Who hasn’t been there? The big meal is over, you’re full, but the craving for sweets remains. Researchers from the Max Planck Institute for Metabolism Research have now discovered that what we call the “dessert stomach” is rooted in the brain. The same nerve cells that make us feel full after a meal are also responsible for our craving for sweets afterwards.
To find the cause of the “dessert stomach”, the researchers investigated the reaction of mice to sugar and found that completely satiated mice still ate desserts. Investigations of the brain showed that a group of nerve cells, the so-called POMC neurones, are responsible for this. These neurones become active as soon as the mice were given access to sugar which facilitated their appetite.
When mice are full and eat sugar, these nerve cells not only release signaling molecules that stimulate satiety, but also one of the body’s own opiate: ß-endorphin. This acts on other nerve cells with opiate receptors and triggers a feeling of reward, that causes the mice to eat sugar even beyond fullness. This opioid pathway in the brain was specifically activated when the mice ate additional sugar, but not when they ate normal or fatty food. When the researchers blocked this pathway, the mice refrained from eating additional sugar. This effect was only observed in full animals. In hungry mice, the inhibition of ß-endorphin release had no effect.
Interestingly, this mechanism was already activated when the mice perceived the sugar before eating it. In addition, the opiate was also released in the brains of mice that had never eaten sugar before. As soon as the first sugar solution entered the mice’s mouths, ß-endorphin was released in the “dessert stomach region”, which was further strengthened by additional sugar consumption.
What happens in humans? #
The scientists also carried out brain scans on volunteers who received a sugar solution through a tube. They found that the same region of the brain reacted to the sugar in humans. In this region, as in mice, there are many opiate receptors close to satiety neurons.
“From an evolutionary perspective, this makes sense: sugar is rare in nature, but provides quick energy. The brain is programmed to control the intake of sugar whenever it is available,” explained Henning Fenselau, research group leader at the Max Planck Institute for Metabolism Research and head of the study.
Relevance for the treatment of obesity #
The research group’s findings could also be important for the treatment of obesity. “There are already drugs that block opiate receptors in the brain, but the weight loss is less than with appetite-suppressant injections. We believe that a combination with them or with other therapies could be very useful. However, we need to investigate this further,” Fenselau said.
To pay attention #
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Our brain’s principal nerve cell of satiety also mediates sugar cravings by releasing the opiate ß-endorphin.
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In mice and humans, the “dessert-stomach pathway” is activated by mere perception, which makes evolutionary sense because sugar provides quick energy.
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Blocking opiate signaling of this pathway may support current and future obesity treatments.
Some words from Science’s editor, Peter Stern #
In his abstract, Stern pointed that “although overall food intake is attenuated when we feel sated or full, this state is associated with an increased desire to eat sweet foods such as desserts. It is unclear why sugar appetite is selectively stimulated in satiety states”. “Minère et al. -added Stern- found that pro-opiomelanocortin (POMC) neurons from the arcuate nucleus send projections to the paraventricular thalamus. Unlike most other POMC neuron projections, these do not release α-melanocyte–stimulating hormone. Rather, they produce the appetite-stimulating opioid β-endorphin, which selectively inhibits postsynaptic neurons in the paraventricular thalamus expressing µ-opioid receptors, and this drives sugar consumption in the fed state (suggest to read Sadaf Farooqi’s paper: Understanding the desire for dessert, also published yesterday in Science). Finally stands out that “blocking this opioid transmission could thus reduce sugar intake and potentially combat binge eating and obesity**.
Minère et al. abstract #
“High sugar–containing foods are readily consumed, even after meals and beyond fullness sensation (e.g., as desserts). Although reward-driven processing of palatable foods can promote overeating, the neurobiological mechanisms that underlie the selective appetite for sugar in states of satiety remain unclear. Hypothalamic pro-opiomelanocortin (POMC) neurons are principal regulators of satiety because they decrease food intake through excitatory melanocortin neuropeptides. We discovered that POMC neurons not only promote satiety in fed conditions but concomitantly switch on sugar appetite, which drives overconsumption. POMC neuron projections to the paraventricular thalamus selectively inhibited postsynaptic neurons through mu-opioid receptor signaling. This opioid circuit was strongly activated during sugar consumption, which was most notable in satiety states. Correspondingly, inhibiting its activity diminished high-sugar diet intake in sated mice.
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The paper Thalamic opioids from POMC satiety neurons switch on sugar appetite, was published in Science. Authors: Marielle Minère, Hannah Wilhelms, Bojana Kuzmanovic, Sofia Lundh, Debora Fusca, Alina Claßen, Stav Shtiglitz, Yael Prilutski, Itay Talpir, Lin Tian, Brigitte Kieffer, Jon Davis, Peter Kloppenburg, Marc Tittgemeyer, Yoav Livneh & Henning Fenselau
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The article Dessert stomach emerges in the brain -our source- was published in Max Planck Institute for Metabolism Research website.
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Many thanks Minère et al., Max Planck Institute for Metabolism Research, Science magazine, Peter Stern & Sadaf Farooqi!!!
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Notaspampeanas contact: notaspampeanas@gmail.com
Citation #
Thalamic opioids from POMC satiety neurons switch on sugar appetite
Marielle Minère, Hannah Wilhelms, Bojana Kuzmanovic, Sofia Lundh, Debora Fusca, Alina Claßen, Stav Shtiglitz, Yael Prilutski, Itay Talpir, Lin Tian, Brigitte Kieffer, Jon Davis, Peter Kloppenburg, Marc Tittgemeyer, Yoav Livneh & Henning Fenselau
Science
13 Feb 2025
Vol 387, Issue 6735
pp. 750-758