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 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?

Researchers say a new method of replacing unhealthy trans fats by modifying fat in commercial products has been found to raise blood glucose and depress insulin in humans -- both common precursors to diabetes. If that wasn't bad enough -- it still adversely affects the beneficial HDL-cholesterol.

The study demonstrates the process of rearranging molecules in the fat adversely affect human metabolism of fats and glucose. The metabolism of unmodified natural saturated fat is healthier, in comparison. The trans fats are replaced with interesterified fat, which is a modified fat that includes hydrogenation followed by rearrangement of fat molecules by the process called interesterification. The rearranged fats are then enriched with saturated stearic acid. Experts on human lipid metabolism noted this study shows the specific location of individual fatty acids, particularly saturated fatty acids, seems to make a difference on fat and glucose metabolism.

New York City has already outlawed the use of trans fats in restaurants. Several U.S. cities have or are considering banning them as well. However a safe replacement for these fats has not yet been agreed upon. Looks like the Micronutrient Monitors will have to congregate at the kitchen table to chew the fat on this one a little more.