Scientists are linking obesity with inflammation and scarring in the
key brain area that controls body weight - a finding that could explain
why it's so hard to lose weight and keep it off.
When researchers switched mice and rats genetically bred to become obese from regular low-fat chow to high-fat and highly palatable chow, the rodents began showing signs of inflammation in the hypothalamus within 24 hours of the diet switch.
The hypothalamus takes signals from body fat and other tissues that tell the brain that we need food or that we've had enough. It also regulates how much energy or fat we burn.
"We saw direct evidence of neuron injury and, ultimately, after months on the diet, a loss of neurons in this hypothalamic area that's vital for body weight control," said lead researcher Dr. Michael Schwartz, professor of medicine and director of the Diabetes and Obesity Center of Excellence at the University of Washington, Seattle.
The switch to the high-fat diet "is actually injuring the neurons that are supposed to protect them from obesity," he said.
When the team next compared MRI scans of the brains of 34 otherwise healthy people, obese people had more gliosis - scarring in the brain from injured neurons - in the hypothalamus than those of normal weight.
The more obese the person, the higher their gliosis score.
Gliosis is normally seen after a stroke.
"We don't know that this is a cause of obesity, or a consequence of obesity," Schwartz said. But it fits with what they observed in the animal experiments. "It suggests that what we have seen in the mouse and rats is also occurring in the human."
The work was based on the hypothesis that changes in the brain conspire to keep weight on once it's gained.
"Our paper provides direct evidence to support that hypothesis," Schwartz said, "because we do find evidence of fixed structural change in the brain area most important for bodyweight control in obese individuals and animals."
"This may help to explain why it's so hard for obese people - they can lose weight but they can't keep it off because their hypothalamus is reading them as basically weighing the right amount."
Inflammation disrupts the action of insulin as well as leptin - a hormone produced by fat cells that tells the brain how much fat and energy is stored.
If the brain can't read the leptin signals properly, it takes more leptin to get the message to the hypothalamus to stop eating.
"And the only way to have more leptin is to have more body fat," Schwartz said.
When researchers switched mice and rats genetically bred to become obese from regular low-fat chow to high-fat and highly palatable chow, the rodents began showing signs of inflammation in the hypothalamus within 24 hours of the diet switch.
The hypothalamus takes signals from body fat and other tissues that tell the brain that we need food or that we've had enough. It also regulates how much energy or fat we burn.
"We saw direct evidence of neuron injury and, ultimately, after months on the diet, a loss of neurons in this hypothalamic area that's vital for body weight control," said lead researcher Dr. Michael Schwartz, professor of medicine and director of the Diabetes and Obesity Center of Excellence at the University of Washington, Seattle.
The switch to the high-fat diet "is actually injuring the neurons that are supposed to protect them from obesity," he said.
When the team next compared MRI scans of the brains of 34 otherwise healthy people, obese people had more gliosis - scarring in the brain from injured neurons - in the hypothalamus than those of normal weight.
The more obese the person, the higher their gliosis score.
Gliosis is normally seen after a stroke.
"We don't know that this is a cause of obesity, or a consequence of obesity," Schwartz said. But it fits with what they observed in the animal experiments. "It suggests that what we have seen in the mouse and rats is also occurring in the human."
The work was based on the hypothesis that changes in the brain conspire to keep weight on once it's gained.
"Our paper provides direct evidence to support that hypothesis," Schwartz said, "because we do find evidence of fixed structural change in the brain area most important for bodyweight control in obese individuals and animals."
"This may help to explain why it's so hard for obese people - they can lose weight but they can't keep it off because their hypothalamus is reading them as basically weighing the right amount."
Inflammation disrupts the action of insulin as well as leptin - a hormone produced by fat cells that tells the brain how much fat and energy is stored.
If the brain can't read the leptin signals properly, it takes more leptin to get the message to the hypothalamus to stop eating.
"And the only way to have more leptin is to have more body fat," Schwartz said.
No comments:
Post a Comment