scholarly journals The metabolism of lipids in mouse pancreatic islets. The biosynthesis of triacylglycerols and phospholipids

1975 ◽  
Vol 152 (3) ◽  
pp. 667-673 ◽  
Author(s):  
C Berne
Keyword(s):  
B Cells ◽  
Pancreatic Islets ◽  
Glucose Concentration ◽  
Secretory Granules ◽  
Phospholipid Biosynthesis ◽  
Glucose Carbon ◽  
Glucose Incorporation ◽  
Extracellular Glucose ◽  
Mouse Pancreatic Islets ◽  
Total Glucose

The rate of incorporation of [U-14C]glucose and [u-14C]palmitate into the lipids of the pancreatic islets of obese-hyperglycaemic mice was examined. The following main observations were made. 1. Both glucose and palmitate were incorporated into lipids in the islets. The fraction of glucose utilized for lipid biosynthesis was calculated to be 3-6% of that oxidized at high and low glucose concentrations, whereas palmitate was about equally divided between oxidation and esterification into lipids. 2. Glucose was primarily incorporated from sn-glycerol 3-phosphate. Of the total glucose carbon incorporated, only 2-4% was recovered as fatty acids. 3. A major portion of both glucose and palmitate was incorporated into phospholipids, whereas 10-30% went into triacylglycerols, depending on the extracellular glucose concentrations. 4. An increase in the glucose concentration from 3.5 to 17 mM caused a twofold increase in the rate of glucose incorporation into triacylglycerols and a fivefold increase in the rate of incorporation into phospholipids. Similar effects were also obtained with normal mouse islets. Palmitate was also preferentially directed into phospholipids by an increased glucose concentration. 5. Islets pre-labelled with radioactive palmitate showed a decrease in triacylglycerol radioactivity when they were subsequently incubated in the absence of exogenous sources of energy. 6. Mannoheptulose inhibited the rate of glucose incorporation into phospholipids, whereas omission of Ca2+ and adrenaline left phospholipid biosynthesis unimpaired. The results suggest that pancreatic B-cells have the capacity to store and utilize energy in the form of triacylglycerols. A stimulation of the B-cells by glucose is followed by an increased rate of phospholipid biosynthesis. However, this does not seem to be directly linked to the release of secretory granules.

scholarly journals Long-term effects of glucose on insulin release and glucose oxidation by mouse pancreatic islets maintained in tissue culture

1974 ◽  
Vol 140 (3) ◽  
pp. 377-382 ◽  
Author(s):  
Arne Andersson
Keyword(s):  
Tissue Culture ◽  
B Cells ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
High Glucose ◽  
Glucose Concentration ◽  
Glucose Oxidation ◽  
Extracellular Glucose Concentration ◽  
Extracellular Glucose ◽  
Mouse Pancreatic Islets

Rates of glucose oxidation and insulin release in response to a wide range of glucose concentrations were studied in short-term experiments in isolated mouse pancreatic islets maintained in tissue culture for 6 days at either a physiological glucose concentration (6.7mm) or at a high glucose concentration (28mm). The curves relating glucose oxidation or insulin release to the extracellular glucose concentration obtained with islets cultured in 6.7mm-glucose displayed a sigmoid shape similar to that observed for freshly isolated non-cultured islets. By contrast islets that had been cultured in 28mm-glucose showed a linear relationship between the rate of glucose oxidation and the extracellular glucose concentration up to about 8mm-glucose. The maximal oxidative rate was twice that of the non-cultured islets and the glucose concentration associated with the half-maximal rate considerably decreased. In islets cultured at 28mm-glucose there was only a small increase in the insulin release in response to glucose, probably due to a depletion of stored insulin in those B cells that had been cultured in a high-glucose medium. It is concluded that exposure of B cells for 6 days to a glucose concentration comparable with that found in diabetic individuals causes adaptive metabolic alterations rather than degeneration of these cells.

