Starved mice had a greater preference for sweetness and a decreased sensitivity to aversive tastes, said researchers.

TOP INSIGHT
During hunger not only does food taste sweeter when our stomachs are rumbling, but bitter food also becomes less difficult to eat, scientists have revealed that these effects are moderated by a neural circuit in the hypothalamus.
Optogenetic and chemogenetic techniques are popular methods for studying neuronal activity because they can manipulate neural activity very precisely. Optogenetics introduces light-sensitive agents into target neurons, whose activity can then be manipulated by light, and chemogenetics introduces designer receptors to affect the target neurons' activity by their specific synthetic ligands.
After AgRP-expressing neuron activation, downstream glutamate neurons in the lateral hypothalamus in turn modulated mice's taste preferences via two different pathways. Glutamate neurons projecting to the lateral septum increased the preference for sweet tastes, and those projecting to the lateral habenula decreased the sensitivity to bitter tastes.
"The next steps will be to investigate whether these hypothalamic neuronal pathways are altered in pathophysiological conditions such as diabetes and obesity," says Yasuhiko Minokoshi, co-author of the study. "For example, we already know that people with obesity have a strong preference for sweetness; this might be associated with a change in the activity of the glutamate neurons projecting to the lateral septum."
These new findings could therefore provide the groundwork for the future development of methods to control taste preferences, which would have significant health benefits. However, much work remains to be done before this becomes a reality.
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