Well, the recent study has shown that fatty food disrupts appetite control and it causes fatness. A new study has discovered a previously nameless mechanism explains the causes of fatness or obesity. It says that high-fat diets can disrupt the appetite-suppressing signals from the brain and lead to overeating. It says that Leptin is a hormone with a range of functions but it is probably best known for regulating appetite
The interesting research revealed a hormone in the gut, triggered by high-fat meals, actually induces the body to keep eating.
Fatty food and Fatness
According to the study published in Journal of Clinical Investigation suggests a previously unknown gut-brain connection that helps explain how extra servings lead to weight gain. On the other hand, corresponding author Dr Makoto Fukuda said, “We have uncovered a new piece of the complex puzzle of how the body manages energy balance and affects weight.”
So, fat cells produce leptin, and the hormone communicates with the hypothalamus to let someone know when they should stop eating. Well, overweight people obviously have more fat cells, so they are known to have higher levels of leptin, however this counter-intuitively does not result in a suppressed appetite. This scenario is called leptin resistance, and scientists weren’t sure exactly what causes the body to block these leptin signals in the brain and cause a person to overeat.
Researchers found that mice consuming a high-fat diet showed increased levels of gastric inhibitory polypeptide (GIP). This hormone is produced in the gut and is involved in managing the body’s energy balance.
Thus, GIP, or gastric inhibitory polypeptide, is concealed by the gut in response to food. It is part of a family of molecules called incretins, known to help regulate insulin and energy expenditure. The scientists acknowledge that while more research is needed, they speculate that these findings might one day be translated into weight loss strategies that restore the brain’s ability to respond to leptin by inhibiting the anti-leptin effect of GIP.