Avtor/Urednik | Battelino, Tadej | |
Naslov | Neurejenost presnove glukoze in spremembe mRNA za glukozne prenašalce pri modelu neonatalnega endotoksičnega šoka | |
Prevedeni naslov | Glucose metabolism dyshomeostasis and changes in glucose transporter mRNA abudance in a model of neonatal endotoxic shock | |
Tip | monografija | |
Kraj izdaje | Ljubljana | |
Založnik | Medicinska fakulteta | |
Leto izdaje | 1996 | |
Obseg | str. 101 | |
Jezik | slo | |
Abstrakt | Newborns with shock are prone to develop hypoglycemia. Glucose dyshomeostasis due to endotoxic was investigated on a model of 10 day old rats. measurements of 14C-2-deoxyglucose showed increased peripheral glucose uptake in the euglycemic phase of endotoxic shock, which contributed to the development of hypoglycemia. Increased glucose uptake was not accompanied by an icrease of plasma insulin concentration, which suggested differences in regulation of glucose metabolism in newborn rats compared to adult rats. Messenger RNA abundance of the ubiquitous glucose transporter GLUT 1 incrased concomitantly with the incrased glucose uptake, especially in liver and fat tissue. In the liver, GLUT 1 mRNA abudance increased both in the hepatocytes and the non-parenchymal cells. Messenger RNA abundance of tissue specific glucose transporters GLUT 2 and GLUT 4, which are not predominant in 10 day old rats, did not change significantly. Phosphoenolpyruvate carboxykinase (PEPCK) mRNA abudance was decreased suggesting decresed gluconeogenesis. Growth hormone (GH) was investigated in the hypoglycemic phase of endotoxic chock. Plasma GH concentration as well as pituitary GH mRNA abudance were decreased. Further on, TNF alpha effects on glucose homeostasis were shown to be comparable to those of endotoxin, proving TNF alpha to be an important mediator of glucose metabolism alterations in endotoxic shock, TNF alpha also caused an increase in GLUT 1 and a decrease in PEPCK mRNA abundance. TNF alpha induced changes in glucose homeostasis were attenuated by a ciclooxygenase inhibitor indomethacin, implying the role of prostaglandins. | |
Deskriptorji | SHOCK, SEPTIC RNA, MESSENGER HYPOGLYCEMIA RATS ANIMALS, NEWBORN DISEASE MODELS, ANIMAL DEOXYGLUCOSE INSULIN MONOSACCHARIDE TRANSPORT PROTEINS SOMATOTROPIN TUMOR NECROSIS FACTOR INDOMETHACIN DEXAMETHASONE LIPOPOLYSACCHARIDES SALMONELLA ENTERITIDIS |