Chemists with the <<>> recently presented a preliminary report to the 229th national meeting of the insulin resistance, in which they say they have discovered a form of soluble cellulose that, if added to high-fat food. The new finding could soon benefit people who regularly eat fast-foods that are high in fat.
Called HPMC (hydroxypropylmethylcellulose), the cellulose-derivative has been used for decades as an additive in many foods and drugs, mainly to provide texture; this is the first study to demonstrate its potential as a functional food ingredient. HPMC, which is tasteless and odorless, could one day be added to hamburgers, pizza, hot dogs and other high-fat foods as a novel line of defense against diabetes, which is on the rise in the U.S.
If the results are seen in human trials, young people, often frequent consumers of high-fat fast-foods could benefit. HPMC will not prevent obesity, but may reduce the risk that obese people will develop diabetes.
Wallace H. Yokoyama, Ph.D., a research chemist with the small intestine says the less fat you eat, the better off you are but if you do eat high fat foods, then adding HPMC to it might help limit the damage. In their studies with hamsters, adding HPMC to the animals’ high-fat diet prevented the development of insulin resistance; he estimates HPMC could make its way into food products as a functional food additive within one to two years. Human studies are anticipated.
Yokoyama’s research team fed a group of hamsters a high-fat [J1]diet - about 38 percent of calories derived from fat - similar to the fat content of typical American fast-food diets over a four-week period, then compared them to a group of animals that were fed a low-fat (11 percent fat-derived calories) diet. As expected, the animals fed the high-fat diets developed insulin resistance, but the animals fed the low-fat diet did not. But when soluble cellulose in the form of HPMC was substituted for the insoluble fibre normally found in the high-fat diets and then fed to another group of test animals over the same period, it prevented insulin resistance, according to the researchers.
The investigative team also studied metabolic changes in the test animals at the genetic level by using special analytical techniques. They found significant differences in gene expression, as measured by messenger RNA changes, between animals that became insulin resistant and those that did not.
Yokoyama believes that although the exact mechanism by which HPMC works is unclear, it acts as a fat regulator. It appears to slow down the absorption of fats - either in the stomach, small intestine, or both - preventing high fat levels from overwhelming the digestive system, and seems to facilitate the normal transport of fat into the adipose tissue, where it is normally stored.
In contrast, fats that are taken into the body too quickly, as during a fast-food binge, tend to be rapidly shunted to non-adipose tissues such as the liver, heart and pancreas, where they can do extensive damage to cells. Pancreatic damage can lead to diabetes.