Epinephrine modifications of insulin release and of 86Rb+ or 45Ca2+ fluxes in rat islets

1983 ◽  
Vol 244 (3) ◽  
pp. E245-E252 ◽  
Author(s):  
T. Tamagawa ◽  
J. C. Henquin
Keyword(s):  
Amino Acid ◽  
Insulin Release ◽  
Maximum Effect ◽  
Rat Islets ◽  
High K ◽  
Net Uptake ◽  
Insulinotropic Effect ◽  
Camp Levels ◽  
K Permeability ◽  
86Rb Influx

The effects of epinephrine on insulin release, 86Rb+ fluxes, and 45Ca2+ fluxes were measured in rat islets. In the presence of 10 mM glucose, epinephrine did not affect 86Rb+ influx and slightly increased net uptake. It caused a monophasic inhibition of release and a biphasic decrease in 86Rb+ efflux. A maximum effect was observed with 1 microM epinephrine, but release was more markedly inhibited by lower concentrations of the catecholamine than was the efflux. Epinephrine inhibition of release and efflux was reversed by phentolamine and yohimbine but not by prazosin or propranolol. It was mimicked by norepinephrine and clonidine. The inhibition of 86Rb+ efflux persisted when insulin release was prevented by omission of extracellular calcium. Ouabain or high K+ markedly increased 86Rb+ efflux in the presence of glucose and epinephrine; theophylline and quinine had a similar but smaller effect. None of these agents restored insulin release. Epinephrine abolished the insulinotropic effect of arginine without altering the rise in 86Rb+ efflux triggered by the amino acid. Epinephrine abolished insulin release but inhibited 45Ca2+ efflux only partially during stimulation by glucose or by barium plus theophylline. The results show that epinephrine does not inhibit insulin release by activating the Na pump or by increasing K permeability of the B cell membrane. On the contrary, the inhibition of release is accompanied by a decrease in 86Rb+ efflux. Both result from activation of alpha 2-receptors but are not causally related; they could be due to remodeling of Ca2+ fluxes and/or changes in cAMP levels.

Cobalt inhibition of insulin release: evidence for an action not related to Ca2+ uptake

1984 ◽  
Vol 246 (1) ◽  
pp. C57-C62 ◽  
Author(s):  
C. B. Wollheim ◽  
D. Janjic
Keyword(s):  
Tissue Culture ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Release Process ◽  
Cyclic Monophosphate ◽  
Rat Islets ◽  
Camp Levels ◽  
Stimulation Of

Insulin release, Ca2+ fluxes, and adenosine 3',5'-cyclic monophosphate (cAMP) levels were measured under various conditions to test the selectivity of cobalt (Co2+) actions in pancreatic islets. Insulin release was measured simultaneously either with 45Ca2+ uptake or 45Ca2+ efflux from rat islets maintained 2 days in tissue culture. Glucose (16.7 mM)-stimulated insulin release was inhibited by Co2+ (0.25, 0.5 mM) without concomitant inhibition of glucose-stimulated 45Ca2+ uptake. At higher concentrations of Co2+ (1.0, 2.5 mM) glucose- as well as K+-stimulated insulin release were inhibited in parallel with 45Ca2+ uptake. In the presence or the absence of external Ca2+, Co2+ (0.5 mM) also decreased 3-isobutyl-1-methylxanthine-stimulated insulin release, which does not depend on the stimulation of Ca2+ uptake. Co2+ did not alter islet cAMP levels. Co2+ also did not affect the unidirectional basal 45Ca2+ efflux measured in the absence of Ca2+ but completely overcame the stimulated 45Ca2+ efflux evoked by the removal of external Mg2+. Under the latter conditions, 50, but not 5 microM verapamil, decreased the stimulated 45Ca2+ efflux. It is concluded that Co2+ is able to inhibit insulin release and lower Ca2+ efflux without apparent interference with Ca2+ uptake. This suggests that Co2+, in addition to its well-known inhibition of Ca2+ uptake, may exert its action at a distal step in the insulin release process.

scholarly journals Metabolism of lysophospholipids in intact rat islets. The insulin secretagogue p-hydroxymercuribenzoic acid impairs lysophosphatidylcholine catabolism and permits its accumulation

1987 ◽  
Vol 241 (3) ◽  
pp. 863-869 ◽  
Author(s):  
S A Metz
Keyword(s):  
Insulin Release ◽  
Acyltransferase Activity ◽  
Base Exchange ◽  
Future Studies ◽  
Rat Islets ◽  
Stimulus Secretion Coupling ◽  
Toxic Concentrations ◽  
Insulinotropic Effect ◽  
Hydrolysis Of ◽  
Lysophospholipase Activity

