Eine Methode der Gewebsumströmung für Fluorescenzmessungen

Panten, U.; Ri, H. dal; Poser, W.; Hasselblatt, A.

doi:10.1007/bf00586569

Cited by 14 publications

(9 citation statements)

References 8 publications

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“…Both G6P and FDP rose significantly before there was any sign of stimulated secretion. This result is consistent with the demonstration of a prompt increase of reduced nicotinamide dinucleotides after exposing islets of ob/ob-mice to a sudden rise of the peri-insular glucose concentration [25,26]. Somewhat conflicting results have been presented by Matschinsky et al [27], who reported that the islet concentration of G6P or 6-phosphogluconate did not rise until 5 min after the in vivo administration of glucose to rats.…”

Section: Discussionsupporting

confidence: 90%

Dynamics of pancreatic ?-cell responses to glucose

Idahl

1973

Diabetologia

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5iicroperifusion was used to study the dynamics of insulin release and metabolic changes in pancreatic islets microdissected from ob/ob-miee. When the islets were suddenly exposed to a high glucose eonccntxation, their content of glucose-6-phosphate and fructose-1, 6-diphosphate started to rise immediately, whereas a secretory response was not observed until after about 80 see. This is consistent with the hypothesis that glucose metabolism initiates insulin release. Fasting the donor animMs for 18 h reduced the initial phase of glucosestimulated release but left the rise of gtucose-6-phosphate, as well as the late phase of sustained' release, unaffected. The use of a tissue culture meditml (TCM 199) instead of Krebs-Ringer bicarbonate buffer as the basal medium increased the secretory responses to glucose, particularly the initial phase, both in islets from fed and fasted mice. However, the difference between fed and fasted mice remained. Theophylline did not restore the impaired initial secretory response after fasting. The responses of islet fruetose-l,6-diphosphate and adenosine-5-triphosphate to glucose depended on the nutritional state of the animals and on the type of basal medium. No consistent correlation was observed between the changes of these substrates and the dynamics of insulin release.

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Section: Discussionsupporting

confidence: 90%

Dynamics of pancreatic ?-cell responses to glucose

Idahl

1973

Diabetologia

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“…Our previous work (Dean & Matthews, 1972) has shown that to remain an effective stimulant D-glyceraldehyde requires an intact NAD+/NADH redox system, for the electrical activity elicited by glyceraldehyde (and by glucose) is obliterated by streptozotocin, a diabetogenic agent which severely reduces NAD levels in islet cells (Schein, Cooney, McMenamin & Anderson, 1973). Furthermore, glucose metabolism in islet cells is normally associated with a very rapid and marked increase in reduced pyridine nucleotides (Panten, Dal Ri, Poser & Hasselblatt, 1971) which is not seen in the absence of Ca2+. It seems therefore more than mere coincidence that it is the conversion of glyceraldehyde-3-phosphate to 1 ,3-diphosphoglycerate by glyceraldehyde-3-phosphate dehydrogenase which is responsible for the reduction of NAD+ in the glycolytic pathway.…”

Section: Discussionmentioning

confidence: 99%

Pancreatic islet cells: effects of monosaccharides, glycolytic intermediates and metabolic inhibitors on membrane potential and electrical activity.

Dean¹,

Matthews²,

Sakamoto³

1975

The Journal of Physiology

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SUMMARY1. The effects of monosaccharides, glycolytic intermediates, metabolic inhibitors and anoxia, have been studied on the membrane electrical activity of mouse pancreatic islet cells in vitro using a single intracellular micro-electrode for both voltage recording and current injection. 4. Electrical activity induced by D-glucose 28 mm, was progressively inhibited by phloridzin, 10 mm, if the cells were exposed to D-glucose and inhibitor simultaneously, and abolished on pretreatment with inhibitor for 30-60 min. Phloridzin also caused depolarization of the islet cells which was independent of extracellular glucose.5. Anoxia completely blocked the electrical activity induced by glucose but not that evoked by D-glyceraldehyde, L-leucine, tolbutamide or glibenclamide.6. Jodoacetic acid, 5 mm, rapidly blocked glucose-induced electrical activity whilst that elicited by tolbutamide was relatively resistant to inhibition. 7. The nature and possible location of the glucoreceptor in pancreatic

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“…Perifusion at 85 91/rain and ~ 36 ~ was performed as described [11]. The medium consisted of Krebs-Ringer bicarbonate buffer.…”

Section: Perifusion Of Pancreatic Isletsmentioning

confidence: 99%

Effect of carbohydrates upon fluorescence of reduced pyridine nucleotides from perifused isolated pancreatic islets

et al. 1973

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In perifused pancreatic islets, the fluorescence of reduced pyridine nucleotides (NAD(P)H) was measured continuously. Elevation of glucose concentration in the medium from 0-5 mM to 20 mlVl led to an increase in l~AD(P)H-fluorescence beginning 10-20 sec after change of medium. Perifusion with calcium-free media had no influence on this effect. It was, however, partially or completely blocked by 2-deoxy D-glucose, D-glucosamine, or D-mannoheptulose. D-mannose, but not D-fructose and L-lactate, enhanced ~qAD(P)I-I-fluorescence from pancreatic islets. Pyruvate caused but a small fluorescence increase. From these observations it is concluded that D-glucose leads to the increase of NAD(P)I-i-fluorescence by mediation of the phosphoglyceraldehyde dehydrogenase reaction.

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Eine Methode der Gewebsumströmung für Fluorescenzmessungen

Cited by 14 publications

References 8 publications

Dynamics of pancreatic ?-cell responses to glucose

Dynamics of pancreatic ?-cell responses to glucose

Pancreatic islet cells: effects of monosaccharides, glycolytic intermediates and metabolic inhibitors on membrane potential and electrical activity.

Effect of carbohydrates upon fluorescence of reduced pyridine nucleotides from perifused isolated pancreatic islets

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