Plasma glucose, immunoreactive somatomedin-C (Sm-C), GH, insulin (IRI) and T3 were measured daily in 20 obese subjects before and during a 9-day fast. Control levels of Sm-C were normal and exhibited no significant correlation with any of the other parameters investigated. During fasting there were no consistent variations in GH, but significant decreases occurred in blood glucose, IRI, T3 and Sm-C levels. While individual Sm-C patterns varied widely, as a group the fasting Sm-C values showed a positive correlation with the fasting IRI and T3 levels, and with control body weight. These findings suggest that the decrease in Sm-C which occurs during caloric deprivation may be the result of concomitant decreases occurring in T3 and IRI levels.
To identify alternative interventions in neonatal hypoxic-ischemic encephalopathy, researchers’ attention has been focused to the study of endogenous neuroprotective strategies. Based on the preconditioning concept that a subthreshold insult may protect from a subsequent harmful event, we aimed at identifying a new preconditioning protocol able to enhance Ca2+-dependent neurogenesis in a mouse model of neonatal hypoxia ischemia (HI). To this purpose, we also investigated the role of the preconditioning-linked protein controlling ionic homeostasis, Na+/Ca2+ exchanger (NCX). Hypoxic Preconditioning (HPC) was reproduced by exposing P7 mice to 20’ hypoxia. HI was induced by isolating and cutting the right common carotid artery. A significant reduction in ischemic damage was observed in mice subjected to 20’ hypoxia followed,3 days later, by 60’ HI, thus suggesting that 20’ hypoxia functions as preconditioning stimulus. HPC promoted neuroblasts proliferation in the dentate gyrus mirrored by an increase of NCX1 and NCX3-positive cells and an improvement of behavioral motor performances in HI mice. An attenuation of HPC neuroprotection as well as a reduction in the expression of neurogenesis markers, including p57 and NeuroD1, was observed in preconditioned mice lacking NCX1 or NCX3. In summary, PC in neonatal mice triggers a neurogenic process linked to ionic homeostasis maintenance, regulated by NCX1 and NCX3.
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