| First Author | Li QC | Year | 2018 |
| Journal | Int J Mol Med | Volume | 41 |
| Issue | 3 | Pages | 1635-1642 |
| PubMed ID | 29328403 | Mgi Jnum | J:273727 |
| Mgi Id | MGI:6282453 | Doi | 10.3892/ijmm.2018.3365 |
| Citation | Li QC, et al. (2018) Arcuate nucleus neurons are not essential for the preprandial peak in plasma ghrelin after neonatal monosodium glutamate treatment. Int J Mol Med 41(3):1635-1642 |
| abstractText | The aim of the present study was to determine whether arcuate nucleus (ARC) lesions affect the ghrelin level in the plasma and the stomach in monosodium glutamate (MSG)treated mice. The aim of the present study was to investigate whether the ARC was destroyed in mice treated neonatally with MSG, and whether the ARC lesions affect the ghrelin level in the plasma and lipid mobilization in MSGtreated mice. The results revealed that MSG led to a marked reduction in ARC cresyl violet staining, tyrosine hydroxylase-immunoreactive (IR) neurons and neuropeptide YIR fibers, compared with saline controls. MSGtreated mice exhibited significantly increased body mass compared with saline controls, and MSG treatment did not prevent food deprivationinduced decrease in white adipose tissue mass compared with controls. Plasma ghrelin levels were significantly increased in MSGtreated mice that were fasted for 48 h, compared with the levels prior to fasting and refeeding, and the preprandial peak of plasma ghrelin persisted in MSGtreated mice. In summary, the ARC was not found to be essential for food deprivationinduced lipid mobilization and preprandial peak in MSGtreated 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. |