scholarly journals Glucose metabolism in mouse pancreatic islets

1970 ◽  
Vol 118 (1) ◽  
pp. 143-154 ◽  
Author(s):  
S. J. H. Ashcroft ◽  
C. J. Hedeskov ◽  
P. J. Randle
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Glucose Oxidation ◽  
Phosphate Concentration ◽  
Lactate Output ◽  
Extracellular Glucose Concentration ◽  
Extracellular Glucose ◽  
Mouse Pancreatic Islets ◽  
Glucose Phosphorylation

1. Rates of glucose oxidation, lactate output and the intracellular concentration of glucose 6-phosphate were measured in mouse pancreatic islets incubated in vitro. 2. Glucose oxidation rate, measured as the formation of 14CO2 from [U-14C]glucose, was markedly dependent on extracellular glucose concentration. It was especially sensitive to glucose concentrations between 1 and 2mg/ml. Glucose oxidation was inhibited by mannoheptulose and glucosamine but not by phlorrhizin, 2-deoxyglucose or N-acetylglucosamine. Glucose oxidation was slightly stimulated by tolbutamide but was not significantly affected by adrenaline, diazoxide or absence of Ca2+ (all of which may inhibit glucose-stimulated insulin release), by arginine or glucagon (which may stimulate insulin release) or by cycloheximide (which may inhibit insulin synthesis). 3. Rates of lactate formation were dependent on the extracellular glucose concentration and were decreased by glucosamine though not by mannoheptulose; tolbutamide increased the rate of lactate output. 4. Islet glucose 6-phosphate concentration was also markedly dependent on extracellular glucose concentration and was diminished by mannoheptulose or glucosamine; tolbutamide and glucagon were without significant effect. Mannose increased islet fructose 6-phosphate concentration but had little effect on islet glucose 6-phosphate concentration. Fructose increased islet glucose 6-phosphate concentration but to a much smaller extent than did glucose. 5. [1-14C]Mannose and [U-14C]fructose were also oxidized by islets but less rapidly than glucose. Conversion of [1-14C]mannose into [1-14C]glucose 6-phosphate or [1-14C]glucose could not be detected. It is concluded that metabolism of mannose is associated with poor equilibration between fructose 6-phosphate and glucose 6-phosphate. 6. These results are consistent with the idea that glucose utilization in mouse islets may be limited by the rate of glucose phosphorylation, that mannoheptulose and glucosamine may inhibit glucose phosphorylation and that effects of glucose on insulin release may be mediated through metabolism of the sugar.

Defective regulation of glucokinase in rat pancreatic islet cell tumours

1987 ◽  
Vol 115 (4) ◽  
pp. 514-520 ◽  
Author(s):  
Sigurd Lenzen ◽  
Markus Tiedge ◽  
Peter R. Flatt ◽  
Clifford J. Bailey ◽  
Uwe Panten
Keyword(s):  
B Cells ◽  
Pancreatic Islets ◽  
Islet Cell ◽  
Pancreatic Islet Cell ◽  
Hexokinase Activity ◽  
Radiation Induced ◽  
Glucose Phosphorylation ◽  
Islet Cell Tumours ◽  
Total Glucose ◽  
Rat Pancreatic Islet

Abstract. The role of glucokinase in the regulation of insulin secretion was examined in normal rat pancreatic islets and in chemically- and radiation-induced rat pancreatic B-cell tumours which show an impaired insulin secretory response to glucose. In normal rats glucokinase activity in cytoplasmic fractions of pancreatic islets was decreased with the duration of fasting and increased by refeeding or insulin administration. This observation is consistent with the induction of glucokinase by insulin. Hexokinase activity was only slightly reduced during fasting. Glucokinase activity decreased in cytoplasmic fractions of streptozotocin-nicotinamideinduced rat pancreatic islet cell tumours. Glucokinase activity contributed about 75% to the total glucose phosphorylation capacity in cytoplasmic fractions of normal pancreatic islets and of small (< 1 mg) streptozotocin-nicotinamide-tumours. This proportion decreased to about 20% in the large streptozotocin-nicotinamide tumours. Glucokinase activity in cytoplasmic fractions of transplantable radiation-induced NEDH (New England Deaconess Hospital) rat B-cell tumours was seven times lower than in normal pancreatic islets and contributed only 15% to the total glucose phosphorylation capacity. In contrast, hexokinase activity of the NEDH tumour B-cells was 2.5 times higher than normal. Decreased glucokinase activity in the chemically- and radiation-induced tumour B-cells appears to result from a loss of the ability of insulin to induce this enzyme and may explain the lack of insulin secretory responsiveness of these tumour B-cells.

