Hypoglycemia
Malaria infantile: zucchero per l'ipoglicemia
La somministrazione di zucchero per via sublinguale è paragonabile a quella di glucosio per via endovenosa nella correzione dell'ipoglicemia associata alle forme gravi di malaria infantile. L'ipoglicemia infatti non è soltanto un indicatore della gravità della malattia, ma è anche un fattore prognostico negativo nel bambino: nelle zone rurali delle aree scarsamente sviluppate le infusioni endovenose sono raramente disponibili per via della mancanza di equipaggiamenti e di personale addestrato. Lo zucchero però può essere degradato dagli enzimi della cavità orale, e successivamente il glucosio può essere trasportato attraverso la mucosa. Se questa semplice misura venisse adottata come procedura d'emergenza in attesa della somministrazione endovenosa di glucosio, essa potrebbe salvare molte vite. (Malaria J online 2008, pubblicato il 12/12)
Hypoglycemia may be counteracted by:
Biochim Biophys Acta. 1985 May 29;840(1):37-42.
Interleukin 1-like factors can accumulate 5-hydroxytryptamine in the liver of mice and can induce hypoglycaemia. 1985
Endo Y, Suzuki R, Kumagai K.
Abstract
After the injection into mice of culture medium of P388D1 cells, a murine macrophage cell line, 5-hydroxytryptamine accumulated in the liver and blood glucose declined. The factors capable of inducing these responses were purified by gel filtration and chromatofocusing. With these procedures, the activity to induce the increase in 5-hydroxytryptamine in the liver accompanied the activity to induce hypoglycaemia. Moreover, through the purification, the factors were found in the fraction of interleukin 1, a lymphocyte-activating factor. These results suggest that the factors capable of inducing the increase in 5-hydroxytryptamine and hypoglycaemia are likely to be interleukin 1 molecules or molecules closely related to interleukin 1. The present and previous findings together with those in the literature support the idea that the increase in 5-hydroxytryptamine in the liver might be a cause of hypoglycaemia. These findings may provide new and important information about the roles of macrophages in inflammation or in immune responses.
Am J Physiol. 1989 Aug;257(2 Pt 1):E269-76.
Fuel-mediated teratogenesis: biochemical effects of hypoglycemia during neurulation in mouse embryos in vitro. 1989
Hunter ES 3rd, Sadler TW.
Department of Cell Biology and Anatomy, School of Medicine, University of North Carolina, Chapel Hill 27599.
Abstract
Hypoglycemia has been reported to induce congenital malformations and growth retardation in rodent embryos during the period of neural tube closure in vitro. However, the biochemical alterations responsible for the production of the dysmorphogenic effects have not been evaluated. Therefore, the rates of glucose metabolism by glycolysis, citric acid cycle, oxidative pentose phosphate pathway (PPP), and anabolic utilization were evaluated in mouse embryos and extraembryonic membranes using the whole embryo culture technique. Altered glucose metabolism by glycolysis and oxidative PPP, as well as altered anabolic synthesis, were produced by exposure to hypoglycemia. In embryos exposed to mild hypoglycemia (80 mg/dl) altered metabolism by the PPP and an associated effect on nucleic acid synthesis were in part responsible for the dysmorphogenic effects of this treatment. In contrast, severe hypoglycemia (40 mg/dl) appeared to have an immediate effect on glycolytic metabolism in addition to effects on the PPP and nucleic acid synthesis. Therefore, a multifactorial biochemical mechanism contributes to the induction of malformations by severe hypoglycemia in mouse embryos in vitro. Furthermore, the differential effects of moderate vs. severe hypoglycemia on glycolytic metabolism, and possibly energy production, may account for the differences in the severity of these treatments on embryonic growth and the incidence of malformations.
A hypothesis linking hypoglycemia, hyperuricemia, lactic acidemia, and reduced gluconeogenesis in alcoholics to inactivation of glucose-6-phosphatase activity by acetaldehyde. 1996
