A brain-derived insulin signal encodes protein satiety for nutrient-specific feeding inhibition

Cell Rep. 2024 Jun 25;43(6):114282. doi: 10.1016/j.celrep.2024.114282. Epub 2024 May 24.

Abstract

The suppressive effect of insulin on food intake has been documented for decades. However, whether insulin signals can encode a certain type of nutrients to regulate nutrient-specific feeding behavior remains elusive. Here, we show that in female Drosophila, a pair of dopaminergic neurons, tritocerebrum 1-dopaminergic neurons (T1-DANs), are directly activated by a protein-intake-induced insulin signal from insulin-producing cells (IPCs). Intriguingly, opto-activating IPCs elicits feeding inhibition for both protein and sugar, while silencing T1-DANs blocks this inhibition only for protein food. Elevating insulin signaling in T1-DANs or opto-activating these neurons is sufficient to mimic protein satiety. Furthermore, this signal is conveyed to local neurons of the protocerebral bridge (PB-LNs) and specifically suppresses protein intake. Therefore, our findings reveal that a brain-derived insulin signal encodes protein satiety and suppresses feeding behavior in a nutrient-specific manner, shedding light on the functional specificity of brain insulin signals in regulating behaviors.

Keywords: CP: Neuroscience; brain insulin signals; dopaminergic neurons; feeding inhibition; protein satiety.

MeSH terms

  • Animals
  • Brain / metabolism
  • Dopaminergic Neurons / metabolism
  • Drosophila Proteins* / metabolism
  • Drosophila melanogaster / metabolism
  • Feeding Behavior
  • Female
  • Insulin* / metabolism
  • Nutrients / metabolism
  • Satiety Response
  • Signal Transduction*

Substances

  • Drosophila Proteins
  • Insulin