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Better understanding satiety feeling

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Publié le lundi 23 mars 2020

Researchers from the Universities of Burgundy, Paris, and Luxembourg together with other scientists from CNRS, INRA and INSERM groups have just highlighted a mechanism in the brain that led to satiety after a standard meal. It is based on a cascade of events, called neuroglial plasticity, that engages pre-synaptic mechanisms, which do not involve structural remodelling of synapses but retraction of glial coverage. This study, conducted in mice, is published in the renowned journal Cell Reports in March 2020.

Regulation of dietary behaviour

The neuronal circuits that govern the sensations of hunger and satiety in our brain have the ability to modify their connections, allowing us to adjust eating behaviour to living conditions and maintain a balance between energy intake and expenditure. Scientists suspect that this plasticity may be altered in obese subjects.

In a new study conducted in mice, researchers have demonstrated that synaptic plasticity happens at the scale of a meal and likely contributes to short-term control of food intake. However, this activation does not require a change in the "connections" of the circuit.

Key role of POMC neurons

Scientists have focused on the pro-opiomelanocortin (POMC) neurons of the hypothalamus, located at the base of the brain. These neurons are known to control food intake. The electrical activity of POMC neurons is regulated according to the prandial state: a hyperactivity can be detected after a meal. This postprandial hyperactivity of POMC neurons engages presynaptic modifications affecting the excitatory tone applied on these neurons. This phenomenon was already known after high metabolic changes.

In this work, the novelty is that synaptic plasticity can be recapitulated at the timescale of meals in physiological context and day-to-day life in response to subtle metabolic changes. Researchers have observed that this POMC postprandial hyperactivity is not associated with a structural synaptic remodelling but with a structural astroglial plasticity, implicating a cyclic AMP-dependent signalling pathway in astrocytes.

Astrocytes are star-shaped glial cells, known for their role in brain homeostasis and support for neurons. In this work, under normal conditions, it has been detailed that astrocytes closely cover the POMC neurons and act somewhat like brake pads, limiting their activity. After a meal, the blood glucose level (glycemia) rises transiently and this signal is felt by the astrocytes, which retract quickly in less than an hour. When the "brake" is lifted, the POMC neurons are activated, which ultimately promotes a feeling of satiety.

Concerning the in vitro part of this study, primary astrocyte cultures have been performed at the University of Luxembourg by Dr Tony Heurtaux from the Department of Life Sciences and Medicine at the University of Luxembourg and Luxembourg Centre of Neuropathology. This in vitro method validated the effectiveness of a viral construction, used in mice to inhibit cyclic adenosine monophosphate (cAMP) levels in astrocytes. 

Surprisingly, a meal rich in fat does not induce this remodelling. Does this mean that lipids are less effective in cutting hunger? Scientists are trying to determine whether they would not trigger satiety by another circuit. It also remains to be seen whether sweeteners have the same effects or whether they are real lures for the brain, which only provide the addictive sweet sensation without cutting off hunger.

Article: “Postprandial Hyperglycemia Stimulates Neuroglial Plasticity in Hypothalamic POMC Neurons after a Balanced Meal”, Cell Reports, 3 March 2020

Pictures: © Alexandre Benani / CNRS / CSGA