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The sight or smell of something delicious is often enough to put your mouth watering, but the physiological response to the perception of food can go far beyond your salivary glands. New research on mice shows that the sight and smell of food can be enough to revive the liver processes that help digest food. The study appears on November 15 in the newspaper Cell.
"This discovery changes our vision of one of the body's most basic processes," says lead author Jens Brüning, endocrinologist and geneticist and director of the Max Planck Institute for Metabolism Research in Cologne, Germany. "The perception of food in the brain activates the liver so that it starts to get ready to receive the nutrients it expects to receive."
An earlier study published in Cell In 2015, another team of researchers discovered that sensory perception of food by laboratory mice was enough to trigger the neural pathways normally fed by food. In particular, the perception of food-inhibited agRP neurons, which stimulate appetite, and activated POMC neurons, which induce satiety and suppress diet. The new study builds on this research and looks at how changes in these neural pathways send signals that affect the metabolic activities of the liver.
Here, the researchers found that within five minutes after the laboratory mice saw the food, changes in POMC neuron activity were sufficient to induce a rapid signaling cascade that activated the mTOR signaling pathways and XBP1. These pathways are normally activated when the liver absorbs amino acids from digested foods and helps increase the ability of proteins to fold the endoplasmic reticulum (ER), which assembles the amino acid proteins present in foods.
"Our research shows that these changes in the liver occur when mice see and smell food," says Brüning. "It's all a coordinated program to start the emergency system and prepare it for more protein to be synthesized and folded after eating."
The researchers explain that the results of this research could have implications for the links between obesity and diabetes, including examining the effects of protein folding on insulin release. "Obesity could interfere with the priming of the liver depending on the sensory cells. It could be a mechanism that contributes to insulin resistance, "says Brüning. "Obesity can leave the liver poorly prepared for protein folding after eating, which could disrupt the normal response to insulin. This is something we plan to consider in future studies using mouse obesity models. "
Further research is needed before results in mice can be linked to humans. Researchers are currently planning translational studies on insulin sensitivity in human volunteers who are allowed to see and smell, but not eat, food.
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