Glucose-induced pulsatile insulin release from single islets at stable and oscillatory cytoplasmic Ca2+

1998 ◽  
Vol 274 (5) ◽  
pp. E796-E800 ◽  
Author(s):  
Peter Bergsten
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Small Amplitude ◽  
Similar Frequency ◽  
Secretory Rate ◽  
Mouse Pancreatic Islets

The cytoplasmic Ca2+ concentration ([Ca2+]i) and insulin release were measured simultaneously in mouse pancreatic islets cultured overnight. [Ca2+]iwas 105 nM and insulin release 3 pmol ⋅ g−1 ⋅ s−1at 3 mM glucose. An increase to 7 mM glucose reduced [Ca2+]itransiently, whereas insulin release doubled and was pulsatile with a frequency of 0.47 min−1. [Ca2+]i oscillations with similar frequency appeared at 11 mM glucose associated with increased amplitude of the insulin oscillations, raising the secretory rate 10-fold. In the presence of 16 and 20 mM glucose [Ca2+]iwas >300 nM and showed no oscillations apart from two islets, which demonstrated [Ca2+]ioscillations with small amplitude at 16 mM glucose. Insulin release with maintained frequency increased by 46 and 31%, respectively. When the glucose concentration was increased from 3 to 11 mM, [Ca2+]idecreased with a nadir that appeared significantly earlier than when the glucose concentration was raised from 3 to 7 mM. Glucose-induced insulin release from the isolated islet is pulsatile both at stable and oscillatory [Ca2+]i, with changes in secretory rate caused by the sugar also when [Ca2+]iis unchanged.

scholarly journals Glucose Acutely Decreases pH of Secretory Granules in Mouse Pancreatic Islets

2006 ◽  
Vol 281 (31) ◽  
pp. 22142-22151 ◽  
Author(s):  
Patrick Stiernet ◽  
Yves Guiot ◽  
Patrick Gilon ◽  
Jean-Claude Henquin
Keyword(s):  
Pancreatic Islets ◽  
Secretory Granules ◽  
Mouse Pancreatic Islets

scholarly journals Long-term effects of a high glucose concentration on cyclic nucleotide phosphodiesterase activity in mouse pancreatic islets maintained in tissue culture

1976 ◽  
Vol 156 (2) ◽  
pp. 461-463 ◽  
Author(s):  
C Berne ◽  
A Andersson
Keyword(s):  
Cyclic Amp ◽  
Pancreatic Islets ◽  
Glucose Concentration ◽  
Phosphodiesterase Activity ◽  
Long Term Effects ◽  
Isolated Pancreatic Islets ◽  
Cyclic Amp Phosphodiesterase ◽  
Extracellular Glucose Concentration ◽  
Extracellular Glucose

It has been suggested that the stimulatory effect of glucose on insulin release may be mediated by the adenylate cyclase-cyclic AMP phosphodiesterase system. In this study it was found that exposure of isolated pancreatic islets to an elevated extracellular glucose concentration for 1 week in vitro caused an increase of the cyclic AMP phosphodiesterase activity in the islet cells. These and previous data indicate that there is an increased turnover of cyclic AMP in B-cells exposed for a prolonged time to a high extracellular glucose concentration, which also causes an increased turnover rate of insulin.

scholarly journals The pentose cycle and insulin release in mouse pancreatic islets

1972 ◽  
Vol 126 (3) ◽  
pp. 525-532 ◽  
Author(s):  
S. J. H. Ashcroft ◽  
L. C. C. Weerasinghe ◽  
J. M. Bassett ◽  
P. J. Randle
Keyword(s):  
Glucose Metabolism ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Glucose Utilization ◽  
Fold Increase ◽  
Primary Role ◽  
Mouse Pancreatic Islets ◽  
Oxidation Of Glucose

