Bev did a great job covering the study of obese mice having protection from elevated blood sugar due to a plethora of adiponectin. Adiponectin was shown to enhance insulin signaling which transported the excess glucose to less harmful areas of the body, rather than the cells which would endure diabetes complications. The results of this study created a condition called ratones mórbidamente obesos - which sounds better in Spanish because in English this means morbidly obese mice.

You know what they say about hindsight, right? A study from a year ago revealed some good news and some bad news. Good news first - turns out Type 2 diabetes drugs using troglitazone increased adiponectin. Rezulin was one of these drugs, but it was removed from the US market March 21, 2000. Now the bad news, the Type 2 diabetes drugs made with metformin were shown to reduce adiponectin. A few of the drugs that use metformin are Fortamet, Glucophage, Glucophage XR, and Riomet.

So why must diabetics be led with imperfect vision? Because the bottom line is researchers and doctors believe they are saving lives every day. Yes, they do. But there is a lot to behold when you tinker with His design. Remember the movie Malice? These lines don't make it into movies for nothing. Producers know human nature and they stretch it to the extreme. Whether or not you want to admit it - you know a few people with a complex like Alec Baldwins. Alec Baldwin says, "You ask me if I have a God complex. Let me tell you something: I am God". Click for the entire 1:30 scene, courtesy of YouTube.

Far from being inert and unchanging, a mere scaffolding to which the body's muscles and organs attach themselves, bones change constantly. Old bone cells die. New ones are born. But that's not all. According to an exciting new discovery, bones play a role in regulating blood sugar levels and fat deposits.

How is this possible? Bones act like a kind of endocrine organ, releasing osteocalcin, a hormone that influences bone formation. This hormone also increases both insulin production and the body's insulin sensitivity. It also reduces fat stores. Basically, osteocalcin levels in the bones are linked to blood sugar and body fat levels, and there is some sort of interaction back and forth.

It's a surprising finding for the uninitiated. However, some scientists are saying it makes sense when you think about it. Says Ronald Kahn, director of Harvard's Joslin Diabetes Center, "Obviously there does need to be some coordination between skeletal growth and body mass. If you carry around extra weight, your bones need to hold up under the extra pressure, so it's not surprising that your bones have a sense of body fat."

Dr. Faustman's lab is currently collecting blood samples from individuals with established Type 1 diabetes. These samples are being used to quantify the number of autoreactive T-cells and develop the adequate dosage for Phase 1 of human trials to cure Type 1 diabetes.

The research has been presented and the NIH confirmed it. By reeducating the confused T-cells and instructing them not to attack healthy islets, an apparent cure of established type 1 diabetes in non-obese diabetic mice is possible. Now, Dr. Faustman is collecting human samples to bestow the same cure for diabetes in humans.

If you wish to be a part of this revolutionary event for curing Type 1 diabetes, please contact the Clinical Coordinator or call Dr. Faustman's lab at (617) 726-4084. Each participant is asked to bring a control person along with them - an unrelated person without Type 1 diabetes or another autoimmune disease. Diabetic or not - you can be a part of history in curing Type 1 diabetes!

Did you hear about renowned Harvard scientist Barbara Kahn's latest published research? I blogged about it recently. Kahn and colleagues state, in a report published in Cell Metabolism (July 2007), that it's possible to use a simple blood test to detect the presence of a specific protein called RBP4. Kahn et al say the presence of RBP4 can be used to measure accumulations of deep belly fat. Underpinning this research is a belief that such accumulations of belly fat increase risk for metabolic syndrome, leading to various maladies including heart disease and diabetes.

However, not everyone accepts this point of view. A Yale research team says that deep belly fat may not be so evil after all. The researchers, who are based at Yale University School of Medicine in Chevy Chase, Maryland, assert that metabolic syndrome is caused not by belly fat but by insulin resistance in skeletal muscle. This resistance, they state, makes it tough for the body to manufacture glycogen, so - in people who are insulin resistant - energy that cannot be stored as glycogen gets diverted into fatty acid production, which then contributes to metabolic syndrome.

