Proton microprobe analysis of 15 elements in pancreatic B cells and exocrine pancreas in diabetic Chinese hamsters

1987 ◽  
Vol 7 (1) ◽  
pp. 33-41 ◽  
Author(s):  
Lisa Juntti-Berggren ◽  
Ulf Lindh ◽  
Per-Olof Berggren ◽  
Barbara J. Frankel
Keyword(s):  
B Cells ◽  
Exocrine Pancreas ◽  
Molar Ratio ◽  
X Rays ◽  
Chinese Hamsters ◽  
High K ◽  
Freeze Dried ◽  
Diabetic Chinese Hamsters ◽  
Pancreatic B Cells

Diabetes mellitus spontaneously develops in certain sublines of non-obese Chinese hamsters, and the diabetic L-subline is known for subnormal pancreatic insulin release in vitro. The cause of the secretory defect is unknown. Freeze-dried pancreas sections from genetically diabetic Chinese hamsters and normal controls were subjected to proton bombardment and the concentration of 15 elements in B cells and acini was calculated from the X-rays emitted. Diabetic B cells contained significantly less Al (−61%) and significantly more Cu (+92 %), Mg (+6 %) and Rb (+13 %) than their normal counterparts. The diabetic acini showed similar, significant changes. The molar ratio between K and Na was about 10 in endocrine as well as exocrine pancreas from both groups of animals, implying that neither sample preparation nor irradiation had induced significant diffusive changes. In conclusion, the high K/Na ratio suggests that the diabetic B cell has a well-functioning Na+/K+ pump. However, significant and parallel changes in Al-, Cu-, Mg- and Rb-levels were found in both the B cells and acinar portion of the diabetic pancreas. It is not clear whether these elemental changes cause the islet secretory defect or result from it.

Diabetes is not associated with a change in the elemental composition of the pancreatic B cell in diabetic C57BL KsJ-db/db mice

1990 ◽  
Vol 10 (2) ◽  
pp. 217-223 ◽  
Author(s):  
Lisa Juntti-Berggren ◽  
Ulf Lindh ◽  
Per-Olof Berggren ◽  
Ove Berglund ◽  
Barbara J. Frankel
Keyword(s):  
B Cells ◽  
B Cell ◽  
Elemental Composition ◽  
Exocrine Pancreas ◽  
X Rays ◽  
Proton Bombardment ◽  
Pancreatic B Cell ◽  
Freeze Dried ◽  
Different Ages ◽  
Onset Of Diabetes

Freeze-dried pancreas sections from 7-, 17-and 27-week-old genetically diabetic (db/db) and normal (±/±) mice were subjected to proton bombardment and the concentrations of 15 elements in B cells and exocrine pancreas were calculated from the characteristic X-rays emitted. In the 7-week-old diabetic animals, B cells contained significantly above-normal levels of Na and S, while exocrine pancreas contained subnormal levels of Ca, and excess Mn. The B cells from the 17-week-old diabetic animals contained subnormal levels of Cu and the exocrine pancreas of the 27-week-old diabetic animals was deficient in Cd. The 7-, 17- and 27-week-old, genetically diabetic (db/db) mice were hyperglycemic, hyperinsulinemic and heavier than age-matched normal (±/±) mice. Although significant changes were found in elemental composition when comparing both B cells and exocrine pancreas at different ages, the changes were not consistent. Therefore, it appears as if the measured elemental changes were random and not related to the onset of diabetes.

Glucokinase in pancreatic B-cells and its inhibition by alloxan

1987 ◽  
Vol 115 (1) ◽  
pp. 21-29 ◽  
Author(s):  
Sigurd Lenzen ◽  
Markus Tiedge ◽  
Uwe Panten
Keyword(s):  
Insulin Secretion ◽  
B Cells ◽  
B Cell ◽  
Metabolic Flux ◽  
Inhibitory Concentration ◽  
Pancreatic B Cell ◽  
High K ◽  
Pancreatic B Cells ◽  
Low K

