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Results for “NICOTINIC ACID”

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At least 991 records · Page 55Linked to original sources
PubMed2002

Cell side-specific sensitivities of intracellular Ca2+ stores for inositol 1,4,5-trisphosphate, cyclic ADP-ribose, and nicotinic acid adenine dinucleotide phosphate in permeabilized pancreatic acinar cells from mouse.

In pancreatic acinar cells hormonal stimulation leads to a cytosolic Ca(2+) wave that starts in the apical cell pole and subsequently propagates toward the basal cell side. We used permeabilized pancreatic acinar cells from mouse and the mag-fura-2 technique, which allows direct monitoring of changes in [Ca(2+)] of intracellular stores. We show here that Ca(2+) can be released from stores in all cellular regions by inositol 1,4,5-trisphosphate. Stores at the apical cell pole showed a higher affinity to inositol 1,4,5-trisphosphate (EC(50) = 89 nm) than those at the basolateral side (EC(50) = 256 nm). In contrast, cADP-ribose, a modifier of Ca(2+)-induced Ca(2+) release, and nicotinic acid adenine dinucleotide phosphate (NAADP) were able to release Ca(2+) exclusively from intracellular stores located at the basolateral cell side. Our data agree with observations that upon stimulation Ca(2+) is released initially at the apical cell side and that this is caused by high affinity inositol 1,4,5-trisphosphate receptors. Moreover, our findings allow the conclusion that in Ca(2+) wave propagation from the apical to the basolateral cell side observed in pancreatic acinar cells Ca(2+)-induced Ca(2+) release, modulated by cADP-ribose and/or NAADP, might be involved.

Adenosine Diphosphate Ribose↗
PubMed2003

Ryanodine receptor type I and nicotinic acid adenine dinucleotide phosphate receptors mediate Ca2+ release from insulin-containing vesicles in living pancreatic beta-cells (MIN6).

We have demonstrated recently (Mitchell, K. J., Pinton, P., Varadi, A., Tacchetti, C., Ainscow, E. K., Pozzan, T., Rizzuto, R., and Rutter, G. A. (2001) J. Cell Biol. 155, 41-51) that ryanodine receptors (RyR) are present on insulin-containing secretory vesicles. Here we show that pancreatic islets and derived beta-cell lines express type I and II, but not type III, RyRs. Purified by subcellular fractionation and membrane immuno-isolation, dense core secretory vesicles were found to possess a similar level of type I RyR immunoreactivity as Golgi/endoplasmic reticulum (ER) membranes but substantially less RyR II than the latter. Monitored in cells expressing appropriately targeted aequorins, dantrolene, an inhibitor of RyR I channels, elevated free Ca(2+) concentrations in the secretory vesicle compartment from 40.1 +/- 6.7 to 90.4 +/- 14.8 microm (n = 4, p < 0.01), while having no effect on ER Ca(2+) concentrations. Furthermore, nicotinic acid adenine dinucleotide phosphate (NAADP), a novel Ca(2+)-mobilizing agent, decreased dense core secretory vesicle but not ER free Ca(2+) concentrations in permeabilized MIN6 beta-cells, and flash photolysis of caged NAADP released Ca(2+) from a thapsigargin-insensitive Ca(2+) store in single MIN6 cells. Because dantrolene strongly inhibited glucose-stimulated insulin secretion (from 3.07 +/- 0.51-fold stimulation to no significant glucose effect; n = 3, p < 0.01), we conclude that RyR I-mediated Ca(2+)-induced Ca(2+) release from secretory vesicles, possibly potentiated by NAADP, is essential for the activation of insulin secretion.

Animals↗
PubMed1986

Effect of a high fat diet on rat adipocyte lipolysis: responses to epinephrine, forskolin, methylisobutylxanthine, dibutyryl cyclic AMP, insulin and nicotinic acid.

An earlier report from this laboratory showed that feeding rats a high fat diet decreased epinephrine-stimulated lipolysis in their adipose tissue. Experiments were designed to explore further the effects of such diets on adipocyte response to epinephrine and to several other lipolytic and antilipolytic agents. Rats were fed diets with 67% of energy consisting of glucose or lard for 5 to 7 d. Adipocytes were prepared from epididymal fat pads and lipolysis measured by the release of glycerol into the medium during 1-h incubations. The cells from the rats fed the high fat diet showed lower lipolytic responses to stimulation by epinephrine, forskolin and dibutyryl cyclic AMP than those from rats fed the high glucose diet. The lard diet effect on the lipolytic response to isobutylmethylxanthine varied among experiments, but it also decreased it in some of them. However, the high fat diet did not induce decreased sensitivity or responsiveness to the antilipolytic effect of insulin, although previous reports have demonstrated resistance to other actions of insulin in rats fed a high fat diet. The antilipolytic effect of nicotinic acid was also similar in cells from rats fed a high fat diet to that found for cells from rats fed the high glucose diet.

1-Methyl-3-isobutylxanthine↗