Insulin not only moves glucose into the cells, but it also escorts Vitamin C. Blood sugar hogs the seats on the bus in most diabetics, therefore reducing the amount of Vitamin C we can absorb. This is the premise of The GAA Theory: high glucose levels hinder vitamin C entry into cells.

Vitamin C is vitally important for many functions throughout the body - a big one being metabolism. Glucose and Vitamin C are similar in the way they enter the cells. Both molecules require help from insulin. The name for the process that brings glucose and Vitamin C through cell membranes is insulin-mediated uptake. The insulin-mediated uptake of glucose and vitamin C uses white blood cells. White blood cells have more insulin pumps and they may contain 20 times the amount of vitamin C as ordinary cells.

So does increasing your Vitamin C help boost your glycemic control? Diabetes Health cited a study that confirms daily doses of 2,000 mg of absorbic acid improved both fasting blood glucose and HbA1c readings in patients with type 2 diabetes. Next time you swing by the store - see if some Emergen-C can help you achieve better glycemic control. With 1,000 mg of Vitamin C per packet - their homepage says: Feel The Good. Little did they know how good it could be for Type 2 diabetics!

The American Association of Clinical Endocrinologists (AACE) has released its new medical guidelines for diabetes. Needless to say, the 66-page guidelines are intended for your doc, not for you. Unless you are having trouble getting to sleep at night...

But they're important for you to know about. Very. The guidelines are the first reference point for physicians determining the best course of care for diabetes patients. Blood sugar, blood pressure, type 1, type 2, pregnancy, metabolism, prevention etc etc. It's all in there.

So what's new? According to AACE president Dr. Richard Hellman, the focus is, for the first time, on patient safety - specifically, reducing the incidence of medical errors involving diabetes patients. "These guidelines are the first that specifically point to how best to protect the patient with diabetes against mistakes and misjudgments by all those who directly or indirectly impact their diabetes care, including themselves," said Dr. Hellman. "Patient safety is not a given."

The guidelines are being published as a supplement to the latest issue of Endocrine Practice (May/June 2007), the journal of the AACE. They can also be accessed online. Click here to view the pdf.

A study has explained why sleep loss may contribute to the development of obesity and type 2 diabetes. Think appetite.

The study found that sleep loss reduced glycogen release from the liver. Since the patient was still awake, requiring energy (and none was being supplied) - the islets withheld production of insulin to sustain existing blood sugar. The aftermath of this suspended glucose metabolism resulted in increased hunger. Yikes.

This study may hint at reasons behind the dubious freshman fifteen for a lot of college students. Can the body adapt to being up all night studying and snacking without jolting the counter regulatory response of metabolism?

Central obesity is associated with insulin resistance through factors that are not fully understood. Researchers studied the effects of three different diets on body fat distribution, insulin sensitivity and peripheral adiponectin gene expression.

Adiponectin is secreted from fat tissue into the blood. The presence of adiponectin can result in improved insulin sensitivity and glucose tolerance, and can assist in mobilizing sugar out of the blood The hormone plays a role in the suppression of the metabolic derangements that may result in type 2 diabetes, obesity, atherosclerosis and non-alcoholic fatty liver disease.

The study involved 11 volunteers who were the offspring of obese type 2 diabetic patients with noticeable abdominal fat deposits. The volunteers were considered insulin resistant and they maintained average hemoglobin A1c levels of greater than 6.5% without medication. All subjects underwent three dietary periods of 28 days each in a crossover design: a) diet enriched in saturated fat (SAT), b) diet rich in monounsaturated fat (MUFA; Mediterranean diet) and c) diet rich in carbohydrates (CHO). Weight, body composition and resting energy expenditure remained unchanged during the three dietary periods. However, when patients were fed a CHO-enriched diet their fat mass was redistributed towards their abdominal region and their periphery fat accumulation decreased compared with a diet MUFA-rich and high SAT diets. Changes in fat deposition were associated with decreased levels of adiponectin after meals and lower insulin sensitivity.

The results of this study conclude a diet rich in monounsaturated fat prevents central fat redistribution and a decrease in after meal adiponectin levels. These findings support the belief that a carbohydrate-rich diet in insulin-resistant subjects exacerbates the insulin resistance. The moral of the story is: to enhance insulin sensitivity - look for a diet rich in monounsaturated fats and less dense in carbohydrates. Chances are if you've tinkered around with your food pyramid - you already knew the results of this study.

