrong
Some meters and/or test strip batches, even when not expired, seem to produce terribly inaccurate results! In one morning with my Bayer Contour 7151H meter with Bayer strips from Amazon that expire 2015-09 (lot DW3JJ3F03D), I had readings between 82 and 131. Am I under 100? No idea. Others have had problems with the Contour’s accuracy. I called Bayer, highly annoyed, and they are sending me the new latest model which they say is 10% to 15% more accurate. After months of testing, and using my morning result to change my behavior the next day, I discovered that my data may be useless? That is, apparently, a lot of sticking myself for nothing. And, yes, I washed my finger each time and quickly used the first blood that came out (evaporation concentrates blood sugar quickly in that little drop.) Even the test solution shaken each time and dropped with a fresh drop onto wax paper had a 10 point spread with the same batch of strips. As you can see, it appears that my blood sugar fell from 122 mg/dL to 82 mg/dL in three minutes, then then went up to 131 mg/dL four minutes later.
Unanswered Question: Can blood sugar change that fast, every few minutes, as fast as blood pressure?
The first drop of blood you squeeze out of your finger may contain more interstitial fluid the solution surrounding your cells, which can give a lower reading… but as you can see, my first test was higher than the next 5. Throwing out the highest (131 & 122) and lowest (82 & 85) readings my average this morning is 106.
Meters like this measure glucose in “whole blood” which consists of plasma (liquid), and cells, mainly red cells. The hematocrit is the percentage of red cells in your blood, normally about 45% for men and 40% for women according to this. The meter has no way of knowing your current hematocrit, so it uses a set reference to yield “plasma-equivalent” results. This is why the reading is only an estimate.
According to Kaiser, the standard range is 39.0 – 51.0 % and my latest reading was 43.2. From one study, it seems that athletes have lower hemocrits:
“… physiological values of hematocrit in these athletes are comprised between 36 and 48%; (b) “low” hematocrit (<40%) was associated with a higher aerobic capacity; (c) subjects with the higher hematocrits (>44.6%) were frequently overtrained and/or iron-deficient… ” – link
Some foods like red meat and dark green leafy veggies, beans, raisins, prunes, broccoli, citrus fruit and tomatoes can increase your heamatocrit, according to this page. If my hematocrit goes up from 43 to say, 45, and my meter has a set standard, this would, I assume, change make my “plasma-equivalent” glucose reading. With more red blood cells per volume, I would have (false) higher glucose readings.
How much does hematocrit vary from minute to minute, hour to hour?
Verify the reason for the high fasting glucose with a C-peptide test. My 5.5 A1C reading says my average blood glucose over the past 3 months has been 110mg/dL which is high. My 1.4 ng/mL C-peptide test says I’m still making insulin, so I probably have an insulin-resistance problem (type 2) rather than an autoimmune problem (type 1).
Fix Your Liver
The pancreas regulates blood sugar when you eat, but a larger organ, your liver, regulates your blood sugar while you are not eating.
The liver, your largest internal organ at 3-4 lbs, works 24 hrs/day to keep you alive by performing hundreds of critical functions, including the ability of the body to store and synthesize glucose.
Claims about things that help the liver:
Drink green tea which helps prevent fat build up in your liver, get enough B vitamins, eat bitter raw greens like kale and dandilion greens, take fish oil, raw milk from pastured grass-fed cows, eat two heaping tablespoons of ground organic flax meal which binds to hormone receptor sites, preventing excess hormones including synthetic xenoestrogens from plastics and other chemicals, from floating around your bloodstream.
Avoid these to protect your liver :
Pesticides prevalent in non-organic foods, especially non-organic meat, dairy products, butter, and eggs which have more pesticides than even non-organic greens and vegetables, avoid food additives, bottled water from plastic bottles, all sodas and soft drinks except sparkling water in glass bottles.
An hour of afternoon exercise may lower glucose levels until the next morning, affecting the fasting blood sugar test.
Some people respond very well to short high intensity training three times per week, combined with simply moving as much as possible (not sitting) during the day. In four weeks, one BBC reporter had a 20% improvement in insulin resistance in a lab glucose tolerance test. I’ve started push-ups, sprints (high intensity training), and walking 10,000 steps per day as monitored by my FitBit.
Note: Don’t overdo it. In my fanatical attempt to get my blood sugar down, three days in a row of high intensity training caused heart attack symptoms and almost sent me to the ER. It takes a full 24 to 48 hours for muscle (including your heart) to recover fully after being torn down. Do only three days a week of high intensity training, skipping a full day between sessions to recover.
The ideas is that if I clear my glucose by breakfast each day, then my pancreas will have a chance to rest (no need to produce insulin) and I should be able to regulate my blood sugar better.
