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."

Summer is here (from where I'm sitting -- in 90-plus degree temps -- it's Definitely here!), which means that it's beach season again. And while it's cool to float around the pool in an inner tube, looking like you ate one might not be the look you're going for this year. What's more, it's certainly not a healthy look, for an excess of abdominal fat can greatly raise a person's risk of developing type 2 diabetes. So, if this whole enlarged waist issue happens to be one to which you can relate, I've outlined some easy and healthy ways to help make this summer your healthiest ever.

1 - Cut Back on the Carbs. For people with type 2 diabetes, this is nothing new. The key, as you likely know, is to avoid refined carbs (pasta, white rice, candy, etc.) like the plague, as they will spike your insulin levels, leading to the storage of more fat. Stick to slower-digesting carb sources like vegetables and whole grains.

2 - Reduce Your Caloric Intake. This pretty basic tenet is one that people, for some reason or another, tend to be the worst at adhering to. For best results, try cutting about 20% of your normal caloric intake. This way, you don't run the risk of catabolizing muscle, too, by restricting your diet to too few calories. If you don't know how many calories you're currently consuming, start checking nutritional labels today. Or, you can visit www.fitday.com for a complete listing of how many calories are in some of your favorite foods. Then, once you've established how many calories you're currently eating, take that number and reduce it by 20%.

3 - Trim the Fat. Remember, fat is not always a bad thing. But, it's also important to bear in mind that for each gram of fat you consume, you're taking in 9 calories. So, without going too crazy, you may want to try cutting back your fat consumption by one-third. The best way to do this is to try low-fat versions of foods (providing they haven't upped the carb/sugar content to make up for the flavor void), eat leaner choices of meat and poultry, and skip a yoke now and again with your eggs. Be this all as it may, do not go as far as to neglect your body of the healthy fats found in fish, avocados, nuts, and olive oil.

4 - Go Pro. To make up for the small caloric deficit left by cutting back on fat and carbs, try eating a bit more protein. Because protein is relatively slow-digesting, it requires your body to burn more calories for it to be processed, thereby amping up your metabolic rate. Also, protein helps curb hunger by increasing certain peptide levels, which signal your brain that you are satiated.

5 - Eat More. Seems counterintuitive, doesn't it? The key is to make sure that you are eating small meals throughout the day. Gone are the days when three squares is the norm (that is, unless you're in prison). Most people by now are hip to the concept that eating five to six small meals at regularly scheduled times of the day is the best way to rev up your metabolism and burn more calories. This isn't to say that you have to eat like a bird all day. Breakfast and dinner, in particular, can still be larger in portion size (lunch can be sizeable, as well). But, you don't want to starve yourself in between those meal times. This is where the other small meals come into play. As a result, you won't end up gorging a few Big Macs for dinner because you're level of hunger won't necessitate such indulgence. Instead, you might opt for a small piece of fish or chicken and a side of vegetables.

I'm not a dietitian, nor have I ever played one on TV, so you may want to consult with a professional before making some or all of the above dietary changes. Still, in my personal opinion -- and based on years of experience with health and fitness -- I can say with confidence that these are healthy and effective ways to help deflate that inner tube of yours.

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?

Eli Lilly partnered with OSI Pharmaceuticals by funding an experimental diabetes medication, PSN010. The partnership will cost Eli Lilly $25 million upfront and possibly $385 million, in total.

Eli Lilly said that it will pay OSI Pharmaceuticals for its pipeline drug, PSN010. This drug represents a new class of diabetes medications aimed at controlling blood sugar in patients with type-2 diabetes by stimulating glucokinase. Glucokinase is a protein that spurs the pancreas to produce more insulin and helps the liver to control glucose.

So this is a good thing. It looks like Eli Lilly is writing checks again - but this time it's for a good cause. This is a genuine attempt to restore street cred with those who butter their bread: the diabetes community!

Some White Coats over at NYU and the Scripps Research Institute have discovered a new enzyme, GAPDH -- found to regulate insulin pathways. This discovery, published in the journal Nature Chemical Biology, could be a new possibility in the treatment of diabetes.

GAPDH, which stands for Great Adventures in the Pursuit for Diabetes Health (okay, that's not what it stands for. It really stands for Glyceralehyde-3-Phosphate Dehydrogenase), was before unknown to be play a role in the development of diabetes in humans. And, a quote from the source adds "It has also been discovered that the inhibition of GAPDH attenuates the diabetic disease symptom in model animals." I'm not sure if I know what model animals are (animals that behave well?), but this is promising news for GAPDH's ability to actively regulate the insulin pathway. The reason why this is such a breakthrough is that because diabetes has so many causes, targeting several different proteins (which is what GAPDH does) offers the most promising method for treatment.

To that I say "Keep up the good work, smart people with long, white coats. And a big thank you to your selfless, model animals, too." Sometimes I just don't know how to end these blog posts.