Acetylcholine increases the level of diglyceride in mouse pancreas

Banschbach, Martin W.; Geison, R. L.; Hokin-Neaverson, Mabel

doi:10.1016/s0006-291x(74)80476-6

Cited by 55 publications

(18 citation statements)

References 7 publications

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“…The level of DG has been shown to increase in certain other tissues during secretion (34)(35)(36)(37), and Allan and Michell have suggested that DG promotes membrane fusibility in such processes (35). Under certain conditions, DG facilitates fusion of hen erythrocytes (38).…”

Section: Discussionmentioning

confidence: 99%

Production of diglyceride from phosphatidylinositol in activated human platelets.

1979

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Section: Discussionmentioning

confidence: 99%

Production of diglyceride from phosphatidylinositol in activated human platelets.

1979

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“…However, there have been reports of stimulated triacylglycerol metabolism, or of diacylglycerol accumulation, in thyrotropin-stimulated thyroid (Scott et al, 1968), in acetylcholine-treated pancreas (Banschbach et al, 1974), and in polymorphonuclear leucocytes (Elsbach & Farrow, 1969;Shohet, 1970), all of which could be a reflection of the activity of a Ca2+-stimulated triacylglycerol lipase in these tissues. Our own preliminary data for polymorphonuclear leucocytes (Table 3) suggest the presence of such an enzyme in these cells.…”

Section: Discussionmentioning

confidence: 99%

A comparison of the effects of phytohaemagglutinin and of calcium ionophore A23187 on the metabolism of glycerolipids in small lymphocytes

Allan¹,

Michell²

1977

Biochemical Journal

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1. The effects of phytohaemagglutinin and of a Ca2+ ionophore (A23 187) on glycerolipid metabolism in lymphocytes from pig lymph nodes were compared (a) by studying the incorporation of [32P] Phytohaemagglutinin only stimulated 32p incorporation into phosphatidylinositol and, to a slight extent, phosphatidate. Removal of most of the extracellular Ca2+ somewhat decreased this response. 3. lonophore A23187 stimulated the labellingofphosphatidateand phosphatidylinositol with 32p to a much greater extent than did phytohaemagglutinin: the increase in phosphatidate labelling, but not that of phosphatidylinositol, was almost abolished by the removal of extracellular Ca2+. 4. The combined effects of phytohaemagglutinin and ionophore appeared to be additive, rather than synergistic. 5. Treatment with ionophore A23187 somewhat decreased the total incorporation of [3H]glycerol into glycerolipids, possibly because it lowered cell ATP content. In these experiments di-and tri-acylglycerol behaved anomalously, triacylglycerol labelling being suppressed completely, whereas that of diacylglycerol was enhanced. The pulse-chase results revealed that triacylglycerol was converted into diacylglycerol in the ionophore-treated cells, and the availability of this diacylglycerol probably led to the enhanced labelling of phosphatidate and phosphatidylinositol in these cells. 6. Thus an increase in intracellular Ca2+ concentration appeared to have three effects on glycerolipid metabolism: (a) slight inhibition of some metabolic step preceding phosphatidate synthesis, (b) inhibition of diacylglycerol acyltransferase and (c) activation of a triacylglycerol lipase. 7. In contrast, it seems likely that the only effect of phytohaemagglutinin is to stimulate phosphatidylinositol breakdown. 8. Pig polymorphonuclear leucocytes treated with ionophore A23187 showed metabolic changes that were similar to those demonstrated with lymphocytes. 9. A possible similarity is suggested between Ca2+-stimulated triacylglycerol lipase in lymphocytes and polymorphonuclear leucocytes and previous observations of enhanced triacylglyerol metabolism in stimulated cells whose metabolic functions involve membrane fusion.

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“…162 phosphodiesteratic cleavage of phosphoinositides and that this may be the primary effect leading to secondary increases in synthesis of phospholipids, particularly phosphatidic acid and phosphatidylinositol. More recently this concept gained support from the studies by Hokin-Neaverson (1974) and her collaborators (Banschbach et al, 1974a) working with pancreas, and Jones & Michell (1974) working with rat parotid fragments, who demonstrated a decrease in phosphatidylinositol in response to acetylcholine.…”

mentioning

confidence: 98%

Acetylcholine increases the breakdown of triphosphoinositide of rabbit iris muscle prelabelled with [32P] phosphate

Abdel‐Latif¹,

Akhtar²,

Hawthorne³

1977

Biochemical Journal

254

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1. Paired iris smooth muscles from rabbits were incubated for 30min at 37°C in an iso-osmotic salt medium containing glucose, inositol, cytidine and [32P]phosphate. 2. One of the pair was then incubated at 37'C for 10min in unlabelled medium containing lOmM-2-deoxyglucose and the other was incubated in the presence of acetylcholine plus eserine (0.05mM each). 2-Deoxyglucose, which was included in the incubation medium to minimize the biosynthesis of triphosphoinositide from ATP and diphosphoinositide, decreased the amount of labelled ATP by 71 % and inhibited further 32p incorporation from ATP into triphosphoinositide by almost 30 %. 3. Acetylcholine (0.05mM) increased significantly the loss of 32P from triphosphoinositide (the 'triphosphoinositide effect') in 32P-labelled iris muscle. This effect was measured both chemically and radiochemically. It was also observed when 32P1 was replaced by myo-[3H]inositol in the incubation medium.4. The triphosphoinositide effect was blocked by atropine but not by D-tubocurarine. Further, muscarinic but not nicotinic agonists were found to provoke this effect. 5. Acetylcholine decreased by 28% the 32p incorporation into triphosphoinositide, presumably by stimulating its breakdown. This decrement in triphosphoinositide was blocked by atropine, but not by D-tubocurarine. 6. The triphosphoinositide effect was accompanied by a significant increase in 32p labelling, but not tissue concentration, of phosphatidylinositol and phosphatidic acid. The possible relationship between the loss of 32p label from triphosphoinositide in response to acetylcholine and the concomitant increase in that of phosphatidylinositol and phosphatidic acid is discussed. 7. The presence of triphosphoinositide phosphomonoesterase, the enzyme that might be stimulated in the iris smooth muscle by the neurotransmitter, was demonstrated, and, under our methods of homogenization and assay, more than 80% of its activity was localized in the particulate fraction.

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Acetylcholine increases the level of diglyceride in mouse pancreas

Cited by 55 publications

References 7 publications

Production of diglyceride from phosphatidylinositol in activated human platelets.

Production of diglyceride from phosphatidylinositol in activated human platelets.

A comparison of the effects of phytohaemagglutinin and of calcium ionophore A23187 on the metabolism of glycerolipids in small lymphocytes

Acetylcholine increases the breakdown of triphosphoinositide of rabbit iris muscle prelabelled with [32P] phosphate

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