Although recent studies implicate lysophospholipids (lyso-PLs) in stimulus-secretion coupling in the pancreatic islet, almost no data on lyso-PL metabolism therein exist. Therefore, intact rat islets were loaded with insulinotropic and non-toxic concentrations of 1-[14C]palmitoyl-lysophosphatidylcholine (lyso-PC) via transbilayer movement, and its metabolic fate was studied. The time-dependent hydrolysis of lyso-PC to fatty acid (lysophospholipase activity), its conversion to phosphatidylcholine (putative acyltransferase activity) and, to a lesser degree, the appearance of label in phosphatidylethanolamine (putative transacylase or base exchange activity) were observed. p-Hydroxymercuribenzoic acid (PHMB) at 100 microM (a concentration previously demonstrated to elicit potent exocytotic insulin release) inhibited all three activities (by 56, 46 and 75%, respectively) and led to the intracellular accumulation of lyso-PC. Antimycin A inhibited phosphatidylcholine formation but not lysophospholipase activity; lyso-PC did not accumulate, implying that blockade of both of the major metabolic pathways is required to induce a detectable increment in lyso-PC levels. Calculations derived from data using the lowest effective insulinotropic concentration of lyso-PC suggested that increments in lyso-PC accumulation at critical membrane sites of less than 10-15% above basal values are sufficient to trigger insulin release. Since PHMB elicited increments of 50-100% in lyso-PC after its translocation into islets, support is provided for the earlier contention that lyso-PLs mediate the insulinotropic effect of PHMB. In addition, these studies may provide a more precise experimental paradigm for future studies of islet lyso-PL metabolism.

scholarly journals Mechanism of 3-phenylpyruvate-induced insulin release. Secretory, ionic and oxidative aspects

1983 ◽  
Vol 210 (3) ◽  
pp. 913-919 ◽  
Author(s):  
A Sener ◽  
M Welsh ◽  
P Lebrun ◽  
P Garcia-Morales ◽  
M Saceda ◽  
...  
Keyword(s):  
Amino Acid ◽  
Cyclic Amp ◽  
Insulin Release ◽  
Inhibitory Effect ◽  
Secretory Response ◽  
Acid Transport ◽  
O2 Uptake ◽  
Net Uptake ◽  
High Concentrations ◽  
Stimulation Of

1. 3-Phenylpyruvate caused a dose-related stimulation of insulin release from rat pancreatic islets deprived of exogenous nutrient or incubated in the presence of 5.6 or 8.3 mM-D-glucose. 2. 3-Phenylpyruvate inhibited insulin release evoked by high concentrations of D-glucose (16.7 or 27.8 mM) or 4-methyl-2-oxopentanoate (10.0 mM). This inhibitory effect appeared to be attributable to impairment of 2-oxo-acid transport into the mitochondria, with resulting inhibition of D-glucose, pyruvate or 4-methyl-2-oxopentanoate oxidation. 3. 3-Phenylpyruvate failed to affect the oxidation of, and secretory response to, L-leucine, and did not augment insulin release evoked by a non-metabolized analogue of the latter amino acid. 4. L-Glutamine augmented 3-phenylpyruvate-induced insulin release. The release of insulin evoked by the combination of 3-phenylpyruvate and L-glutamine represented a sustained phenomenon, abolished in the absence of extracellular Ca2+ or the presence of menadione and potentiated by theophylline. 5. Whether in the presence or in the absence of L-glutamine, the secretory response to 3-phenylpyruvate coincided with an increase in O2 uptake, a decrease in K+ conductance, a stimulation of both Ca2+ inflow and 45Ca2+ net uptake and an increase in cyclic AMP content. 6. It is concluded that the release of insulin induced by 3-phenylpyruvate displays features classically encountered when the B-cell is stimulated by nutrient secretagogues, and is indeed attributable to an increase in nutrient catabolism.

The stimulus-secretion coupling of amino acid-induced insulin release: metabolism and cationic effects of leucine

Diabetes ◽  
1980 ◽  
Vol 29 (6) ◽  
pp. 431-437 ◽  
Author(s):  
W. J. Malaisse ◽  
J. C. Hutton ◽  
A. R. Carpinelli ◽  
A. Herchuelz ◽  
A. Sener
Keyword(s):  
Amino Acid ◽  
Insulin Release ◽  
Stimulus Secretion Coupling

Effect of Intraduodenal Starch Infusion on Net Portal Absorption of Amino Acids in Growing steers Fed Lucerne

1994 ◽  
Vol 1994 ◽  
pp. 28-28
Author(s):  
C.J. Seal ◽  
D.S. Parker ◽  
J.C. MacRae ◽  
G.E. Lobley
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Gastrointestinal Tract ◽  
Protein Turnover ◽  
Portal Blood ◽  
Intestinal Lumen ◽  
Short Term ◽  
Net Uptake ◽  
Amino Acid Requirements ◽  
Glucose Availability

Amino acid requirements for energy metabolism and protein turnover within the gastrointestinal tract are substantial and may be met from luminal and arterial pools of amino acids. Several studies have demonstrated that the quantity of amino acids appearing in the portal blood does not balance apparent disappearance from the intestinal lumen and that changing diet or the availability of energy-yielding substrates to the gut tissues may influence the uptake of amino acids into the portal blood (Seal & Reynolds, 1993). For example, increased net absorption of amino acids was observed in animals receiving exogenous intraruminal propionate (Seal & Parker, 1991) and this was accompanied by changes in glucose utilisation by the gut tissues. In contrast, there was no apparent change in net uptake of [l-13C]-leucine into the portal vein of sheep receiving short term intraduodenal infusions of glucose (Piccioli Cappelli et al, 1993). This experiment was designed to further investigate the effects on amino acid absorption of changing glucose availability to the gut with short term (seven hours) or prolonged (three days) exposure to starch infused directly into the duodenum.

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