Arcuate nucleus neurons are not essential for the preprandial peak in plasma ghrelin after neonatal monosodium glutamate treatment

Abstract

The aim of the present study was to investigate whether the arcuate nucleus (ARC) was destroyed in mice treated neonatally with monosodium glutamate (MSG), and whether the ARC lesions affect the ghrelin level in the plasma and lipid mobilization in MSG-treated mice. The results revealed that MSG led to a marked reduction in ARC cresyl violet staining, tyrosine hydroxylase-immunoreactive (IR) neurons and neuropeptide Y-IR fibers, compared with saline controls. MSG-treated mice exhibited significantly increased body mass compared with saline controls, and MSG treatment did not prevent food deprivation-induced decrease in white adipose tissue mass compared with controls. Plasma ghrelin levels were significantly increased in MSG-treated mice that were fasted for 48 h, compared with the levels prior to fasting and re-feeding, and the preprandial peak of plasma ghrelin persisted in MSG-treated mice. In summary, the ARC was not found to be essential for food deprivation-induced lipid mobilization and preprandial peak in MSG-treated mice. However, this finding does not mean that ARC neurons do not contribute to food sensing and lipid mobilization under normal conditions, as compensatory mechanisms may have emerged after the ablation of ARC neurons.