Fat. Never a good thing, right? At least not in the US, where food is super-abundant. Instead of being rightly grateful for all that food, we blame it for our weight woes. Yes, there's a growing sense that food is the enemy. Food leads to weight gain, which leads to obesity, which leads to heart disease, type 2 diabetes, and on and on. (Read Michael Pollan's The Omnivore's Dilemma for more on what he terms "our national eating disorder.")

But apparently there's a silver lining in all that fat. Says journalist Natalie Angier for The New York Times, "to castigate fat for getting too big and to blame it for high blood pressure or a wheezing heart is like a heavy drinker blaming the liver for turning cirrhotic." That is, if the body couldn't convert energy to fat cells in an efficient manner we'd really be up the proverbial creek. In fact, evolutionary biologists have even speculated that humans' ability to store good-sized quantities of fat has aided the survival of the species and made it possible for our big brains to grow so big and, um, brainy. The fat, you see, helps us through hard times. Food for thought, huh?

Two doctors from the UK warn athletes who take growth hormone in an effort to enhance their performance increase their risk of developing diabetes.

The doctors describe what they believe is the first reported case of diabetes associated with taking high doses of growth hormone. A 36-year-old professional body-builder was admitted to the emergency room and treated for chest pain. He told his doctors that in the past year he had lost 88 pounds and noticed that he had to urinate excessively and was constantly thirsty and hungry. The man admitted to using anabolic steroids for 15 years and high doses of growth hormone for the past 3 years. He said he went on insulin a year after starting growth hormone in an effort to counter the effects of high blood sugar, but he stopped taking insulin after a couple of episodes of sudden low blood sugar while at the gym. Tests showed that the man's liver was inflamed, his kidneys were enlarged and that he had very high blood sugar. He was also dehydrated, and was diagnosed with diabetes. He was admitted to the hospital, treated with intravenous fluids and insulin for five days and then sent home. His symptoms resolved completely, and he was no longer diabetic.

The use of growth hormone has become popular with athletes because it is easy to buy online and difficult to detect in screening tests, unlike anabolic steroids. The internet gives easy access to these drugs as well as the 'best' means to take them. The reporting doctors warn physicians should not dismiss such users as being naïve. They have extensive pseudo-medical knowledge. Sadly, the short term risks are instantly addressed. More concerning is the reality of long term complications. The efficacy of growth hormone for enhancing athletic performance is debatable. The conclusive suggestion is anyone taking high doses of growth hormone should get their blood sugar levels checked regularly.

A diet rich in black soya beans (UK) or soybeans (US) could help control weight and even prevent diabetes. The laboratory research on rats found the beans could also lower cholesterol levels.

Four groups of 32 male rats consumed a fatty diet for 28 days. Each group was given different amounts of black soya beans, with one group receiving none and acting as a control. The rats eating 10% of their energy from black soya beans gained about half as much weight as those in the control group. Total blood cholesterol also fell by 25% and LDL levels ("bad" cholesterol) fell by 60%. Soya protein may have an effect on fat metabolism in the liver and adipose tissue, reducing synthesis of new fatty acids and cholesterol. It is this metabolic effect that may explain the traditional Asian use of black soya in the treatment of diabetes. 'The key problem in type 2 diabetes is impairment of insulin action due to excess abdominal fat tissue. Any loss of weight often improves glycaemic control.

The research is preliminary but the popularity of soya foods has been increasing over the past few years. You've got to cook something for dinner tonight. Why not give black soya beans a try? Cooks.com offers a few recipes to put your soya beans to good use. Anybody up for soya bean burgers or baked soya beans? The Diabetic soya bean cookies caught my attention. Watch-out, Betty Crocker!!

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?

According to scientists at Washington University School of Medicine in St. Louis, interrupting nerve signals to the liver can prevent diabetes and hypertension in mice.

Mice were treated to become diabetic with glucocorticoids, a class of steroid hormones characterized by an ability to bind with the cortisol receptor. Once diabetes was established, the researchers surgically removed the vagus nerve. The vagus nerve is the only nerve that starts in the brainstem and extends all the way down to the abdomen. More impressive is the fact that once the nerve was removed from the diabetic mice, insulin resistance and high blood pressure was prevented or reversed. This is an interesting discovery because people with asthma, arthritis, and organ transplants often rely on steroid treatments. It just so happens that many of them go on to develop insulin resistance.

Don't go ripping your vagus nerve out just yet. A fun fact about the vagus nerve is that it's name is taken from the Latin word meaning "wanderer". The vagal nerve pathway can influence seizures, depression and other disorders. Although the research is thoroughly enlightening, it is still very green. Hang on to your vagus nerve while the research continues.

In the January 2007 issue of the the journal Liver Transplantation, the official journal of the American Association for the Study of Liver Disease (AASLD), French scientists published an article suggesting a link between certain risk factors and new-onset diabetes mellitus (NODM) following liver transplantation.

Specifically, a history of impaired fasting glucose, obesity and hepatitis C infection -- when paired with the use of an of immunosppressant -- was shown to be associated with an increased risk of NODM.

The study, conducted by a team of researchers at the Hospital Paul Brousse in Villejuif, France, included 211 patients from 10 transplant centers who had undergone a liver transplant between October of 2003 and June of 2004. The patients' records were reviewed and their fasting blood sugar levels were recorded 3, 6, 12, and 18 months after the surgery. Those patients with NODM had their date of diagnosis noted, in addition to the immunosuppressive treatment and diabetes management they received.

The results demonstrated an incident of NODM of 22.7 percent, with most cases being diagnosed within three months after transplant surgery. Moreover, 12.4 percent of the patients with normal glucose levels before the surgery developed impaired fasting glucose.

Scientists have found that mice lacking a protein known as SH2B1 throughout their body are obese and ultimately develop diabetes. Researchers replaced SH2B1 in the brain of obese mice and it seemed to deter the onset of obesity. The study reveals that targeting SH2B1 in the brain might be a new avenue of treatments for obesity and type 2 diabetes.

SH2B1 is expressed in tissues related to obesity, including the brain, liver, pancreas, and fat tissue. Replacing SH2B1 in the brain of mice lacking SH2B1 prevented the mice from becoming obese. It also prevented the mice from developing obesity after being fed a high-fat diet, indicating that SH2B1 in the brain is required to regulate body weight and fat content.

This study implies that SH2B1 in the brain is a practical target for the development of new drugs to treat obesity and type 2 diabetes.

Anybody ever frustrated with left-field highs? You haven't had a morsel to eat in hours and you're stymied (if not righteously furious) your sugar is off the wall. I've been there. No sir, I don't like it. Where is this high coming from? Thank your liver. Researchers are working on a drug to slow down the body's overproduction of glucose when our bodies lock-down in fasting mode. Halleluiah.

A key enzyzme involved in the metabolic pathway used to produce glucose is phosphoenolpyruvate carboxykinase. This enzyme helps control blood sugar levels during a fasting period. Researchers believe an overproduction of the enzyme might lead to the bamboozling highs we sometimes encounter after a long period of...well...nothing!

A proof of concept study shows that it is possible to alter the activity of phosphoenolpyruvate carboxykinase without directly interfering with homeostatic functions of metabolism. This research could be used to design a drug that can prevent the liver from overproducing glucose in a person with diabetes. I'll thank the Lord when this one hits the shelves.