Brain glucose metabolism in the newborn rat

Tl, Moore; Lione, AP; Regen, DM; Tarpley, HL; Raines, PL

doi:10.1152/ajplegacy.1971.221.6.1746

Cited by 75 publications

(23 citation statements)

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“…The immature brain has a dimin-after induced ketosis (45,46). Indeed, the present findings are ished capacity for glucose uptake from blood and utilization entirely consistent with the original data of Myers and Yamacompared with its adult counterpart (17)(18)(19). Both fetal and guchi (I), which showed improved neurologic outcome of fasted newborn animals use alternate substrates, including lactate, py-monkeys subjected to cardiac arrest compared with either fed or ruvate, and ketone bodies, which supplement glucose to support glucose-infused animals.…”

Section: Discussionsupporting

confidence: 91%

Effect of Insulin-Induced and Fasting Hypoglycemia on Perinatal Hypoxic-Ischemic Brain Damage

et al. 1992

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Section: Discussionsupporting

confidence: 91%

Effect of Insulin-Induced and Fasting Hypoglycemia on Perinatal Hypoxic-Ischemic Brain Damage

et al. 1992

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“…The rats were killed 90 min later. (Preliminary experiments were in agreement with Moore et al (25), establishing that this time allowed stable serum concentrations of both mannitol and 3-0-methylglucose.) The brain uptake of both mannitol and 3-0-methylglucose was increased in rats with meningitis (Table 4).…”

supporting

confidence: 86%

“…Because H. influen zae also contains endotoxin, the dense infection of blood and meninges might result in endotoxin concentrtion high enough to have a pharmacologic effect. In~ddition, the subst~~ti~lly slower utilization of glucose by the infant rat could mmrrmze the effect of any reduction in carrier-mediated tra.nsp?rt (25).…”

Section: Discussionmentioning

confidence: 99%

Brain Carbohydrate Metabolism during Experimental Haemophilus influenzae meningitis

Moxon

1979

Pediatr Res

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SummaryFive-day-old infant rats which acquire Haemophilus intluenzae b bacteremia and meningitis after intranasal inoculation have a transient depression in weight gain (2 days), but then continue to grow at the same rate as strain U-ll inoculated controls. Brain lactate, glucose, and glycogen concentrations increase during the first 5 days of disease in infected animals. The increase in brain glycogen can be accounted for by an influx of glycogen containing polymorphonuclear leukocytes. The increased concentrations of glucose and lactate were found not to be due to a change in brain weight to dry weight ratio or the volume of entrapped blood. The mean cerebrospinal fluid (CSF) glucose concentration was higher in animals with meningitis (2.7 mM) in comparison to U-ll inoculated controls (1.8 mM). This increase in brain and CSF glucose concentration appeared secondary to an increased brain uptake of hexoses as manifested by an increased [3Hlmannitol uptake. Brain lactate accumulation was not explicable from the data available. There was no evidence of cerebral cortical ceUular damage because in vitro oxygen uptake and lactate production were equivalent in control and meningitic animals. The ability of the infant rat brain to maintain cerebral adenosine triphosphate (ATP) content in meningitis and the failure of CSF glucose concentration to decrease might be a reflection of the importance of alternative oxidative substrate (e.g., ,8-hydroxybutyrate) to the cerebral metabolism of the developing rat brain. Speculation iology of postmeningitic central nervous system sequelae is poorly understood.Hypoglycorrachia is observed in patients with pyogenic meningitis. Its mechanism is unclear, but it has been suggested that it results from abnormal cerebral glucose metabolism (23). In dogs with experimental pneumococcal meningitis the passive diffusion of mannitol from blood into CSF was increased 16-fold; however, net facilitated inward diffusion of 3-0-methylglucose was decreased, as was 3-0-methylglucose efflux. The methods used did not permit net balance studies, but the role of the brain in regulating CSF glucose concentration was not excluded. Because hypoglycemia or subarachnoid hemorrhage can be associated with abnormal cerebral glucose metabolism and is associated with permanent neurologic sequelae, we investigated cerebral carbohydrate metabolism in infant rats with H. injluenzae meningitis.These studies utilized an experimental model of H. injluenzae, type b, meningitis in infant rats in which the infection is produced by noninvasive intranasal inoculation of bacteria (27). The occurrence of meningitis can be predicted by the presence of bacteremia 48 hr postinoculation at a density of> 10 4 colony-forming units/rnl (26). In this model the histopathologic characteristics and CSF inflammatory response simulate those occurring in the human (26,27). In addition, postmeningitic survivors show a decreased rate of acquisition of operant conditioning (42) and decreased synaptogenesis and dendritic arborization (5). This...