1. Rates of insulin release, glucose utilization (measured as [3H]water formation from [5-3H]glucose) and glucose oxidation (measured as14CO2 formation from [1-14C]- or [6-14C]-glucose) were determined in mouse pancreatic islets incubated in vitro, and were used to estimate the rate of oxidation of glucose by the pentose cycle pathway under various conditions. Rates of oxidation of [U-14C]ribose and [U-14C]xylitol were also measured. 2. Insulin secretion was stimulated fivefold when the medium glucose concentration was raised from 3.3 to 16.7mm in the absence of caffeine; in the presence of caffeine (5mm) a similar increase in glucose concentration evoked a much larger (30-fold) increase in insulin release. Glucose utilization was also increased severalfold as the intracellular glucose concentration was raised over this range, particularly between 5 and 11mm, but the rate of oxidation of glucose via the pentose cycle was not increased. 3. Glucosamine (20mm) inhibited glucose-stimulated insulin release and glucose utilization but not glucose metabolism via the pentose cycle. No evidence was obtained for any selective effect on the metabolism of glucose via the pentose cycle of tolbutamide, glibenclamide, dibutyryl 3′:5′-cyclic AMP, glucagon, caffeine, theophylline, ouabain, adrenaline, colchicine, mannoheptulose or iodoacetamide. Phenazine methosulphate (5μm) increased pentose-cycle flux but inhibited glucose-stimulated insulin release. 4. No formation of14CO2 from [U-14C]ribose could be detected: [U-14C]xylitol gave rise to small amounts of14CO2. Ribose and xylitol had no effect on the rate of oxidation of glucose; ribitol and xylitol had no effect on the rate of glucose utilization. Ribose, ribitol and xylitol did not stimulate insulin release under conditions in which glucose produced a large stimulation. 5. It is concluded that in normal mouse islets glucose metabolism via the pentose cycle does not play a primary role in insulin-secretory responses.

scholarly journals Immunohistochemical Localization of Monoamine Oxidase Type B in Pancreatic Islets of the Rat

2005 ◽  
Vol 53 (9) ◽  
pp. 1149-1158 ◽  
Author(s):  
Yu-Hong Huang ◽  
Akio Ito ◽  
Ryohachi Arai
Keyword(s):  
B Cells ◽  
Monoamine Oxidase ◽  
Pancreatic Islets ◽  
Pancreatic Islet ◽  
Secretory Granules ◽  
Secretory Process ◽  
Type B ◽  
Electron Microscopic ◽  
Double Labeling ◽  
Outer Membranes

Monoamine oxidase (MAO) is regarded as a mitochondrial enzyme. This enzyme localizes on the outer membrane of mitochondria. There are two kinds of MAO isozymes, MAO type A (MAOA) and type B (MAOB). Previous studies have shown that MAOB activity is found in the pancreatic islets. This activity in the islets is increased by the fasting-induced decrease of plasma glucose level. Islet B cells contain monoamines in their secretory granules. These monoamines inhibit the secretion of insulin from the B cells. MAOB is active in degrading monoamines. Therefore, MAOB may influence the insulin-secretory process by regulating the stores of monoamines in the B cells. However, it has not been determined whether MAOB is localized on B cells or other cell types of the islets. In the present study, we used both double-labeling immunofluorescence histochemical and electron microscopic immunohistochemical methods to examine the subcellular localization of MAOB in rat pancreatic islets. MAOB was found in the mitochondrial outer membranes of glucagon-secreting cells (A cells), insulin-secreting cells (B cells), and some pancreatic polypeptide (PP)-secreting cells (PP cells), but no MAOB was found in somato-statin-secreting cells (D cells), nor in certain other PP cells. There were two kinds of mitochondria in pancreatic islet B cells: one contains MAOB on their outer membranes, but a substantial proportion of them lack this enzyme. Our findings indicate that pancreatic islet B cells contain MAOB on their mitochondrial outer membranes, and this enzyme may be involved in the regulation of monoamine levels and insulin secretion in the B cells.

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