A recent study, published in the journal Cell Metabolism, defines a mechanism that controls if a precursor fat cell matures into a brown fat or white fat cell. Why would this matter?
Most people are undergoing a constant battle to get rid of fat. But, fat cells aren't all the same. Two forms of fat cells exist; white fat and brown fat. White fat is the stuff that stores the excess calories and energy that we taken in, making sure we have enough reserves for lean times when food is scarce. White fat accumulates around the mid-section of our body, along the butt and thighs, and elsewhere. Brown fat is quite different. Brown fat generates heat and burns energy. These cells are filled with energy producing iron-filled mitochondria, hence the brown color, and generates heat for the organism. Brown fat, found mostly in infants (along the spine and shoulders of the back) and hibernating mammals. It's main function is to provide heat to avoid hypothermia in mammals that don't shiver. In adult humans, the amount of brown fat is quite low.
Dr Seale and colleagues have now shown that a protein called early B cell factor-2 or Ebf2 acts like a switch during fat cell development that controls which type of fat cell emerges, a brown fat or white fat cell. It turns out that Ebf2 binds to the promoter of genes involved in brown fat development. This results in the recruitment and binding of another protein, PPAR, and the subsequent expression of these genes. This study also showed that overexpression of Ebf2 in white fat cells converts into brown fat cells. Understanding how these cells develop may help develop new ways to control the amount of white fat cells in the body to help fight obesity.
http://www.alnmag.com/news/how-brown-fat-cells-develop-mice?et_cid=3143363&et_rid=454985655&linkid=http%3a%2f%2fwww.alnmag.com%2fnews%2fhow-brown-fat-cells-develop-mice
Saturday, March 23, 2013
Monday, March 11, 2013
New gene controls obesity
The search for an (the) obesity gene has been a long and arduous one that has implicated many candidate genes during this quest. Although these genes that have had important roles in regulating weight, the common thread linking them together has been that have had some role in metabolism and regulating the cell's ability to use energy.
Researchers at the University of Colorado and Tufts Medical School have recently identified another potential regulator of obesity, Plin2. Like previous candidate genes, Plin2 may play a key role in regulating cellular metabolism. Further, the deletion of this gene in mice prevented weight gain, even when the animal was fed a high fat diet. Surprisingly, researchers found that lack of expression of this gene prevented the onset of other obesity associated outcomes -- like high triglycerides and increased inflammation that are seen along with obesity. Even the adipose (fat) cells in these mice were smaller than their paired control mice that faithfully expressed Plin2.
Work is ongoing to learn more about Plin2 and how this gene controls metabolism and weight gain. http://www.scienceomega.com/article/863/removing-gene-stops-obesity-in-mice
Researchers at the University of Colorado and Tufts Medical School have recently identified another potential regulator of obesity, Plin2. Like previous candidate genes, Plin2 may play a key role in regulating cellular metabolism. Further, the deletion of this gene in mice prevented weight gain, even when the animal was fed a high fat diet. Surprisingly, researchers found that lack of expression of this gene prevented the onset of other obesity associated outcomes -- like high triglycerides and increased inflammation that are seen along with obesity. Even the adipose (fat) cells in these mice were smaller than their paired control mice that faithfully expressed Plin2.
Work is ongoing to learn more about Plin2 and how this gene controls metabolism and weight gain. http://www.scienceomega.com/article/863/removing-gene-stops-obesity-in-mice
Sunday, March 3, 2013
Salt activates different receptors depending on concentration
Do you like lots of salt? You may not be alone -- many people love salt. But, even for these salt-lovers, high concentrations of salt taste transitions from delectable to disgusting. How does this happen? We have taste receptors that recognize the sweet, savory, salty, bitter and sour tastes in the foods we ingest. This is an evolutionary adaptation that prevents us from eating potentially deadly or toxic foods. Sweet and savory foods activate one set of receptors and one pathway. On the other hand, sour and bitter foods stimulate a different set of receptors and pathways. This makes sense; different pathways informs us if a food is acceptable or potentially toxic and shouldn't be eaten.
But what about salt? A new paper published in Nature magazine, by Dr. Y. Oka and colleagues (ePub February 13, 2013, print 494: 472), provides new insight into how salty tastes transition from good to bad. At low concentrations, salt activates the savory and sweet pathways, but switches to the bitter and sour pathways at higher levels. Researchers have begun to identify specific receptors that a involved and have shown how blocking these receptors changes the reaction to salt concentrations. This research opens the door to understanding how and why we like salt at times, but not when there is too much of it.
But what about salt? A new paper published in Nature magazine, by Dr. Y. Oka and colleagues (ePub February 13, 2013, print 494: 472), provides new insight into how salty tastes transition from good to bad. At low concentrations, salt activates the savory and sweet pathways, but switches to the bitter and sour pathways at higher levels. Researchers have begun to identify specific receptors that a involved and have shown how blocking these receptors changes the reaction to salt concentrations. This research opens the door to understanding how and why we like salt at times, but not when there is too much of it.
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