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“…In rats during the 1st wk of life glucose flux into brain from blood is only about 20% of that in adults (29,30). These data suggest that the concentration of the glucose camer per unit of brain weight is lower in the immature brain, probably as a result of lower capillary density.…”

Section: Discussionmentioning

confidence: 77%

Neonatal Seizures in Monkeys and Rabbits: Brain Glucose Depletion in the Face of Normoglycemia, Prevention by Glucose Loads

Dwyer

Wasterlain

1985

Pediatr Res

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ABSTRACT. Sustained convulsive seizures were induced with bicuculline in newborn rabbits and marmoset monkeys. In both species, seizures were predominantly tonic, with generalized polyspikes on the EEG. Brain glucose concentration fell dramatically during seizures in both species, and in many normoglycemic animals reached levels usually associated with severe hypoglycemia, suggesting that glucose transport from blood to brain could not keep pace with glucose utilization. Glucose loads given to rabbits induced hyperglycemia and during seizures maintained brain glucose well above concentrations needed to saturate hexokinase so that glycolytic rates were probably never limited by substrate availability. Blood and brain lactate concentrations rose during seizures but never reached levels considered cytotoxic. These data suggest that epileptic seizures can deplete brain glucose in normoglycemic neonates of several species, including subhuman primates. (Pediatr Res 19: 992-995,1985) Neonatal status epilepticus in rats can result in death or in stunted brain growth (I). During seizures brain glucose fell in these animals despite normal blood glucose levels (2). If rats were made hyperglycemic by injecting them with an isotonic glucose solution before seizure onset the mortality rate from status epilepticus was reduced by 90% during the 1st wk of life, brain glucose was not depleted and deficits in brain growth were reduced (2). The purpose of this investigation was to determine whether these phenomena are peculiar to the rat or occur in other species including subhuman primates. We have induced generalized seizures with bicuculline, a plant alkaloid, which blocks the postsynaptic inhibitory action of GABA on neuronal firing rates (3). We have shown that continuous seizures can deplete brain glucose in newborn rabbits and marmoset monkeys, in the presence of normal blood glucose concentrations, and that brain glucose depletion in seizing rabbits can be prevented if animals are made hyperglycemic prior to seizure onset. MATERIALS AND METHODSAnimals. Rabbits of either sex (12-24 h old) were purchased from Curd's Caviary and Animal Supply (LaPuente, CA). Marmoset monkeys (Callithrixjacchus) aged 4-7 days were obtained from our breeding colony at the Sepulveda V.A. Medical Center.

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Brain glucose metabolism in the newborn rat

Cited by 75 publications

References 0 publications

Effect of Insulin-Induced and Fasting Hypoglycemia on Perinatal Hypoxic-Ischemic Brain Damage

Effect of Insulin-Induced and Fasting Hypoglycemia on Perinatal Hypoxic-Ischemic Brain Damage

Brain Carbohydrate Metabolism during Experimental Haemophilus influenzae meningitis

Neonatal Seizures in Monkeys and Rabbits: Brain Glucose Depletion in the Face of Normoglycemia, Prevention by Glucose Loads

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