This finding provides strong evidence that brain inflammation may be a cause of obesity, rather than obesity causing brain inflammation. It was previously thought that overeating causes stress and damage to cells in the body as well as the brain, leading to an increase in inflammatory markers.
The researchers hope this information can provide promising leads for new anti-obesity therapies.
The brain and obesity
The connection between brain inflammation and obesity has been supported with evidence for some time. Inflammation is also thought to affect regions of the brain that control eating.
More specifically, a hormone called leptin that is released by fat cells generally provides the brain with information about the amount of energy stored as body fat. Neurons (brain cells) in the hypothalamus are sensitive to leptin and use this information to help regulate eating and activity.
Obese individuals have an insensitivity to leptin and as a result, they no longer trigger the decrease in hunger and increase in energy expenditure that should normally occur. This leads to excess weight gain. Brain inflammation is thought to lead to leptin insensitivity.
However, whether brain inflammation actually causes the development is not fully clear yet. This new study finds that the activation of a particular type of brain immune cell, called microglia, kicks off the events that are most definitely linked directly to obesity.
Looking at mouse models
Experiments on mice by researchers at the University of California, San Francisco, and the University of Washington found that altering the activity of microglia in the hypothalamus controlled their body weight. This was also seen to be true no matter how much the mice ate.
The study in question tested these effects by reducing either the number of microglia or the level of activity in the mice subjects. Both instances cut the weight gain in half that resulted from putting the mice on high-fat diets.
Next, the researchers increased the activity of microglia and found that it causes obesity in mice that had been on a normal diet.
They were quite surprised that manipulation of microglia appeared to play a big role in the development of obesity, rather than the brain cells themselves. This indicated that supporting cells, like microglia, can exert control over primary functions like weight gain.
Considering the studies were only carried out in mice, there is no telling whether this holds true for humans as well. But similar instances of brain inflammation in humans have been linked to negative consequences in the human body, with these new results providing a potential solution to the obesity crisis.
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