You may not be hungry, but there is always room for dessert. The neurons that induce the feeling of satiety at the end of a meal are the same as, if there are simple sugars in view, they stimulate us to eat them anyway, according to German researchers of the Max Planck Institute for Metabolism Research. The so -called “dessert stomach” could revolutionize obesity treatments.
What is the “dessert stomach”?
Everyone, after an abundant meal, has thought it has enough. Not even one more gram of rice could enter the organism. However, he is never told not to the chocolate cake or strawberry cake, right?; This phenomenon is known as “dessert stomach.” The scientific community has the concept in mind, but it is not clear what stimulus causes the desire to eat sugar when sufficient calories have already been reached.
The Max Planck Institute team, led by Henning Fenselau, finally gives a specific response. As explained in the study published in the magazine Science, His first approach was with the mice and then analyzed the behavior in humans. In both species, the activation of hypothalamic neurons called pro-opiomelanocortin (POMC) is producedwhich are also responsible for the feeling of satiety.
These cells produce different neurotransmitters: to indicate that it is time to stop eating, they release the alpha-melanocyte-stimulating hormone that binds to melanocortin-4 receptors (MC4R); In turn, it activates the neurons of the nucleus to ventricular of the hypothalamus. But if a sweet food is perceived they also produce another substance: the betaendorphine opioid. This, by joining another receiver called Muopioid (MOR), inhibits the neurons of the paraventricular core of the thalamus, which stimulates the appetite for sugars and, when consuming them, activates the mechanism of enjoying them in abundance.
“From an evolutionary perspective, this makes sense: sugar is scarce in nature, but provides fast energy, the brain is scheduled to control glucose intake whenever it is available,” explains Fenselau.
BENEFITS FOR THE TREATMENT OF OBESITY
The researchers found that it was a specific mechanism of sugar intake and also saw that, By inhibiting the betaendorphine circuit, the mice that were already satiated ceased to feel the temptation to consume more sugar. This observation could be useful in treatments against obesity by combining suppressive drugs with blockers of opioid receptors in the brain. “However, we still have to continue investigating,” concludes Fenselau.
Article originally published in Wired Italy. Adapted by Alondra Flores.
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