Abstract. Characterization of glucokinase in pancreatic B-cells from ob/ob mice and from rat liver revealed identical characteristics. A narrow substrate specificity; high Km values for the two substrates, D-glucose and D-mannose, in the range of 10 and 20 mmol/l, respectively; higher Vmax values for D-glucose than for D-mannose; inhibition of glucokinase activities by D-mannoheptulose and by a specific glucokinase antibody. These characteristics distinguish glucokinase in soluble cytoplasmic fractions of pancreatic B-cells and liver from low Km hexokinases. Alloxan is a pancreatic B-cell cytotoxic agent, which has been widely used as a tool for the elucidation of the mechanisms of insulin secretion, because its inhibitory action on insulin secretion has been presumed to be intimately related to the mechanism of glucose-induced insulin secretion. Alloxan inhibited glucokinase but not hexokinase activity in cytoplasmic fractions of pancreatic B-cells and liver. The half maximal inhibitory concentration of alloxan was 5 μmol/l. Glucokinase activity was protected from alloxan toxicity only by D-glucose and D-mannose; the α anomer of D-glucose provided significantly greater protection than the β anomer. The non-metabolizable sugar 3-0-methyl-D-glucose did not provide protection of glucokinase activity against inhibition by alloxan. Thus, inhibition of pancreatic B-cell glucokinase may contribute to the inhibition of glucose-induced insulin secretion by alloxan. These results support the contention that glucokinase regulates the metabolic flux rate through the glycolytic chain in the pancreatic B-cell and thereby generates the signal for glucose-induced insulin secretion.

scholarly journals Induction of class II MHC antigens in vitro on pancreatic B cells isolated from BB/E rats

Diabetologia ◽  
1986 ◽  
Vol 29 (10) ◽  
pp. 749-751 ◽  
Author(s):  
R. Walker ◽  
A. Cooke ◽  
A. J. Bone ◽  
B. M. Dean ◽  
P. van der Meide ◽  
...  
Keyword(s):  
B Cells ◽  
Class Ii ◽  
Mhc Antigens ◽  
Class Ii Mhc ◽  
Class Ii Mhc Antigens ◽  
Pancreatic B Cells

scholarly journals Die ultrastrukturele, morfometriese evaluering van die mikrotubulere stelsel in gestimuleerde B-selle van die pankreas

1992 ◽  
Vol 11 (4) ◽  
pp. 127-135
Author(s):  
A. Crous ◽  
A. M. De Beer ◽  
E. J. Visser
Keyword(s):  
B Cells ◽  
Insulin Release ◽  
Insulin Response ◽  
High Magnification ◽  
Tissue Samples ◽  
Islet Tissue ◽  
Pancreatic B Cells ◽  
Complete Cell

The intracellular distribution of microtubules in pancreatic B-cells was studied morphometrically to elucidate the positive correlation between microtubular content and the rate of insulin release found by biochemical investigations. Rat islet tissue was glucose stimulated under in vivo and in vitro (isolated islets) conditions and tissue samples taken to represent both phases of the phasic insulin response. Electron micrographs (x40 000) of individual B-cells were assembled into montages to obtain complete cell profiles at high magnification.

scholarly journals Increase of gap junctions between pancreatic B-cells during stimulation of insulin secretion.

1979 ◽  
Vol 82 (2) ◽  
pp. 441-448 ◽  
Author(s):  
P Meda ◽  
A Perrelet ◽  
L Orci
Keyword(s):  
Insulin Secretion ◽  
B Cells ◽  
Gap Junctions ◽  
Freeze Fracture ◽  
Secretory Activity ◽  
Isolated Rat Islets ◽  
Pancreatic B Cells ◽  
Stimulation Of

The development of gap junctions between pancreatic B-cells was quantitatively assessed in freeze-fracture replicas of isolated rat islets under different conditions of insulin secretion. The results show that in resting B-cells, gap junctions are small and scarce but that these junctions increase when insulin secretion is stimulated. Both a short (90 min) stimulation by glucose in vitro and a prolonged (2.5 d) stimulation by glibenclamide in vivo raise the number of gap junctions; in addition, the glibenclamide stimulation causes an increase in the size of individual gap junctions. As a consequence, the total area occupied by gap junctions on the B-cell membrane and the ratio of this area to the cell volume were found significantly increased in the latter condition. The slight increase of these values observed after the glucose stimulation did not reach significance. These data indicate a change of gap junctions during the secretory activity of the pancreatic B-cells. The possibility that the coupling of the cells is affected by the treatment is discussed.

