Metabolic adaptation at birth.
ABSTRACT After birth, the neonate must make a transition from the assured continuous transplacental supply of glucose to a variable fat-based fuel economy. The normal infant born at term accomplishes this transition through a series of well-coordinated metabolic and hormonal adaptive changes. The patterns of adaptation in the preterm infant and the baby born after intrauterine growth restriction are, however, different to that of a full-term neonate, with the risk for former groups that there will be impaired counter-regulatory ketogenesis. There is much less precise linkage of neonatal insulin secretion to prevailing blood glucose concentrations. These patterns of metabolic adaptation are further influenced by feeding practices.
- SourceAvailable from: Piotr Bregestovski[Show abstract] [Hide abstract]
ABSTRACT: While the ultimate dependence of brain function on its energy supply is evident, how basic neuronal parameters and network activity respond to energy metabolism deviations is unresolved. The resting membrane potential (E(m)) and reversal potential of GABA-induced anionic currents (E(GABA)) are among the most fundamental parameters controlling neuronal excitability. However, alterations of E(m) and E(GABA) under conditions of metabolic stress are not sufficiently documented, although it is well known that metabolic crisis may lead to neuronal hyper-excitability and aberrant neuronal network activities. In this work, we show that in slices, availability of energy substrates determines whether GABA signaling displays an inhibitory or excitatory mode, both in neonatal neocortex and hippocampus. We demonstrate that in the neonatal brain, E(m) and E(GABA) strongly depend on composition of the energy substrate pool. Complementing glucose with ketone bodies, pyruvate or lactate resulted in a significant hyperpolarization of both E(m) and E(GABA), and induced a radical shift in the mode of GABAergic synaptic transmission towards network inhibition. Generation of giant depolarizing potentials, currently regarded as the hallmark of spontaneous neonatal network activity in vitro, was strongly inhibited both in neocortex and hippocampus in the energy substrate enriched solution. Based on these results we suggest the composition of the artificial cerebrospinal fluid, which bears a closer resemblance to the in vivo energy substrate pool. Our results suggest that energy deficits induce unfavorable changes in E(m) and E(GABA), leading to neuronal hyperactivity that may initiate a cascade of pathological events.Journal of Neurochemistry 11/2009; 112(4):900-12. DOI:10.1111/j.1471-4159.2009.06506.x · 4.24 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: ZusammenfassungDieser Artikel beschreibt die Pathophysiologie des Glukosemetabolismus des Neugeborenen von Müttern mit diabetischer Stoffwechsellage, klinische Zeichen der diabetischen Fetopathie und der Hypoglykämie des Neugeborenen, das klinisch-praktische Vorgehen der postpartalen Blutzuckermessung und Definition der Hypoglykämie sowie die Prophylaxe und Therapie der postpartalen Hypoglykämie. Aufgrund einer möglichen deutlichen Beeinträchtigung der vor allem mentalen Entwicklung in den ersten Lebensjahren nach unmittelbar postpartalen rezidivierenden Hypoglykämien mit oder ohne Symptomen in der Risikogruppe sind regelmässige Blutzuckermessungen am ersten Lebenstag angezeigt. Ein postpartales Schema zur Blutzuckermessung und Therapie findet sich am Ende der Ausführungen.Gynäkologisch-geburtshilfliche Rundschau 01/2009; 49(4):271-276. DOI:10.1159/000301087
Article: Fueling brain neuronal activity[Show abstract] [Hide abstract]
ABSTRACT: The energy requirements of the brain are amazingly high. The brain represents about 2% of the body weight, but it receives 15% of the total blood flow provided by the cardiovascular system and consumes at least 25% circulating glucose plus 20% oxygen available in the body at rest. The cornerstone feature of the brain energy metabolism is its tight coupling with neuronal activity. An abnormality in the sequence of events allowing neurons to be adequately supplied with the necessary energy could have dramatic consequences exemplified in the neurodegenerative diseases such as epilepsy and Alzheimer’s disease. In this paper, we review the current views on the main pathways of neuronal energy supply.Biochemistry (Moscow) Supplement Series A Membrane and Cell Biology 04/2012; 6(2). DOI:10.1134/S1990747812010175