If our scale indicates that we are overweight, perhaps even obese qualify, since it is well known what to do: get their hands on a balanced diet and exercise, formidable remedies to combat obesity.
However, it seems that in our brain there's a remedy, a key to combat obesity: control of the action of a hormone called leptin.
Leptin is secreted by fat cells of the body. Its mission is to send a signal to the brain satiety.
Once the brain receives the signal, it triggers a chain of other indications to stop eating and start burning fat.
However, there is something that does not fit this explanation: if one is obese undoubtedly have more fat cells so more leptin is secreted and therefore receives more satiety signals that should lead to stop eating, burn more fat and prevent fattening. Why not work well?
What happens is that when there is an overdose of the brain becomes leptin deaf to the hormone signal and chain that activates the circuit indications to stop eating and burn fat breaks.
As shown by a team of researchers from the University of Texas Southwestern United States, which analyzed the brains of mice that were created leptin resistance.
The team, led by Joel Elmquist, found that brain action chain that starts with the leptin signal just breaks when the brain is exposed to much of this hormone, as detailed in a report in the journal Cell Metabolism.
What if leptin resistance and it was generated?
A team of researchers from the Weizmann Institute in Israel, believes he has the answer: there is a protein that serves as a signal amplifier of leptin in the brain, if the protein is not present, the hormone signal is weaker and returns to be heard by the brain even if an excess of leptin, so orders satiety and start burning fat are activated.
Protein is tyrosine phosphatase epsilon (PTPE, for its acronym in English) and the initial objective of the research team led by Ari Elson was analyzing its effect on the development of osteoporosis.
They created in laboratory mice lacking PTP, their ovaries removed to accelerate the development of osteoporosis and fed a high-fat diet.
To the surprise of Elson and colleagues, menopausal and under a high-calorie diet did not become obese mice, they remained thin.
Then, as detailed in the study also published in the journal Cell Metabolism, examined the brains of mice and discovered the effect of PTP protein in the action of leptin at the level of the hippocampus.
It should make human studies to know whether to block PTP in our brains helps control obesity similarly as it did in the rodent study.
Yes, there is bad news for men: the block PTP worked only in the brains of mice and may work only in women; will have to see what future research reveals.
However, it seems that in our brain there's a remedy, a key to combat obesity: control of the action of a hormone called leptin.
Leptin is secreted by fat cells of the body. Its mission is to send a signal to the brain satiety.
Once the brain receives the signal, it triggers a chain of other indications to stop eating and start burning fat.
However, there is something that does not fit this explanation: if one is obese undoubtedly have more fat cells so more leptin is secreted and therefore receives more satiety signals that should lead to stop eating, burn more fat and prevent fattening. Why not work well?
What happens is that when there is an overdose of the brain becomes leptin deaf to the hormone signal and chain that activates the circuit indications to stop eating and burn fat breaks.
As shown by a team of researchers from the University of Texas Southwestern United States, which analyzed the brains of mice that were created leptin resistance.
The team, led by Joel Elmquist, found that brain action chain that starts with the leptin signal just breaks when the brain is exposed to much of this hormone, as detailed in a report in the journal Cell Metabolism.
What if leptin resistance and it was generated?
A team of researchers from the Weizmann Institute in Israel, believes he has the answer: there is a protein that serves as a signal amplifier of leptin in the brain, if the protein is not present, the hormone signal is weaker and returns to be heard by the brain even if an excess of leptin, so orders satiety and start burning fat are activated.
Protein is tyrosine phosphatase epsilon (PTPE, for its acronym in English) and the initial objective of the research team led by Ari Elson was analyzing its effect on the development of osteoporosis.
They created in laboratory mice lacking PTP, their ovaries removed to accelerate the development of osteoporosis and fed a high-fat diet.
To the surprise of Elson and colleagues, menopausal and under a high-calorie diet did not become obese mice, they remained thin.
Then, as detailed in the study also published in the journal Cell Metabolism, examined the brains of mice and discovered the effect of PTP protein in the action of leptin at the level of the hippocampus.
It should make human studies to know whether to block PTP in our brains helps control obesity similarly as it did in the rodent study.
Yes, there is bad news for men: the block PTP worked only in the brains of mice and may work only in women; will have to see what future research reveals.
Facebook
Twitter
RSS
0 comments: