Pancreatic β-Cell Function and Content of 6-Phosphogluconate

Idahl, L; Hurme, P.; Wahlquist, Ylva; Hellman, Bo

doi:10.1055/s-0028-1094164

Cited by 10 publications

(3 citation statements)

References 3 publications

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“…With 6-phosphogluconate content exactly the converse is true; there is no rise in 6-phosphogluconate in the fed state but almost a three-fold increase in the starved state. This lack of correlation of 6-phosphogluconate concentration with insulin release agrees with the results of Idahl et al (1971), who showed that the addition of adrenaline to or omission of Ca2+ from a high-glucose medium (both experimental conditions that inhibit insulin release) gave a significant elevation of the islet 6-phosphogluconate content.…”

Section: Discussionsupporting

confidence: 90%

The pentose cycle and insulin release in isolated mouse pancreatic islets during starvation

Hedeskov

Capito

1975

Biochemical Journal

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When islets from mice were incubated with 16.7 mM-glucose, previous starvation for 48 h decreased the rate of insulin release by approx. 50% and glucose utilization was decreased by approx. 35%. The maximally extractable activity of glucose 6-phosphate dehydrogenase was diminished by 28% after starvation. The formation of 14CO2 from both [1-14C]glucose was, however, higher than the rate of oxidation of [6-14C]-glucose in islets from both fed and starved mice. The fraction of glucose utilized that was oxidized (specific 14CO2 yield) ranged from one-fifth to one-third and was higher in islets from starved mice with both [1-14C]glucose and [6-14C]glucose as substrate. The contribution of pentose-cycle oxidation to total glucose metabolism was small (3% in the fed state and 4% in the starved state). The absolute rates of glucose carbon metabolism via the pentose-cycle oxidation to total glucose metabolism was small (3% in the fed state and 4% in the starved state). The absolute rates of glucose carbon metabolism via the pentose cycle and the turnover of NADPH in this pathway were identical in islets from fed and starved animals. After incubation at 16.7 mM-glucose for 30 min the contents of glucose (6-phosphate and 6-phosphogluconate were both unchanged by starvation. It is concluded that there is no correlation between the decreased sensitivity of the insulin secretory mechanism during starvation and the metabolism of glucose via the pentose cycle, the islet content of glucose 6-phosphate or 6-phosphogluconate.

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Section: Discussionsupporting

confidence: 90%

The pentose cycle and insulin release in isolated mouse pancreatic islets during starvation

Hedeskov

Capito

1975

Biochemical Journal

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“…The curve relating glucose-utilization rate to glucose concentration was similar in shape to those described for a number of other glucose-sensitive parameters 1972 of islets, e.g. glucose oxidation rate and islet glucose 6-phosphate concentration , insulin release (Malaisse et al, 1967), islet 6-phosphogluconate concentration (Montague & Taylor, 1970;Idahl et al, 1971) and the incidence of fl-cell membrane action potentials (Dean & Matthews, 1970). The only other published values for the rate of glucose utilization by mammalian islets are those of Snyder et al (1970), who measured glucose uptake by isolated rat islets at 3.3 and 16.7mM extracellular glucose: the rates of 25 and 130pmol/h per islet calculable from their results are comparable with the rates of 19 and 89pmol/h per islet at these two glucose concentrations obtained in the present study (Fig.…”

Section: Glucose Utilization By Mouse Isletssupporting

confidence: 61%

The pentose cycle and insulin release in mouse pancreatic islets

Ltd¹

1972

Biochemical Journal

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“…Previous use of this nucleotide in the same experimental system induced a significant decrease in the amount of glycogen but no alteration in the levels of fructose-1,6-diphosphate or 6-phosphogluconate [Hellman, 1970b;Idahl and Hellman, 1971;. These results might indicate that the effect of dibutyryl cyclic 3,5-AMP on the carbohydrate metabolism of the /9-cells is essentially restricted to glycogen turnover.…”

Section: Discussionmentioning

confidence: 48%

Glucose-6-Phosphate Content in Mammalian Pancreatic β-Cells

Idahl¹

1971

Horm Res Paediatr

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Glucose-6-phosphate was measured in microdissected pancreatic islets obtained from obese-hyperglycemic mice. Exposure of the islets in a low glucose medium to the hypoglycemic sulfonylurea compound glibenclamide resulted in a significant decrease of glucose-6-phosphate. This effect might be due to uncoupling of the oxidative phosphorylation leading to an accelerated glycolytic rate. Under the same experimental conditions another stimulator of insulin release, dibutyryl cyclic 3,5-AMP, induced a slight increase in glucose-6-phosphate. Inhibition of the glucose-induced insulin release by epinephrine, diazoxide or omission of Ca^{+ +} resulted in considerably elevated islet levels of glucose-6-phosphate. A reduced availability of Ca^{+ +} may be a common denominator forthis effect on glucose-6-phosphate.

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Pancreatic β-Cell Function and Content of 6-Phosphogluconate

Cited by 10 publications

References 3 publications

The pentose cycle and insulin release in isolated mouse pancreatic islets during starvation

The pentose cycle and insulin release in isolated mouse pancreatic islets during starvation

The pentose cycle and insulin release in mouse pancreatic islets

Glucose-6-Phosphate Content in Mammalian Pancreatic β-Cells

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