Scientists have revealed an antiobesity gene that has apparently been keeping critters lean during times of plenty since ancient times. The gene, first discovered by another team in flies, also keeps worms and mice trim, as per the new report in the recent issue of Cell Metabolism, a publication of Cell Press. If the gene works similarly in humans, the findings could lead to a new weapon against our burgeoning waistlines, as per the researchers.
Animals without a working copy of the gene, known as Adipose (Adp), become obese and resistant to insulin, while those with increased Adp activity in fat tissue become slimmer, the scientists found. Moreover, the genes dose seems to determine how slender an animal turns out to be.
Maybe if you could affect this gene, even just a little bit, you might have a beneficial effect on fat, said Jonathan Graff of the University of Texas Southwestern Medical Center, noting that people often become overweight very graduallyadding just one or two pounds a year. After 30 years, thats a lot.
While worms and flies are routinely studied as models of human health and disease, that trend has been less true in fat biology, Graff said. Thats because unlike mammals, worms and flies store their fat in multifunctional cells rather than in dedicated fat cells known as adipocytes. However, those differences didnt preclude the possibility that the animals might use similar genes to accomplish their fat storage goals, he added.
In the new study, Graffs team observed that worms lacking Adp activity became fat, eventhough they appeared to be otherwise healthy and fertile. The scientists scoured the genetic database in search of related genes and found one with tremendous similarity in flies.
Indeed, another scientist, Winifred Doane, had found a naturally occurring strain of plump flies in Nigeria almost 50 years ago that carried a mutation in their Adp gene. The flies lived in a climate marked by cycles of famine, where they may have benefited from being highly efficient at fat storage, Doane had suggested.
To explore Adps function even further, Graff and colleagues produced a strain of mutant flies like those that Doane had found years earlier. They observed that the mutant flies were indeed fat and also had trouble getting around. Flies with only one copy of the Adp mutation fell somewhere in between the fat and normal flies, evidence that the genes effects are dose dependent, they reported.
Treatments that increased Adp in the insects fat tissue led them to lose weight, evidence that the gene operates within fat cells themselves. In mice that expressed the gene in fat-storing tissues, the same patterns emerged.
We made mice that expressed Adp in fat-storing tissues, and lo and behold, what happened" Graff said. They were skinnyweighed less with markedly less fatand their fat cells were smaller. Smaller fat cells commonly translate into better metabolic function, he said, including better blood sugar control.
Its a striking conservation of genes that restrain fat, he said. While fat storage is an important mechanism for getting through lean times, too much fat in times of plenty has deleterious consequences.
The search for molecules underlying weight gain and poor blood sugar control has taken on additional urgency due to the recent dramatic increase in obesity and diabetes, Graff said. But in a modern world where a number of people have essentially unlimited access to food, its a wonder that even more people arent overweight, he added. If this gene plays a similar role in humans, it may be that some peoples Adp works very well.
Posted by: Evelyn
Source