The team compared abdominal fat levels in young and healthy individuals, some of whom were insulin sensitive and some of whom were insulin resistant. The result? "There is absolutely no difference in the volume of abdominal fat," states Yale's Gerald I. Shulman, who was lead author of the study. Abdominal fat, says Dr. Shulman, "may come later in the course of the disease [metabolic syndrome], but it's not a primary, underlying factor."

Researchers found that the type of body fat an individual has -- - white and brown-- may explain why one person gains weight easier than another.

White fat is the more familiar form of fat that accumulates in the abdomen, thighs, and buttocks. Brown fat burns energy and generates heat. White fat is deposited around internal organs and as visceral fat - the most harmful form of abdominal fat. Brown fat contains small lipid droplets tucked behind tiny energy factories called mitochondria. These cells are most prevalent in cute, little chubby babies, but tend to mostly disappear by adulthood. A 2005 Joslin study discovered genes that control the creation of the precursor cells that give rise to brown fat cells. This latest study shows that brown fat may not disappear in all adult animals and that little collections of brown fat may account for why some mice are protected from obesity and diabetes and others are not.

This study compared the difference in fat metabolism between the B6 mouse and the 129 mouse. The B6 mouse is one of the most commonly used strains in metabolic research and an established model for diet-induced obesity. When placed on a high-fat diet, the B6 mouse develops severe obesity, high blood glucose and insulin resistance with extremely high insulin levels. By contrast, the 129 mouse gains 30% to 50% less weight than the B6 mouse and is resistant to dietary induced obesity and glucose intolerance.

The only difference between the B6 and 129 mice is the type of body fat. The B6 mice had a majority of white fat cells, whereas the 129 mice had over 100 times the number of brown fat cells than the B6 mice. The mice with more white fat cells had a tendency to gain weight and develop diabetes on a high-fat diet. The study showed that the 129 mice had higher basal energy expenditure than the B6 mouse, resulting in a mitigated response to dietary effects. So I guess this begs the question -- how does one turn white fat into brown fat?

The Spring Point Project is a nonprofit organization created to increase the availability of islet tissue for diabetes care by cultivating medical-grade pigs for islet xenotransplantation.

Dr. Bernhard Hering is the scientific director of the Diabetes Institute for Immunology & Transplantation at the University of Minnesota. He believes the shortage of human donor organs greatly limits the applicability of islet transplants. Of course he does. In 2004, President Bush directed the Diabetes Research Work Group, created by Congress, to develop a comprehensive plan for diabetes research. One of the outgrowths has been the establishment of the NIH (National Institute of Health) Clinical Islet Transplant Consortium. Spring Point Project's consultant Dr. Bernhard Hering, M.D., is one of only five researchers worldwide appointed to serve on it. Hold the cornmeal, Wilbur. Who else has a seat in the NIH panel?These medical-grade pig islets require immunosuppression drugs to sustain the life of the islets without another autoimmune attack taking place. A statement from the faq page on The Spring Point Project site states, "Pig islet graft survival was made possible with a novel immunosuppressive protocol." Okay. Minor detail but very important when you weigh your options.

The Spring Point Project says human trials are slated to begin in 2008. Funny-- that is the same time Massachusetts General Hospital's human trials for Dr. Denise Faustman's proposed cure for type 1 diabetes is set to begin. Dr. Faustman's cure does not require any immunosuppression drugs. In my book - any cure that requires a continuum of drugs is not a cure, at all.

A Harvard Medical School scientist's experiments with fish discarded along the coast near Boston have led to a new class of diabetes drugs. The latest, from Novartis, may get U.S. approval this week.

In the late 1970s, Habener, a doctor specializing in diabetes care, began buying discarded fish to learn about the ways animals controlled blood sugar. By 1987 Habener discovered a protein in the pancreas of anglerfish that tells the pancreas to produce insulin. He called it glucagon-like peptide-1, or GLP-1. In 1995, researchers uncovered another use for Habener's discovery to treat diabetes. The scientists found an enzyme that digests GLP. By blocking the enzyme, they could increase the body's reserves of GLP, thereby raising insulin levels. Twenty years later, we will soon have the pleasure of meeting Novartis' concept for this chronology of discoveries in the form of liraglutide.

