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Updated 2:30 PM September 19, 2005
 

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  Research
Life sciences team learns about the origin of fat cells

A U-M research team has determined some of the crucial steps in how fat cells are formed, and its findings may help in understanding chronic diseases, such as obesity and diabetes.
The cover of the Sept. 13 issue of Cell Metabolism features the article, "Changes in Integrin Expression During Adipocyte Differentiation," which presents results of a study by Life Sciences Institute Director Alan Saltiel and a team of U-M researchers. (Photo courtesy Life Sciences Institute)

Research conducted in the laboratory of Alan Saltiel, director of the Life Sciences Institute, dissected the genetic effects of a hormonal cocktail that induces the transition from fat-cell precursors to full-blown fat cells.

Like all cells, fat cells develop from stem cells. The fate of a stem cell is predetermined. Pre-fat cells are programmed to turn into fat cells when exposed to a certain hormonal environment. Saltiel's group looked at how the hormones affected that cellular change.

"The body needs fat cells," Saltiel says. "They serve as a storage depot for fuel as well as a sensor of hormone and energy status. These cells sense the amount of fat and secrete hormones that maintain energy balance throughout the body."

Everyone needs the right number of fat cells. Too many, too big, fat cells cause obesity, while too few cause a disease called lipodystrophy, where fat has to be stored in muscle or the liver. Both problems can lead to diabetes.

Saltiel's group wanted to figure out how these hormones led to formation of fat cells, so they withheld one ingredient in the cocktail, and then looked at all the genes that changed. Among the hundreds of genetic changes were two receptor proteins called integrins found on the surface of cells. Integrins bind to the extra-cellular matrix that surrounds the cell, and serve as switchboards to control the shape, size and growth of cells.

The crucial event occurred when integrin alpha 5 was decreased and integrin alpha 6 was increased. This "integrin switching" caused cells to stop growing, and cluster together, which ultimately led to changes in the shape of the cells.

"Fat cells require contact in order to stretch and change shape—becoming round enables the cell to accumulate lots of lipids," Saltiel says. "While many changes occur in the generation of fat cells, the transition from one integrin to another is a crucial step."

Saltiel says he believes the study could have implications in understanding obesity and diabetes, and open the door to new explorations centered on how integrins control fat formation.

The article, "Changes in Integrin Expression During Adipocyte Differentiation" is featured on the cover of the Sept. 13 issue of Cell Metabolism.

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