scholarly journals Human pancreatic B cells in vitro: Microtubule and insulin immunofluorescence

Diabetologia ◽  
1982 ◽  
Vol 23 (3) ◽  
pp. 280-283
Author(s):  
W. E. Bolton ◽  
A. E. Boyd ◽  
S. P. Terrell ◽  
K. L. Andrews ◽  
W. A. Redwine
Keyword(s):  
B Cells ◽  
Pancreatic B Cells

scholarly journals Two sites of glucose control of insulin release with distinct dependence on the energy state in pancreatic B-cells

1994 ◽  
Vol 297 (3) ◽  
pp. 455-461 ◽  
Author(s):  
P Detimary ◽  
P Gilon ◽  
M Nenquin ◽  
J C Henquin
Keyword(s):  
Membrane Potential ◽  
B Cells ◽  
Insulin Release ◽  
Cell Function ◽  
Energy State ◽  
Secretory Process ◽  
High K ◽  
Pancreatic B Cells ◽  
Stimulus Secretion Coupling ◽  
Intracellular Targets

The energy state of pancreatic B-cells may influence insulin release at several steps of stimulus-secretion coupling. By closing ATP-sensitive K+ channels (K(+)-ATP channels), a rise in the ATP/ADP ratio may regulate the membrane potential, and hence Ca2+ influx. It may also modulate the effectiveness of Ca2+ on its intracellular targets. To assess the existence of these two roles and determine their relative importance for insulin release, we tested the effects of azide, a mitochondrial poison, on mouse B-cell function under various conditions. During stimulation by glucose alone, when K(+)-ATP channels are controlled by cellular metabolism, azide caused parallel, concentration-dependent (0.5-5 mM), membrane repolarization, decrease in cytosolic Ca2+ concentration [Ca2+]i and inhibition of insulin release. When K(+)-ATP channels were closed pharmacologically (by tolbutamide in high glucose), azide did not repolarize the membrane or decrease [Ca2+]i, and was much less effective in inhibiting insulin release. A similar resistance to azide was observed when K(+)-ATP channels were opened by diazoxide, and high K+ was used to depolarize the membrane and raise [Ca2+]i. In contrast, azide similarly decreased ATP levels and increased ADP levels, thereby lowering the ATP/ADP ratio under all conditions. In conclusion, lowering the ATP/ADP ratio in B-cells can inhibit insulin release even when [Ca2+]i remains high. However, this distal step is much more resistant to a decrease in the energy state of B-cells than is the control of membrane potential by K(+)-ATP channels. Generation of the signal triggering insulin release, high [Ca2+]i, through metabolic control of membrane potential requires a higher global ATP/ADP ratio than does activation of the secretory process itself.

RNA Metabolism, DNA Damage and Cellular Resistance to X-Rays: Investigations in Chick Embryo and Rat Cells

1992 ◽  
Vol 47 (3-4) ◽  
pp. 249-254 ◽  
Author(s):  
A. Link ◽  
K. Tempel ◽  
M. Hund
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Protein Synthesis ◽  
B Cells ◽  
Chick Embryo ◽  
Chicken Embryo ◽  
X Rays ◽  
Embryo Cells ◽  
X Irradiation

Abstract Three hours after X-irradiation in vivo with 8 Gy the in vitro incorporation of [3H]uridine into total RNA of liver(L)- and brain(B)-cells of the chick embryo was reduced to 77% and 90%, respectively; the m RNA fraction was strongest inhibited. Under the same conditions, protein synthesis of L-cells declined to 62%, while protein synthesis of B-cells was not influenced. RNA and protein metabolism was not altered following X-irradiation in vitro (1.75 -56 Gy). - Compared to thymic - and splenic cells of the rat, chicken embryo cells exhibited higher constitutive poly(adenosine diphosphate-ribose)polymerase activity and lower X-irradiation-induced DNA damage. - Whereas the slight inhibition of RNA and protein synthesis by X-irradiation in ovo may be an abscopal and/or secondary phenomenon reflecting DNA and/or cellular damage, the present investigations comprising various cell types argue for an efficient DNA repair in chicken embryo cells caused, at least partly, by a high constitutive activity of DNA repair proteins.

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