So I thought. As I am underweight, this may have been a very bad idea. Waiting until my blood sugar level came down one morning until I ate, the result was that I got very shaky, then started to black out with a blood sugar level of 103 after 14 hours of fasting. I had dull chest pains and an panic adrenaline reaction, tingling in my hands and feet, my left foot cramped up for about 20 minutes and the bottom of my right foot felt like I was standing on a heater. That symptom, the hot foot, remained on and off for days.
Don’t Bloat Yourself with Food
Eat a little less (until no longer hungry, instead of until full), again to get back to an ability to store and clear the glucose with insulin.
Get Enough Deep Sleep
I’ve shifted my work hours so I eat an hour earlier, work out earlier, and get more sleep. It sounds mundane, but getting enough sleep seems to be the key for me. University of Chicago Med Center researchers found that “suppressing deep sleep for just three nights causes a 25 percent drop in insulin sensitivity. the researchers say that the decrease in insulin sensitivity after three nights of bad sleep is equivalent to gaining 20 to 30 pounds.”
I normally pop awake after 6.5 to 7 hours of sleep, but going to sleep extra early and having a swig of raw goat’s milk before bed gave me an 8.5 hour sleep with a decent blood sugar reading the next morning. The effect of proper recovery seems cumulative. 7 hours sleep the following night was enough for my first fasting blood sugar under 100 in a week.
One study found that just a single night of inadequate sleep increases insulin resistance.
Get up! Get on up! Walk or Stand Rather than Sit Most of the Day
Standing at your desk rather than sitting, you burn about 50 calories per hour more and your heart beats about 10 beats per minute more.
“… prolonged sitting has not only been linked to problems with blood glucose control, but also a sharp reduction in the activity of an enzyme called lipoprotein lipase, which breaks down blood fats and makes them available as a fuel to the muscles. This reduction in enzyme activity leads to raised levels of triglycerides and fats in the blood, increasing the risk of heart disease.” – link
Add cinnamon to meals which helps insulin work.
“Yes, it does work,” says , a research nutritionist with the University of California, Davis. He authored a recent published in the Journal of Medicinal Food that concluded that cinnamon lowers fasting blood glucose. “According to our results, it’s a modest effect of about 3 to 5 percent,” Davis says. This is about the level of reduction found in the older generation of diabetes drugs, he says. That makes the findings of interest not just to the 25 million Americans who already have diabetes, but also to the 80 million other people — of us — who have elevated fasting blood-glucose levels.
The most common kind, cassia cinnamon can contain high levels of coumarin, so keep it under 1 teaspoon per day to avoid reversible liver toxicity in case you are one of the few people who is sensitive to it.
- Eat a few fresh basil leaves with meals.
- Cut down from 2 grams/day to 1 gram of Vitamin C which competes with glucose for insulin transport into your cells. One person reported false positive high A1C and FBG readings from 4 grams of vitamin C.
- Started taking chromium picolinate (200 mcg/day) which can lower fasting blood sugar and insulin levels. It seems to help insulin work better in people with type 2 diabetes.
Avoid too much Selenium
Selenium is incorporated into proteins to make selenoproteins, which are important antioxidant enzymes. Selenium is required for proper functioning of the thyroid gland, and may protect against cancer, so you need some. A recommended amount according to the NIH is 55 mcg/day. A long term deficiency can lead to a syndrome where the immune system attacks the thyroid. However, too much can kill you.
“Researchers have identified a hormone, selenoprotein P (SeP), produced and secreted by the liver as a previously unknown cause of insulin resistance. … When the researchers gave normal mice SeP, they became insulin resistant and their blood sugar levels rose. A treatment that blocked the activity of SeP in the livers of diabetic and obese mice improved their sensitivity to insulin and lowered blood sugar levels. ” – link
The evolved reduced utilization of selenium-containing proteins in mammals raises important questions in human and animal nutrition. Selenoprotein expression is regulated such that people don’t need to rely so heavily on dietary selenium which is often present in excess amounts in the diet. – link
Brazil nuts, for example, contain very high amounts of selenium (68–91 mcg per nut) and can cause you to go over the safe upper limit if you eat too many. … Too much over time can also cause garlic breath and nervous system problems, among others. At extremely high intakes, selenium can cause severe problems, including difficulty breathing, tremors, kidney failure, heart attacks, and heart failure. – link
Selenium is found naturally in seafood, meat, poultry, eggs and dairy products as well as breads, cereals and other grains. (more) Is excess selenium causing insulin resistance and diabetes? 400 mcg is probably the safe upper daily limit for Selenium intake for adults. If you’ve watched the movie Evolution, you probably know that selenium is a key ingredient in dandruff shampoo.
