In mice, neural circuits in the brain promote hunger-stimulated food consumption and suppress pleasure-motivated eating.
- American researchers have identified a group of neurons that regulates nutritional balance in the brain.
- These are Penk neurons in the brain region called the diagonal band of Broca (DBB), which increase hunger-motivated eating while reducing pleasure-motivated eating when activated.
- According to the team, these results open new perspectives for the development of strategies to combat obesity.
“Eating behavior is influenced by two main factors: homeostatic needs driven by hunger and hedonic desires for pleasure, even in the absence of hunger. While effective homeostatic feeding is vital for survival, excessive hedonic feeding can have adverse consequences, such as obesity and metabolic dysregulation. However, the neurobiological mechanisms that orchestrate homeostatic versus hedonic food consumption remain largely unknown,” said researchers from Baylor College of Medicine (USA).
That’s why they decided to conduct a study published in the journal Nature Metabolism. The scientists built on previous research that highlighted the role of neurons identified by the GABAergic marker of proenkephalin (Penk), an endogenous opioid hormone, in feeding and body weight control. The problem: their contribution to the regulation of hunger- and pleasure-driven feeding has not been elucidated. In parallel, the team also conducted an experiment on mice that were exposed to food.
Activation of DBB-Penk neurons promotes an ideal feeding pattern
According to the findings, Penk neurons in the brain region called the diagonal band of Broca (DBB) of male mice respond to food presentation. These neurons project to two different brain areas, one regulating hunger-motivated eating and the other regulating pleasure-motivated eating. “A subset of DBB-Penk neurons that projects to the paraventricular nucleus of the hypothalamus is preferentially activated when food is presented during periods of fasting, facilitating hunger-motivated eating. On the other hand, a distinct subset of DBB-Penk neurons that projects to a different brain region, the lateral hypothalamus, is preferentially activated when it detects foods high in fat and sugar and inhibits their consumption,” explained Yong Xu, an author of the work.
Obesity: an alteration in the function of some of the brain circuits involved
When mice, whose entire DBB-Penk population had been eliminated, were given a free choice between a “chow diet” and a high-fat, high-sugar diet, they reduced their consumption of the chow diet but increased their consumption of the high-fat, high-sugar diet, leading to accelerated development of obesity and metabolic disturbances. These findings indicate that the development of obesity is associated with impaired function of some of these brain circuits in mice, the researchers say. “We want to further study the molecular markers of these circuits that could constitute suitable targets for the treatment of diseases, such as obesity,” they concluded.
