Yes, the title conjures up images of a futuristic world in which diabetics puff their way back to health. "New! Insulin Cigarettes!" In fact, it's rather more innocuous than that: scientists have engineered a type of insulin-containing tobacco plant that could - in theory, at least - be used as a diabetes treatment.

A study has just been completed of its use. Once freeze-dried and broken down into powder, the insulin-containing tobacco leaves were administered to mice. The scientists who came up with the plant (and who are based at the University of Central Florida), found the powder successfully prevented diabetes symptoms in the mice after eight weeks. It seems pretty safe to assume, they speculate, that humans with type 1 diabetes could get similar results from ingesting plant-based insulin.

The only snag so far is the image problem associated with tobacco. As a result, lead researcher Henry Daniell, is proposing a switch to lettuce, which is cheap, easy to grow and - oh, yeah! - is not associated with cancer. Good move.

The results of this study appear in the Plant Biotechnology Journal (July 2007).

What makes for a long and healthy life? Why, you say, how about a healthy diet and liberal quantities of exercise? True! A healthy lifestyle keeps you in shape and is one factor that promotes longevity. But have you ever wondered exactly how this works on a physiological level? How does the brain understand you skipped the gym all summer and had French fries for lunch yesterday?

The answer, according to the results of a new study published in Science (July 2007), could relate to insulin levels in the brain. Researchers induced lab mice to overeat until they became obese and some exhibited symptoms of diabetes. Yet some of those same mice actually lived eighteen percent longer than their slender mice buddies. The researchers attributed that longevity to a gene that affects insulin. Put simply: the longevity gene (called Irs2) effectively "tricked" the brains of those mice into thinking they were slim and fit, when in fact the opposite was true.

For diabetics, the study raises an additional question: if raising insulin levels decreases the body's sensitivity to it, is it really desirable to treat type 2 diabetics with insulin over the long-term? Lead author of the study, Morris White of Children's Hospital in Boston, says it's highly preferable (when possible) to get type 2 diabetes under control through old-fashioned diet and exercise, rather than through insulin or other meds.

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?

Doesn't it seem like lab animals are being cured of diseases every day? That, of course, is partially a joke. What's not as funny, however, is the fact that animals are being killed at an alarming rate during laboratory testing. Do the ends justify the means? I'll leave you to answer that for yourself. But, whatever your feeling, I think it's safe to assume that everybody feels a little sorry for the sacrificial mice and other lab animals who, for the betterment of humankind, are often times killed during testing procedures. Again, it's your call as to whether or not the ends justify the means.

But, in the January issue of Clinical Biochemistry, it was reported that scientists and physicians with the Physicians Committee for Responsible Medicine (PCRM) have delineated their method for a new, cruelty-free ELISA (enzyme-linked immunosorbant assay)for human insulin. Using monoclonal antibodies produced by cells cultured in an animal-serum-free medium, PCRM's insulin ELISA (sorry for all the acronyms) is the first of its kind.

Traditionally, lab scientists detect human insulin using antibodies that have been implanted into the abdomens of living mice. If you think this is cruel, you're not the only one, for this procedure has been banned in some European countries. And, even when antibodies are produced from cells in test tubes, the live cells are typically grown using bovine serum. This serum is sourced from bovine fetuses by puncturing their hearts with a needle, a procedure that is completed without anesthesia of any kind.

Fortunately, the PCRM's new method for ELISA does not involve either of the above stated methods. Mice and cattle, feel free to breath a big sigh of relief. I suppose us humans can as well, because this new method not only presents ethical advantages, but growing cells without animal serum ensures that fewer variables are present in experiments.

A study suggests that a bile acid may be used for the treatment of obesity, insulin resistance, and type 2 diabetes. This discovery was made when researchers found colestimide, a resin that eliminates bile acids, as a cholesterol-lowering treatment.

The study was based on the fact that abnormal lipids lead to high mortality in type 2 diabetics. The researchers investigated the effects of colestimide on blood glucose levels in mice that develop a disease akin to type 2 diabetes. Colestimide treatment prevented diet-induced obesity and high blood sugar, and corrected diet-induced obesity in mice. It also showed a significant decrease in levels of "bad" LDL cholesterol without affecting "good" HDL cholesterol levels.

How about that? The unlikely path of colestimide could detour us from hitting the dead end consequences of high blood fats and obesity. All these discoveries on mice eventually will prove something remarkable for us humans. Won't they?

An a very interesting breakthrough, scientists at the University of Pittsburgh have successfully prevented the onset of type 1 diabetes in mice that were prone to its development.

Currently, there are over 700,000 Americans who have type 1. So, if these researchers are truly onto something here, hopefully that number will at the very least not get any higher. In efforts to make this the case, the scientists made this discovery by treating non-obese mice with an antibody -- basically, a type of protein that's produced by the immune system whose function is to identify and do battle with infections and the like -- directed against a receptor known as CD137 on the surface of T-cells. By doing so, the mice with the anti-CD137 antibodies were able to suppress the onset of type 1 diabetes, whereas control mice who were not treated developed diabetes within six months.

Buuuuut, "Suppression" is the key word here. Not to sound negative about this wonderful step forward in the quest for a cure, but I'd be remiss if I didn't stress the operative nature of that term in this case. The mice did, unfortunately, still have lymphocytes in their pancreatic islets, which is a strong indication of pancreatic inflammation and autoimmunity. Still, by no means is all lost. In fact, it's just the opposite. Doctors are calling this a solid step in the right direction, to the point where they are hopeful that it could lead to treatment capable of entirely preventing the disease before it is able to take hold.