You should also be aware that selenium compounds, including those used in some medicated dandruff shampoos, are not easily absorbed through the skin. Most of the selenium that enters the body quickly leaves the body, usually within 24 hours. Beyond what the body needs, selenium leaves mainly in the urine, but also in feces and breath. Selenium in the urine increases as the amount of the exposure goes up. Selenium can build up in the human body, however, if exposure levels are very high or if exposure occurs over a long time. – link
Low carb? Evenly spaced carbs? Low fat or high (good) fat? Is intermittent fasting good for thin prediabetics with no weight issues? Intermittent fasting (IF) when you are prediabetic causes swings in glucose, resulting in mental discomfort and potentially increased cortisol and cardiac death.
‘There seems to be rather a lot of slim, fit people, who have had an excellent diet for years, that seem to be either diabetic or pre-diabetic, What is going on?’ http://www.diabetes.co.uk/forum/threads/thin-fit-prediabetic-is-there-hope.43169/
What else can be done? Even for Type 1, there is new hope:
Sanford-Burnham Medical Research Institute (Sanford-Burnham) and UC San Diego School of Medicine scientists have shown that by encapsulating immature pancreatic cells derived from human embryonic stem cells (hESC), and implanting them under the skin in animal models of diabetes, sufficient insulin is produced to maintain glucose levels without unwanted potential trade-offs of the technology. The research suggests that encapsulated hESC-derived insulin-producing cells hold great promise as 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, Ph.D., adjunct assistant professor in the Development, Aging, and Regenerative Program at Sanford-Burnham, with a joint appointment at UC San Diego.
“We have shown that encapsulated hESC-derived pancreatic cells are able to produce insulin in response to elevated glucose without an increase in the mass or their escape from the capsule. These results are important because it means that the encapsulated cells are both fully functional and retrievable,” said Itkin-Ansari.
In the study, published online in Stem Cell Research, Itkin-Ansari and her team used bioluminescent imaging to see if encapsulated cells stay in the capsule after implantation.
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 mature 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, which secreted insulin only when needed.
“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. Given these goals and continued successful results, I expect to see the technology become a treatment option for patients with insulin-dependent diabetes,” said Itkin-Ansari.
Neurotoxin causes of autoimmunity – The immune system interacts extensively with the nervous system. Some research suggests that the events that control the development of type 1 diabetes involve neurological factors, not only the immune system (Tsui et al. 2007). Over 200 chemicals are known to be neurotoxic in humans, and over 1000 are known to be neurotoxic in experiments. Whether these could be involved in type 1 diabetes development is not known. – link
Pancreatic b-cells – Cells that make up 65-80% of the cells in the islets of Langerhans in the pancreas. The primary function of a beta cell is to store and release insulin. Diabetes mellitus can be experimentally induced for research purposes by streptozotocin or alloxan, which are specifically toxic to beta cells.
Streptozotocin (Streptozocin, STZ, Zanosar®) – a naturally occurring chemical that is particularly toxic to the insulin-producing beta cells of the pancreas in mammals. A glucosamine-nitrosourea compound. As with other alkylating agents in the nitrosourea class, it is toxic to cells by causing damage to the DNA, though other mechanisms may also contribute. DNA damage induces activation of poly ADP-ribosylation, which is likely more important for diabetes induction than DNA damage itself. Streptozotocin is similar enough to glucose to be transported into the cell by the glucose transport protein GLUT2, but is not recognized by the other glucose transporters. This explains its relative toxicity to beta cells, since these cells have relatively high levels of GLUT2.
Alloxan – a toxic glucose analogue, which selectively destroys insulin-producing cells in the pancreas (that is beta cells) when administered to rodents and many other animal species. This causes an insulin-dependent diabetes mellitus (called “alloxan diabetes”) in these animals, with characteristics similar to type 1 diabetes in humans. Alloxan is selectively toxic to insulin-producing pancreatic beta cells because it preferentially accumulates in beta cells through uptake via the GLUT2 glucose transporter.
White flour contains diabetes-causing contaminant alloxan: … Studies show that alloxan, the chemical that makes white flour look “clean” and “beautiful,” destroys the beta cells of the pancreas. That’s right; you may be devastating your pancreas and putting yourself at risk for diabetes, all for the sake of eating “beautiful” flour. Is it worth it? – http://www.naturalnews.com/008191.html
Alloxan, in the presence of intracellular thiols, generates reactive oxygen species (ROS) in a cyclic reaction with its reduction product, dialuric acid. The beta cell toxic action of alloxan is initiated by free radicals formed in this redox reaction. [Some studies] found a significant difference in alloxan plasma levels in children with and without diabetes Type 1.
File under: Damnit, why didn’t someone tell me this years ago when I still had a healthy pancreas!
Prodromal Period ( Prodromic Period ) – the time during which a disease process has begun but is not yet clinically manifest.