The FDA has approved a new over-the-counter weight loss drug called alli (orlistat) that is designed to absorb 25% of the fat from your meal. However, nutrition and fitness expert Dr. Len Lopez, author of "To Burn or Not to Burn, Fat is the Question" shares his reasons why the new approved weight loss drug may not be beneficial to your health.

New research is showing that medications don't make us healthier. Research is showing that losing weight with medications doesn't decrease the rate of heart attacks, strokes or diabetes. Add that to the fact that your body loses nutrients with these medications and you can easily see how these new weight loss drugs can hamper your health. Dr. Lopez discusses practical steps to losing weight which includes diet and exercise, but also covers how stress and adrenal fatigue can disrupt our hormones, such as cortisol and adrenaline. These hormonal imbalances can throw off our metabolism and take us out of our fat burning mode.

Both of Dr.Lopez's books cover a good deal of information to understand how we can correct our imbalances in piecing together the weight loss puzzle. His knowledge explores the roles of insulin and cortisol in weight gain, cravings, fatigue and more. He also explains how stress can take you out of your fat burning zone and helps you regain your blood sugar balance, as well as implementing the "Five and Two" dieting plan.

Say NO to the weight loss drugs and say YES to the empowering knowledge Dr. Lopez has to share.

An enzyme named eIF2alpha kinase (GCN2) was shown to profoundly regulate fat metabolism in mice.

Scientists provoked the mice into starvation mode by removing a single amino acid named leucine from their diets. By doing this, the body represses fat synthesis and consumes virtually all of its stored fat. After 17 days of a leucine-deficient diet, the mice with GCN2 lost 48% of their liver mass and 97% of the fat from their abdomens. In contrast, the mice without GCN2 kept a steady liver mass and lost only 69% of abdominal body fat.

The mice without GCN2 did not lose as much fat as the mice with GCN2. Furthermore, they developed symptoms that could lead to fatty liver disease. In most events of rapid weight loss, the liver tends to take a beating. However, the fastidious weight loss in the mice with GCN2 occurred because of the repressed synthesis of new fats coupled with the depletion of stored fats. This says a lot for safe handling when it comes to teamwork.

Researchers found a protein that coats the liver is directly correlated with visceral-fat induced diabetes, or type 2 diabetes.

When visceral fat accumulates, the amount of a hormone called adiponectin, decreases. Adiponectin is found in fat cells, and plays a role in glucose regulation and fatty acid metabolism. Researchers found two types of protein on the surface of mouse liver cells. When the proteins and adiponectin interact, blood sugar and neutral fat levels fall, boosting fat-burning functions. However, obese mice with accumulated visceral fat have fewer of these proteins on the surface of their liver cells. When these proteins increased in number, blood sugar levels would decline. The study hypothesizes that if the quantity of adiponectin decreases in obese people, a potential cure for type 2 diabetes may be found by increasing the proteins found on the surface of the liver.

Talk about the power of protein! We've all heard about the leaders in the pack when it comes to dropping pounds - eggs, fish, chicken, soy and whey protein. But this discovery reveals a new way to combat the bulge and reduce your chances of developing type 2 diabetes. Although these new proteins won't find accommodations in your local grocery store - perhaps Big Pharma will have a designer label to sport in the near future. You'd buy it, wouldn't you?

A small molecule has been identified that controls diabetes in mice and may pave the way to the development of easier treatment for adult-onset diabetes.

This key molecule, called Boc5, can stimulate insulin function and reduce body weight by 20%. The molecule stimulates the production of the glucagon-like peptide1 (GLP1), responsible for metabolizing glucose. The study intended to discover ways to sensitize insulin by stimulating production of GLP1. Boc5 is not powerful enough to become a diabetes or weight loss drug. But researchers suggest that similar compounds could join the latest generation of diabetes drugs, called "incretin mimetics." The first FDA-approved incretin mimetic was Byetta. A second such drug, with the generic name liraglutide, is in clinical trials.

The problem with the existing FDA approved incretin mimetic treatments is that they are large molecules that must be administered through injection. Boc5 is a small fry with big potential. Being a smaller molecule gives hope for a new generation in diabetes treatment in the form of a pill many of us would be happy to swallow.

Elixir Pharmaceuticals is a company focused on age-related diseases such as diabetes and obesity. Elixir released new data on research that ultimately could lead to a treatment for type 2 diabetes.

