Glycogen Metabolism in Neonatal Rat Brain During Anoxia and Recovery

Abstract

Metabolic alterations in glycogen and in glycogen-related metabolites were studied in neonatal rat brain during controlled anoxia and recovery. One-day postnatal rats were exposed to 100% N, at 37°C for up to 20 min; some rats were allowed to recover in air. Animals were frozen in liquid N, and the brains were prepared for fluorometric analysis of compounds involved in glycogen turnover. During anoxia, glycogen decreased by 29% and 42% at 10 and 20 min, respectively; the free (soluble) and bound (insoluble) components of glycogen decreased in nearly equal proportions. Brain glucose decreased by 72% at 10 min with little further change thereafter; G-6-P, G-I-P, and UDPG also declined. During recovery from anoxia, glucose and G-6-P increased above control levels for up to 60 min. G-1-P paralleled G-6-P levels, but UDPG remained low. Glycogen returned to control values by 4 h. The findings suggest that although glycogen is mobilized slowly in newborn rat brain, the metabolite contributes at least one-third of the cerebral energy supply during anoxia.Presumably, readily available stores of glycogen combined with low cerebral metabolic requirements underscore the known tolerence of immature animals to hypoxic stress. Glycogen accumulation during recovery appears to be facilitated at the synthetase step, since equilibrium measurements of the phosphoglucomutase and pyrophosphorylase systems indicate that these reactions are not rate-limiting for glycogen synthesis.

Sp1 and Sp3 Regulate Transcriptional Activity of the Facilitative Glucose Transporter Isoform-3 Gene in Mammalian Neuroblasts and Trophoblasts

“…Levels of Sp1 mRNA in cerebral and cerebellar cortex reveal higher levels immediately after birth with a nadir around day 11-20 postnatal age (55). This developmental expression pattern reciprocates the postnatal day 14 to 21 increase in Glut 3 expression, which is noted in negligible amounts prior to this age (3,57). Thus, it is feasible that Sp1 represses Glut 3 in neuronal cells during the different stages of development.…”

Postnatal age influences hypoglycemia-induced neuronal injury in the rat brain

“…A number of factors may be responsible for the relative resistance of the early postnatal brain during hypoglycemia. When compared with the P28 and mature brains, the P7 and P14 brains have lower energy requirement, higher brain glycogen stores, and are capable of efficient transport and utilization of non-glucose energy substrates, such as ketone bodies [22,38]. Moreover, unlike in the adult, insulin does not suppress ketogenesis during hypoglycemia in neonatal rats [43].…”

Glucose Transporter Asymmetries in the Bovine Blood-Brain Barrier

“…␥-glutamyltranspeptidase and System A amino acid transport activity with N-(methylamino)isobutyric acid as substrate, respectively (8). Rat microvessels and vascular-free rat brain membranes were prepared as previously described (15,16).…”

“…␥-glutamyltranspeptidase and System A amino acid transport activity with N-(methylamino)isobutyric acid as substrate, respectively (8). Rat microvessels and vascular-free rat brain membranes were prepared as previously described (15,16).Western Blot-Western blot analysis was performed as previously described (17) and quantified by chemiluminescence and image analysis (18). Human erythrocyte and rat brain membrane samples were included on all blots as internal GLUT1 standards for quantitation.…”