FRIDAY, Sept. 18, 2008 (HealthDay News) — Scientists believe they have discovered a new class of hormones in mice, one of which may help stop or reverse obesity-related conditions such as insulin resistance and fatty liver, a new study says.
The Harvard School of Public Health researchers, whose work was published in the Sept. 19 issue of Cell, said their discovery — if applicable to humans — may allow the development of therapeutic or preventive treatments to counter rising obesity and resulting increases in potentially fatal metabolic disorders such as diabetes and atherosclerosis.
Lipokines, unlike other hormones which are steroid- or protein-based, were found in the fat cells of the genetically engineered mice. One of these hormones, “C16:1n7” or palmitoleate, appears to flag the muscles and liver to increase cell sensitivity to insulin and block fat accumulation in the liver. Palmitoleate also appeared to halt inflammation, a primary factor leading to metabolic disease.
The research team had noticed that genetically altered mice were remarkably resistant to the metabolic problems, like diabetes and heart disease, normally linked to a long-term, high-fat diet. In these mice, whose fat cells lacked proteins to chaperone the fat to their normal storage cells, palmitoleate production was much higher. The excess palmitoleate signaled the muscles and the liver to improve insulin function, so the cells could better absorb nutrients.
“We believe that it might be possible to chemically stimulate cells to manufacture their own ‘good’ fat, which could have beneficial effects on metabolism through increased palmitoleate signaling,” lead researcher Gokhan Hotamisligil, a professor at the Harvard School of Public Health, said in a university news release.
If the palmitoleate effect is similar in people, Hotamisligil said it may be a potential treatment for metabolic disorders.
The U.S. National Institute of Diabetes and Digestive and Kidney Diseases has more about adult obesity.
SOURCE: Harvard School of Public Health, news release, Sept. 18, 2008