A team of Swedish researchers has characterized novel systems properties of insulin signaling in human fat cells. Their mathematical modeling, described in an article published June 20th in the open-access journal PLoS Computational Biology, provides further insight into energy level maintenance (via the hormone insulin) within our bodies.

New research by the Gladstone Institutes of Cardiovascular Disease (GICD) and the University of California, San Francisco (UCSF), has revealed the genetic determinants of fat storage in cells, which may lead to a new understanding of and potential treatments for obesity, diabetes, and heart disease.

The radioactive carbon-14 produced by above-ground nuclear testing in the 1950s and ’60s has helped researchers determine that the number of fat cells in a human’s body, whether lean or obese, is established during the teenage years. Changes in fat mass in adulthood can be attributed mainly to changes in fat cell volume, not an increase in the actual number of fat cells.

The machinery responsible for energy production in fat cells is working poorly as a result of obesity. Finnish research done at the University of Helsinki and the National Public Health Institute shows that this may aggravate and work to maintain the obese state in humans.

The body's fat cells help the pancreas do its job of secreting insulin, according to research at Washington University School of Medicine in St. Louis. This previously unrecognized process ultimately could lead to new methods to improve glucose metabolism in type 2 diabetic or insulin-resistant people.

The surface of fat cells contains many small pockets called caveolae (because they look like caves in an electron microscope). Although their role is not clear, Paul F. Pilch and colleagues review current knowledge about caveolae and conclude that one of their major functions is to regulate the movement and production of fats in fat cells.

Researchers report that fasting or eating half as much as usual every other day may shrink your fat cells and boost mechanisms that break down fats.

In obese individuals, fat cells are bloated and inflamed because they receive too many nutrients, including lipids. In these cells, various components cannot work properly anymore and, instead, they activate new proteins to cope with the situation.

Scientists have shown for the first time that a protein involved in the transfer of fat in the blood may also influence how fat cells store fat. Richard E. Morton and Lahoucine Izem, research scientists at the Cleveland Clinic Foundation, have shown that the protein, called cholesteryl ester transfer protein (CETP), is involved in the cellular storage and regulation of cholesterol and other fats and, as a result, probably has unexpected contributions to obesity and diabetes.