The research explains the role of ghrelin, a hormone secreted by the stomach. Ghrelin controls appetite by increasing levels before meals and decreasing levels after meals. A lack of sleep produces ghrelin, which stimulates appetite and creates less leptin which, amongst its many other effects, suppresses appetite. Research scientists have developed an anti-obesity vaccine, which is directed against the hormone ghrelin. The vaccine uses the immune system antibodies to prevent ghrelin from reaching the central nervous system, thus producing a desired reduction in weight gain.

The research conducted by Elixir, as well as the obesity vaccination, shows compelling evidence that ghrelin plays a pivotal role in metabolic regulation. Scientists have shown pharmacologic inhibition of the ghrelin receptor results in a reduction in fasting glucose levels, reduction in insulin resistance, and weight loss. This could lead to victorious battle for science in the war on obesity.

Those of us who don't have a metabolism like Sea biscuit might fall for the too good to be true ads every time. This time the object of my curiosity is Diamaxol. The product was formerly called Diabeticine, but the FDA didn't like the hint of medicine in the name, so the manufacturers changed it.

The product supposedly reduces blood sugar levels, eliminates (strong word) insulin resistance, and normalizes insulin production. A partial list of Diamaxol ingredients include: Banaba, Guggle (Guggul), Bitter Melon, Licorice extract, Cinnamon herb powder, Gymnema Sylvestre, Yarrow, Cayenne, Juniper Berries, Huckleberry, and Vanadyl Sulfate How exactly does Diamaxol claim to work it's magic? It's not magic - it's simply science. The magic behind the formula is actually the miraculous human body doing its job. Diamaxol is more like the stage crew for David Copperfield, rather than the show itself.

Diamaxol interferes with glucose absorption and prevents the stimulation of glucose from the liver. This effectively reduces blood sugar levels. It also eliminates insulin resistance by repairing cell receptors to better handle insulin. Scientists agree, insulin resistance is one of the leading causes of type 2 diabetes. The normalization of insulin production is restored (in type 2) and replaced (in type 1) by an organic compound. Curiously enough, banaba is at the top of the list of ingredients. Banaba contains corosolic acid, which activates the transport of glucose across cell membranes, resulting in blood sugar reductions. It has been used in the Philippines for years to treat diabetes. Because the FDA has approved Diamaxol as a supplement, at least we know that it can't hurt. Sounds interesting, perhaps worth looking into - but is it worth the $75 to $100 a bottle?

Based on studies conducted at Georgetown University Medical Center, the best-selling wellness author recommends niacin-bound chromium supplementation to improve blood sugar levels, regulate proper insulin function and maintain healthy body weight.

Type 2 diabetics are commonly believed to suffer from a chromium deficiency. Chromium is very important in promoting normal insulin function and is essential for proper protein, fat and carbohydrate metabolism. Elevated levels of insulin and blood sugar significantly accelerate cellular aging. Research now shows that the type of chromium known as NBC (niacin-bound chromium) has a superior anti-aging profile.

Studies conducted at Georgetown University Medical reveal that Chromium polynicotinate (a generic term for ChromeMate) promote: proper insulin function, normal blood sugar levels, healthy blood cholesterol levels, normal blood pressure, cardiovascular health and healthy body weight and lean body mass. Chromium looks like a strong defense for diabetics in the battle against aging and blood sugar control.

Okay, so it's not just an immune blunder anymore. Canadian-led research suggests immune cells aren't the only culprits in developing type 1 diabetes - the nervous system also plays a pivotal role.

With Type 1 diabetes, the destruction of the islet cells in the pancreas leaves the body without insulin to regulate the metabolism of blood glucose, or sugar. In studies of laboratory mice specially bred to make them susceptible to Type 1 diabetes, researchers discovered that a control circuit exists between insulin-producing cells and their associated sensory, or pain-related, nerves. It turns out that this control circuit is necessary to retain the health and normal function of islet cells. Researchers have found that the immune system is under much closer control by the nervous system than previously thought.

In other words, a dysfunctional immune response is not the only thing needed to get diabetes - the nerve cells are also critical. The researchers also found that injecting a substance into mice whose islet cells were inflamed and on the way to being destroyed not only eliminated the inflammation but actually reversed it. "The blood glucose normalizes overnight and it stays low for weeks to months - this is with a single shot," enthused one researcher. "We now have four-month-old mice that are non-diabetic that used to be diabetic" - a period equivalent to six to eight years in humans. Heck, I'll take a 6 to 8 year vacation from 10 finger sticks a day, 3 SYMLIIN injections a day, and a bi-weekly pump change. O Canada!