09-02-2008, 06:35 AM
A genetic link controlling both appetite and fertility has been found by US researchers.
A gene, TORC1, appears to act as a "master switch", switching off food intake and allowing pregnancy.
The gene probably offered an evolutionary advantage, by stopping women getting pregnant in times when food was scarce, the researchers said.
Mice lacking the gene were unable to reproduce, and grossly overweight, reported the journal Nature Medicine.
Both underweight and severely overweight women may have fertility problems, and the research at Salk Institute in California is suggesting that TORC1 may play a role in both.
In normal circumstances, when food intake is sufficient, fat cells produce a hormone called leptin, which in turn, say the researchers, switches on TORC1, decreasing appetite, and enabling reproduction.
In times of food shortage, a lack of leptin leaves TORC1 switched off, leaving appetite unchecked and preventing pregnancy, which would use too much of a woman's energy.
This, said the Salk researchers, would be an important evolutionary advantage in times of famine.
However, they argued that a subtle mutation in the TORC1 gene might also play a role in obesity, by failing to pass on the "stop eating" signal even when food is plentiful.
If passed from generation to generation, it could mean an inherited extra risk of obesity, they said.
The failure of the gene to work properly could also affect fertility, by not allowing reproduction to proceed.
Infertile and overweight
To test this the scientists bred mice without TORC1, which after just eight weeks began to gain weight, becoming obese. In addition, both sexes were infertile.
Professor Marc Montminy, who led the study, said that TORC1 presented a good target for drugs.
He said: "This gene is crucial to the 'daisy-chain' of signals that run between body fat and the brain.
"It likely plays a pivotal role in how much we, as humans, eat, and whether we have offspring."
Professor Stephen Bloom, from Imperial College London, said that the findings made sense, although it was too early to say whether TORC1 was the most important point in the "cascade" of signals generated by leptin.
He said: "It's an extremely interesting observation. We've known for a long time that if you haven't got any fat as a girl your periods stop, and if you give leptin, the periods start again.
"However, I don't think they have yet established whether this is just a stepping stone, or the key link in the chain."
A gene, TORC1, appears to act as a "master switch", switching off food intake and allowing pregnancy.
The gene probably offered an evolutionary advantage, by stopping women getting pregnant in times when food was scarce, the researchers said.
Mice lacking the gene were unable to reproduce, and grossly overweight, reported the journal Nature Medicine.
Both underweight and severely overweight women may have fertility problems, and the research at Salk Institute in California is suggesting that TORC1 may play a role in both.
In normal circumstances, when food intake is sufficient, fat cells produce a hormone called leptin, which in turn, say the researchers, switches on TORC1, decreasing appetite, and enabling reproduction.
In times of food shortage, a lack of leptin leaves TORC1 switched off, leaving appetite unchecked and preventing pregnancy, which would use too much of a woman's energy.
This, said the Salk researchers, would be an important evolutionary advantage in times of famine.
However, they argued that a subtle mutation in the TORC1 gene might also play a role in obesity, by failing to pass on the "stop eating" signal even when food is plentiful.
If passed from generation to generation, it could mean an inherited extra risk of obesity, they said.
The failure of the gene to work properly could also affect fertility, by not allowing reproduction to proceed.
Infertile and overweight
To test this the scientists bred mice without TORC1, which after just eight weeks began to gain weight, becoming obese. In addition, both sexes were infertile.
Professor Marc Montminy, who led the study, said that TORC1 presented a good target for drugs.
He said: "This gene is crucial to the 'daisy-chain' of signals that run between body fat and the brain.
"It likely plays a pivotal role in how much we, as humans, eat, and whether we have offspring."
Professor Stephen Bloom, from Imperial College London, said that the findings made sense, although it was too early to say whether TORC1 was the most important point in the "cascade" of signals generated by leptin.
He said: "It's an extremely interesting observation. We've known for a long time that if you haven't got any fat as a girl your periods stop, and if you give leptin, the periods start again.
"However, I don't think they have yet established whether this is just a stepping stone, or the key link in the chain."