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Obesity is an alarming problem that is behind a huge percentage of death every single year that not many are even aware of. While the prospect of overeating and a sedentary lifestyle was regarded as the common reason behind the condition, a new study conducted can shed some better light on the condition.
A new study (R) conducted by the researchers from the Baylor College of Medicine suggests a previously known gut brain connection behind the obesity which is associated with the overeating. The researchers were finally able to get a better idea on how the same affects and propagates the condition even more so.
When you overeat, the momentary satisfaction and happiness is something unexplainable but why the same contributed to weight gain was still unclear up until now. The research has been conducted by a multi-institute team of researchers that have shed some better light on how the same affects the overall gut-brain connection and can end up contributing to obesity.
The study was conducted on mice to get a better perspective on why this happens and how it happens as well.
The mice which were fed with a high fat diet were found to have increased levels of the gastric inhibitory polypeptide (GIP) which is a hormone that is produced in the gut to ensure better energy levels in the body. The study has found that the excess GIP in the bloodstream travels along the blood up till the brain where it ends up inhibiting the action of leptin which is the satiety hormone in the body.
What this does is blur out the line when you are full, thus making you eat more than your capacity and contributing to the risks of obesity. Simultaneously, successfully blocking the interaction of GIP with that of the brain helps in restoring the normal functioning of the leptin, thus contributing to weight loss.
Dr. Makoto Fukuda, assistant professor of pediatrics at Baylor and the USDA/ARS Children’s Nutrition Research Center at Baylor and Texas Children’s Hospital, who is also the corresponding author of the study suggested saying that they have successfully uncovered yet another prospect on how the body manages the balance and how the same affects the weight.
It is know by the researchers that leptin does play a very crucial role when it comes to the control of the body weight in both the humans as well as the mice. Given that it is the satiety hormone, it triggers our brain to make up stop eating when we have reached our satiety, thus preventing us from overeating.
On the contrary, for people suffering from obesity, this mechanism of the leptin is disrupted. The body stops responding to the leptin signals and makes is overeat which further worsens the condition of weight gain even more so.
Fukuda further shed some light stating that they weren’t aware that the leptin resistance in the body is caused when we eat a high fat diet on a consistent basis. The researchers then went on to find the reasons that could be contributing to the leptin resistance in the brain on the consumption of the fatty foods.
Following years of research surrounding the screen blood circulating factors with that of the leptin reactions, the researchers did establish the fact that there is a strong connection between the levels of brain GIP with that of leptin that could be the primary contributing factor to the condition of obesity.
For the ones who aren’t aware, GIP is an incretin hormone which is produced and secreted in the gut and is responsible for the energy balance and management in the body. In order to establish for sure whether or not the GIP hormone has any kind of influence in the leptin resistance, the researchers confirmed for a fact that the GIP receptor is expressed in the brain for better binding.
Following that, the researchers wanted to test the kind of effect it would bring around if one blocked the GIP receptor. The same was done by infusing a monoclonal antibody directly into the brain by Dr Peter Ravn who is from AstraZeneca. This was found to prevent the direct interaction between two GIP molecules. This was one of the factors that were found to have beneficial impacts on the body weight of the obese mice.
Fukuda said that they found that following doing that, the mice not just ate less, they also did have a reduced fat mass as well as controlled blood glucose levels in the body.
In contrast to these findings, the researchers also did find that the normal chow fed lean mice when treated with the monoclonal antibody didn’t show any drastic differences in the body indicating the fact that the same is prevalent in the diet induced obesity, for the most part.
Other experiments further showed for a fact that if the animals were then genetically engineered to be leptin deficient, the same doesn’t have any kind of impacts on the weight loss or even the reduction of appetite in the obese mice. This further suggests that the GIP in the brain does act via the leptin signaling.
Concluding it all, Fukuda finally said that eating a balanced diet doesn’t cause any kind of difference in the GIP levels in the brain and thus the leptin works in its optimal function. It effectively triggers the brain to stop eating when one is full.
On the contrary, when the person is eating a diet filled with high fat food and then become obese, the same can end up increasing the levels of GIP in the blood stream. This excess level of GIP then flows round to the hypothalamus and ends up inhibiting the function of the leptin. This result in making the person end up eat more, because they aren’t aware when they are full.
The successful blocking of the GIP with that of the hypothalamus is what ends up helping with proper regulation of one’s appetite, thus keeping the risk of obesity in control and in check. More research is necessary in this prospect which is what the researchers are also working on currently.