In clinical trials, patients taking liraglutide attained normal blood sugars without the common side effect of weight gain. In fact, liraglutide was more likely to make the patients slightly leaner. Depending on dosage and length of treatment, it may help patients to lose weight. The drug does not cause a change in appetite. Furthermore, none of the liraglutide patients experienced episodes of low blood sugar levels throughout the trials.

I'm no fisherman, but if all the seagulls of Big Pharma are swarming overhead - there's bound to be a school of fish below. However, this school is quite competitive. At last count, the five largest diabetic drug makers are using Habener's findings to create new medicines.

Many of us fear what we do not know, which could be why the diagnosis of diabetes is so harrowing. Fear no more. Amy Tenderich has teamed up with Dr. Richard Jackson, MD of the Joslin Diabetes Center to shed some light on the heaps of material we must digest to control our diabetes. Amy and Dr. Jackson have simply explained it all in Know Your Numbers, Outlive Your Diabetes: 5 Essential Health Factors You Can Master to Enjoy a Long and Healthy Life (Marlowe Diabetes Library).

The book is a priceless addition to any diabetic library. It begins by explaining the five tests that are the cornerstones for monitoring your overall health with diabetes. These tests are: A1c, blood pressure, lipids, microalbumin, and an annual eye exam. You may think you know it all because you've been there, done that. But do you really know - what it tests, why it's done, and what your numbers should look like? After you learn what those tests mean to you and your health - Amy and Dr. Jackson help you develop a plan of action. They build a road, paved with easy to understand (and explained remarkably well) information about nutrition, medicine, organic treatments, support, and specialized shopping sites for diabetes.

I was impressed beyond my expectations. Knowing the award winning caliber of work Amy produces, and the integrity of Dr. Jackson's work with Joslin Diabetes Center and Harvard Medical - I was looking for a good guidebook on diabetes care. No ma'am. This book is AWESOME! I knew it would be good, Amy. You've outdone yourself, once again. I hope this book motivates everyone who reads it to know their numbers and outlive their diabetes. And when it does - remember us little people, ok? Thanks a million, Amy!

One of the many shining stars of dLife, and a father of a type 1 diabetic, Tom Karlya, shares his reflections on 2006 through a satirical piece where he personifies 2006 and pays respect to the accomplishments of the diabetic community.

Reflections include the Team Type 1 fundraising event. The mission of Team Type 1 is to increase the general public's awareness of diabetes as a disease that can be managed effectively - allowing those with this condition to continue active, healthy lives and permitting them to perform well in athletic events. Another monumental accomplishment this year was a DVD created for the Public Health Foundation. The DVD addresses a topic most people consider unspeakable. You have to watch the video teaser online to get the picture. Last but certainly not least, Tom mentions the controversial but promising cure research of Dr. Denise Faustman.

Tom makes a great point when he says, "Same actions will never yield different results. .. Show me something that was not a biomedical finding funded by private industry." Take a minute to indulge in the victorious ending of 2006. Ring in the New Year with an optimistic smile of what's to come in the days ahead.

Lately a lot of attention has been focused on the Massachusetts General Hospital, one of the largest teaching hospitals of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of nearly $463 million. With deep pockets and medical moxie like that-would you expect the potential cure for type 1 diabetes to come from anywhere else?

In 1999, a MGH research study identified a gene malfunction that plays a pivotal role in the development of type 1 diabetes. The study showed that a gene required to help teach the immune system to recognize so-called "self" proteins is somehow inactivated, causing type 1 diabetes. Sounds like tricky stuff, but it prefaced a strong foundation for the prototype to cure type 1 diabetes. In 2001 MGH researchers found that by retraining the animal's immune system not to attack insulin-producing pancreatic beta cells, it would correct the autoimmune dysfunction causing type 1 diabetes. This research, in concert with a discovery made in 2003, whereby spleen cells appear to develop into insulin-producing cells, provided a revolutionary approach to curing type 1 diabetes. The National Institute of Health has recently confirmed this as a potential cure for type 1 diabetes.

Think of the illustrious contributions Harvard has bestowed on modern society in the form of witty-banter. The Harvard Lampoon, the Simpsons, and of course -- Conan O'Brien. It's only fitting that the cure for type 1 diabetes and other autoimmune diseases would come from the motherland of such mental marvels.