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R Staudt

Publications and source records attributed to R Staudt.

6 recordsLinked to original sources

Increased cerebral glucose utilization and decreased glucose transporter Glut1 during chronic hyperglycemia in rat brain.

Whereas acute hyperglycemia has been shown to result in an unchanged local cerebral glucose utilization (LCGU) the changes of LCGU during chronic hyperglycemia are a matter of dispute. The present study had three aims: (1) To compare the effects of acute and chronic hyperglycemia on LCGU and to investigate in vivo the lactate level as a potential indicator of glycolytic flux. (2) To investigate local changes in brain Glut1 and/or Glut3 glucose transporter densities during chronic hyperglycemia. (3) To analyze the relationship between LCGU and local Glut densities during chronic hyperglycemia. To induce chronic hyperglycemia in rats steptozotocin was given i.p. and experiments were performed 3 weeks later. LCGU was measured by the 2-[14C]deoxyglucose method and intraparenchymal lactate concentration by MR-spectroscopy. Local densities of the glucose transport proteins were determined by immunoautoradiographic methods. During chronic hyperglycemia weighted average of LCGU increased by 13.9% whereas it remained unchanged during acute hyperglycemia. The cerebral lactate/choline ratio was increased by 143% during chronic hyperglycemia. The average density of glucose transporters Glut1 decreased by 7.5%. Local densities of Glut1 were decreased in 12 of 28 brain structures. Glut3 remained unchanged. Positive correlations were found between LCGU and local Glut densities during control conditions and during chronic hyperglycemia. It was concluded that (1) Chronic, but not acute hyperglycemia is followed by an increased LCGU. (2) The capacity to transport glucose is decreased during chronic hyperglycemia. (3) Increased LCGU and decreased densities of Glut1 are matched on a local level.

Animals↗

Increase in glucose transporter densities of Glut3 and decrease of glucose utilization in rat brain after one week of hypoglycemia.

The present study addresses the question whether a chronic decrease of plasma glucose concentration for 1 week induces a global or local increase in glucose transporter densities Glut1 and Glut3 in the brain. To induce chronic hypoglycemia insulin was infused into rats by osmotic minipumps for 1 week resulting in a mean plasma glucose concentration of 3.1+/-0.5 mmol/l (control group: 8.1+/-0.5 mmol/l). Global and local densities of Glut1 and Glut3 glucose transporters were measured by immunoautoradiographic methods. The mean density of glucose transporters Glut1 remained unchanged, whereas the mean density of Glut3 increased slightly, although significantly. To determine whether the increased density of Glut3 is related to a change in glucose metabolism, the local cerebral metabolic rate of glucose (lCMR(glc)) was quantified by the 2-deoxyglucose method. Mean glucose utilization was decreased by 15%. Local analysis of transporter densities (Glut1 and Glut3) and glucose utilization showed a significant correlation between local glucose transporter densities (Glut1 and Glut3) and lCMR(glc) during hypoglycemia as already previously observed during normoglycemia. It is concluded that 1 week of hypoglycemia is a stimulus for the induction of additional glucose transporters Glut3 in the brain. These additional neuronal glucose transporters may support the maintenance of glucose utilization which is not completely maintained under these conditions.

Acute Disease↗

Increase of glucose transporter densities (Glut1 and Glut3) during chronic administration of nicotine in rat brain.

Chronic infusion of nicotine is known to result in a distinct pattern of increases in local cerebral glucose utilization (LCGU). The present study addresses the question whether this increase in LCGU is paralleled by (1) a local increase in Glut1 and/or Glut3 glucose transporter densities and (2) a local increase in capillary density in the brain. Nicotine was infused by osmotic minipumps for one week. In cryosections of rat brains local densities of Glut1 (vascular) and Glut3 (neuronal) glucose transporters were measured by immunoautoradiographic methods whereas local capillary densities were determined by an immunofluorescent method. Densities of glucose transporters Glut1 and Glut3 were increased in 12 of the 27 structures investigated. Glut1 was elevated in four additional structures and Glut3 in two more structures. Comparison of the changes in transporter densities with the changes of LCGU measured in a previous study during chronic nicotine infusion showed that LCGU was also elevated in most of these structures. In contrast, capillary density remained unchanged in all structures investigated. It is concluded that one week of nicotine infusion is sufficient to raise the densities of Glut1 and Glut3 glucose transporters predominantly in those structures in which LCGU is elevated. The unchanged capillary density under these conditions indicates an increased density of Glut1 transporters per capillary.

Animals↗

Local transport kinetics of glucose during acute and chronic nicotine infusion in rat brains.

Acute and chronic infusion of nicotine is known to result in a distinct increase in local cerebral glucose utilization (LCGU) in several brain structures. The present study addresses the question whether this increase in LCGU is paralleled by a local change in glucose transport in rat brain. Nicotine was infused either acutely for 3 hours or chronically by osmotic minipumps for one week. Local rate constants for glucose transport were measured in brain cryosections using the 3-O-[14C]methylglucose method. Local rate constants K1 and k2 were lower in part of the brain structures during acute (-10% to -20%) and in nearly all structures during chronic (-39% to -41%) nicotine. The finding of a decreased glucose transport during chronic nicotine was confirmed by additional experiments of 3-O-[14C]methylglucose transfer in an epithelial cell culture. It is concluded that acute and chronic nicotine infusion results in decreased glucose transport although LCGU is either unchanged or increased.

3-O-Methylglucose↗

Chondroectodermal dysplasia (Ellis--van Creveld syndrome) with dysplasia of renal medulla and bile ducts.

A case of a 28-month-old boy with chondroectodermal dysplasia (Ellis-van Creveld syndrome) is reported. Besides polydactyly, ectodermal dysplasia, acromelic dwarfism and congenital heart defect, which are characteristic morphologic features of the syndrome, additional dysplastic developmental defects were discovered in the kidneys, liver, and lungs. Detailed histopathologic studies of the growth plates of tibia, femur and ribs disclosed an irregular, partly hyperplastic, partly dystrophic appearance of the epiphyseal cartilage, which was not resorbed properly by the invading blood vessels. Focal areas of necrosis occurred and barriers of tongue-shaped cartilaginous peninsulas persisted. Regular enchondral ossification was hindered and compensatory membrane ossification was found in the fibrosing metaphyseal bone marrow adjacent to the cartilage. Dysplasia and fibrosis of the renal medulla plus interstitial fibrosing nephritis in the cortex resulted in kidney contraction and renal failure. Hepatomegaly, portal fibrosis and bile duct hyperplasia and dysplasia were detected at autopsy, but did not have any clinical significance. These findings once again emphasize that derivatives of all three germ layers are involved in the Ellis-van Creveld syndrome. The possibility that a single metabolic or structural abnormality of the mesenchymal tissues could be responsible for the various organ dysplasias is discussed.

Bile Ducts↗

[Poliomyelitis epidemic in a district of Freiburg i. Br. in autumn 1975 (author's transl)].

In the autumn of 1975 five cases of poliomyelitis occurred within 6 weeks in German children of families of low socioeconomic class. They lived in two districts of Freiburg with close familial and occupational contacts. One child had been immunised against polio once orally several years ago and none of the others were immunised. The clinical course and results of investigations of the environment are reported. Included is the state of immunisation of 472 school beginners in Freiburg schools and the antibody levels of 284 children aged 1 to 10 years from Freiburg and the adjoining areas.

Adolescent↗