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Pregnancy Timeline by SemestersFemale Reproductive SystemFertilizationThe Appearance of SomitesFirst TrimesterSecond TrimesterThird TrimesterFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterDevelopmental Timeline
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March 6, 2013--------News Archive Return to: News Alerts

m


The Plin2 gene produces a protein that regulates fat storage
and metabolism. Researchers found that mice created without
the Plin2 gene were resistant to obesity.










WHO Child Growth Charts

       

Discovered—Gene that Causes Obesity in Mice

Researchers have discovered that deleting a specific gene in mice prevents them from becoming obese even on a high fat diet, a finding they believe may be replicated in humans. Deleting the gene in mice eliminates obesity, which is highly significant for humans

by David Kelly | University Communications

"When fed a diet that induces obesity these mice don’t get fat," said Prof. James McManaman, Ph.D., lead author of the study and vice-chairman of research for Obstetrics and Gynecology at the University of Colorado School of Medicine. "It may be possible to duplicate this in humans using existing technology that targets this specific gene."

The two-year study, funded by the National Institutes of Health and the U.S. Department of Agriculture, was published last month in The Journal of Lipid Research.


The research team created a strain of mice without the Plin2
gene which produces a protein that regulates fat storage
and metabolism. They immediately found that the mice
were resistant to obesity.

Usually, mice fed a high fat diet will eat voraciously,
yet these showed an unusual restraint. Not only did they
eat less, they were more active.

Their fat cells were also 20 percent smaller than typical mice
and did not show the kind of inflammation usually associated
with obesity, the study found. Obesity-associated fatty
liver disease, common in obese humans and rodents,
was absent in the mice without the Plin2 gene.


"The mice were healthier," McManaman said. "They had lower triglyceride levels, they were more insulin-sensitive, they had no incidents of fatty liver disease and there was less inflammation in the fat cells."

The absence of the gene may cause fat to be metabolized faster, McManaman believes.

"Now we want to know why this works physiologically," McManaman said. "We want to better understand how this affects food consumption."

According to the study, understanding how Plin2 is involved in the control of energy balance will provide new insights into "the mechanisms by which nutrition overload is detected, and how individuals adapt to, or fail to adapt to, dietary challenges."


The consequences for people are highly
significant as we also possess the Plin2 gene.


"It could mean that we have finally discovered a way to disrupt obesity in humans," he added. "That would be a major breakthrough."

The study’s co-authors include David Orlicky, Ph.D., and Paul MacLean, Ph.D., associate professors at the CU School of Medicine and Andrew Greenberg, MD, senior scientist and director of the The Obesity and Metabolism Laboratory at Tufts University.

Original article: http://www.ucdenver.edu/about/newsroom/newsreleases/Pages/Researchers-discover-gene-that-causes-obesity-in-mice.aspx