n completely corrected the metabolic disorders that the knockout mice had developed, but also improved the brain cells’ ability to respond to leptin signals and produce further signals that regulate eating.
What’s more, the mice that were treated to make extra SH2B1 didn’t become obese or lose their ability to respond to leptin signals even after being fed a high-fat diet that caused those effects in other mice.
“Obesity, whether in mice or humans, is the product of an altered balance between energy intake and energy use. The imbalance is linked to alterations in leptin and insulin signaling that lead to excess weight gain and Type 2 diabetes, respectively,” says Rui, an assistant professor of molecular and integrative physiology at U-M. “SH2B1 appears to play a key regulatory role in this system, through its direct influence on the processing of leptin and insulin signals in cells of the brain’s hypothalamus.”
Rui, who first discovered SH2B1’s metabolic importance as a graduate student at U-M in the 1990s, worked on the new paper with postdoctoral fellow Decheng Ren, Ph.D., who also collaborated on a paper in the journal Cell Metabolism in 2005 that first indicated SH2B1’s key role in obesity.
The team and other researchers have found that SH2B1, which was previously called SH2-B, is a kind of jack-of-all-trades in the world of cell signaling. Able to shuttle between the area just beneath the cell membrane and the nucleus, it can bind to many different molecules and facilitate signaling.
Specifically, it can bind to a variety of molecules called tyrosine kinases, including ones that serve as receptors for insulin and growth factors that circulate in the brain and body. One of its most important binding partners is JAK2, which is activated every time a leptin molecule binds to a cell.
Since leptin is the body’s messenger boy to the brain for “stop eating, we’re full” messages, and JAK2 helpsPage: 1 2 3 4 Related medicine news :1
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