Central administration of prolactin-releasing peptide shifts the utilities of metabolic fuels from carbohydrate to lipids in chicks

- Central administration of prolactin-releasing peptide stimulates feeding behavior in chicks.
- Prolactin-releasing peptide decreases respiratory quotient.
- Plasma glucose and insulin concentrations are decreased by prolactin-releasing peptide.
- Prolactin-releasing peptide might be related to glucose and lipid metabolism in the brain of chicks.

We have recently identified prolactin (PRL)-releasing peptides (PrRPs) and their stimulating effects on feeding behavior in chicks. To investigate further metabolic functions of PrRP, the present study was performed to clarify whether intracerebroventricular (ICV) injection of PrRP31, an active form of PrRP in chicks, affects heat production (HP), respiratory quotient (RQ) and plasma concentrations of metabolic fuels in chicks. The ICV injection of PrRP31 (94 and 375 pmol) did not affect HP but significantly lowered RQ. The change in RQ implies that PrRP31 shifted the utility of metabolic fuels in the body. This idea was confirmed by subsequent results in which ICV injection of PrRP31 significantly reduced glucose but increased non-esterified fatty acid concentrations in plasma. These shifts in blood metabolic fuels would not be through the increased plasma insulin, because the ICV injection of PrRP31 significantly decreased plasma insulin concentration. On the other hand, ICV injection of another orexigenic peptide, neuropeptide Y (NPY) also induced the insulin release and the metabolic effects were similar to those of PrRP31. Because ICV injection of PrRP31 increased NPY mRNA in the diencephalon, the NPY may mediate the metabolic functions of PrRP31. In summary, the present study suggests that central PrRP31 shifts the utilities of peripheral energy sources, which is not via hyperinsulinemia but via the diencephalon.