The brain and intestine are closely related, and the intestine is also called the “second brain” because it has the most neurons after the brain and spinal cord.
Several studies on the gut microbiota show that it takes part in the communication between the intestine and the brain.
This would influence brain function , having a direct impact on certain psychic disorders , neurodegenerative diseases and eating behaviors .
Uncontrolled eating and extra portions usually appear on the scale later, but the precise operation is not yet clear to scientists.
A study published August 12, 2019 in the journal Journal of Clinical Investigation reveals a previously unknown gut-brain link that helps explain how these extra portions lead to weight gain .
Conducted in the laboratory, this study shows that mice that follow a high-fat diet show an increase in levels of gastric inhibitory polypeptide (GIP). This hormone produced in the gut participates in the management of the energy balance of the body .
The study reports that the excess of this hormone spreads in the blood to the brain where it inhibits the action of leptin , the hormone of satiety.
As a result, the animals continue to eat and gain weight. Blocking the interaction of this hormone with the brain restores leptin’s ability to suppress appetite and leads to weight loss in mice.
A new major light against obesity
Researchers have discovered a new complex key to how the body manages energy balance and affects weight.
They know that leptin, a hormone produced by fat cells , plays an important role in the control of body weight in both mice and humans.
Leptin works by causing the feeling of satiety in the brain when we have eaten enough food and stop eating.
However, in the case of obesity resulting from a diet too fat, the body stops reacting to leptin signals.
The consequence is that he does not feel full and continues to eat, resulting in weight gain .
Until then, researchers did not know how a high-fat diet or excessive diet led to leptin resistance .
The fruit of several years of research
The results of this study are the result of several years of research into the causes of leptin resistance in the brain.
To do this, they examined the ability of blood circulation factors to stop the actions of leptin , and found a connection between the intestinal hormone and leptin.
GIP hormone is one of the incretin hormones produced in the gut in response to diet and known for their ability to influence energy management by the body.
To determine if this hormone was involved in leptin resistance , the researchers first confirmed that the GIP receptor (the molecule on cells that binds to GIP and moderates its effects) is expressed in the brain.
Next, they evaluated the blocking effect of the GIP receptor on obesity by injecting a monoclonal antibody directly into the brain, which effectively prevents receptor interaction.
They found that it significantly reduced the weight of obese mice fed a high fat diet.
According to the researchers, “the animals ate less and also reduced their body fat and blood sugar levels. In contrast, lean mice fed normally, treated with the monoclonal antibody, did not reduce their food consumption, or lost body weight or body fat .
This indicates that the effects are specific to diet-induced obesity.
Other experiments have shown that if animals were genetically modified to be leptin deficient, treatment with the specific monoclonal antibody did not reduce appetite and weight in obese mice, indicating that GIP in the brain was acting leptin signaling bias.
In addition, researchers identified intracellular mechanisms involved in modulating leptin activity through GIP.
A balanced diet allows leptin to work properly
In summary, when the diet is balanced, GIP levels do not increase and leptin acts as expected.
“This causes the brain to feel satiated when the animal has eaten enough and the mice stop eating. “
“But when animals have a high fat diet and become obese, blood GIP levels increase. The GIP then enters the hypothalamus where it inhibits the action of leptin. “
“As a result, animals become less sensitive, do not eat and do not gain weight. Then, the interaction of GIP with the hypothalamus of obese mice restores leptin’s ability to suppress appetite and reduce body weight. “
Finally, these data indicate that gastric inhibitory polypeptide (GIP) and its receptor in the hypothalamus , a region of the brain that regulates appetite, are necessary and sufficient to induce leptin resistance. This is a previously unrecognized role of the GIP on obesity that plays directly in the brain.
To conclude, the researchers indicate that “even if additional research is needed, these results could soon be translated into weight loss strategies that restore the brain’s ability to respond to leptin by inhibiting the anti-leptin effect of GIP.” .
External sources
Kentaro Kaneko, Yukiko Fu, Hsiao-Yun Lin, Elizabeth L. Cordonier, Qianxing Mo, Yong Gao, Ting Yao, Jacqueline Naylor, Victor Howard, Kenji Saito, Pingwen Xu, Siyu S. Chen, Miao-Hsueh Chen, Yong Xu, Kevin W. Williams, Peter Ravn, Makoto Fukuda. Gut-derived GIP activates central Rap1 to odd neural leptin sensitivity during overnutrition . Journal of Clinical Investigation , August 2019; DOI: 10.1172 / JCI126107, https://jci.org/articles/view/126107