Appetite control is often associated with risk of obesity and Type 2 Diabetes. Researchers at the University of California, San Diego have found that leptin resistance may have a significant impact on hunger and satisfaction. In animal studies, a high-fat diet increases the amount of an enzyme named MMP-2, which damages leptin receptors that signal your brain when you’re full. When the hormone leptin’s receptor sites are damaged, the neurons do not send a satiety signal to the stomach to stop eating. This may explain why obese individuals often eat past the point of fullness. 

Leptin is released from white fat tissue, the most predominant form of fat, when a person is eating a meal. “Leptin travels through the bloodstream to the brain, specifically the hypothalamus, where it stimulates neural receptors to signal that the stomach is full.” Individuals who are overweight or obese typically have plenty of leptin in the blood, but due to the abundance of the MPP-2 enzyme, the system fails to send the signal of satiety to the hypothalamus.

This study found the enzyme MMP-2 is responsible for the damage to leptin receptors. Subjects who did not produce the MMP-2 enzyme gained less weight overall. Their leptin receptors still remained in tact. Researchers of this study, believe that, “other membrane receptors may be destroyed in the same way.” Further research must be conducted to determine if this is the case for other receptors as well. 

This research team is calling for a large-scale clinical trial to investigate whether MMP-2 inhibitors might help people lose weight

For more information on leptin resistance, check out at the study Leptin Resistance and Appetite Control.

Contributed By: Sofia Sepulveda