Stimulation of Insulin Release In Vivo by the Methyl Esters of Succinic Acid and Glutamic Acid

1997 ◽  
pp. 231-234 ◽  
Author(s):  
Isabel Valverde ◽  
David Vicent ◽  
Marisa L. Villanueva-Peñacarrillo ◽  
Francine Malaisse-Lagae ◽  
Willy J. Malaisse
Keyword(s):  
Glutamic Acid ◽  
Succinic Acid ◽  
Insulin Release ◽  
Methyl Esters ◽  
Stimulation Of

Respiratory, ionic, and functional effects of succinate esters in pancreatic islets

1993 ◽  
Vol 264 (3) ◽  
pp. E428-E433 ◽  
Author(s):  
W. J. Malaisse ◽  
J. Rasschaert ◽  
M. L. Villanueva-Penacarrillo ◽  
I. Valverde
Keyword(s):  
Succinic Acid ◽  
Insulin Release ◽  
Methyl Esters ◽  
O2 Uptake ◽  
Biosynthetic Activity ◽  
Insulin Secretagogues ◽  
Net Uptake ◽  
Characteristic Features ◽  
45Ca Efflux ◽  
Stimulation Of

The methyl esters of succinic acid were introduced a few years ago as new potent insulin secretagogues. In the present study, they were found to increase O2 uptake by rat islets incubated in the absence or presence of D-glucose; to decrease 86Rb outflow from prelabeled islets; to stimulate biosynthetic activity in the islets, with a preferential effect on the synthesis of proinsulin; to inhibit 45Ca efflux from prelabeled islets perifused in the absence of extracellular Ca2+ but to augment 45Ca net uptake and to cause a biphasic stimulation of 45Ca outflow in islets incubated or perifused in the presence of extracellular Ca2+; and to evoke a biphasic stimulation of insulin release. The insulinotropic action of these methyl esters coincided with a shift to the left of the sigmoidal relationship between insulin output and D-glucose concentration, was concentration related in the 2-10 mM range, failed to be duplicated by succinic acid, displayed both Ca2+ dependency and resistance to a lowering of extracellular pH, and was operative in the absence of D-glucose whether or not the islets were stimulated by non-nutrient secretagogues. It is concluded that the respiratory, cationic, biosynthetic, and secretory responses of the islets to succinate methyl esters display the characteristic features usually encountered in the process of nutrient-stimulated insulin release.

The release of labeledl-glutamic acid from rat neostriatum In vivo following stimulation of frontal cortex

Neuroscience ◽  
1980 ◽  
Vol 5 (12) ◽  
pp. 2151-2154 ◽  
Author(s):  
O.V. Godukhin ◽  
A.D. Zharikova ◽  
V.I. Novoselov
Keyword(s):  
Glutamic Acid ◽  
Frontal Cortex ◽  
Stimulation Of

Effect of fatty acids on isolated ovine pancreatic islets.

1978 ◽  
Vol 234 (2) ◽  
pp. E162 ◽  
Author(s):  
H N Jordan ◽  
R W Phillips
Keyword(s):  
Fatty Acids ◽  
Plasma Membrane ◽  
Insulin Release ◽  
Chain Length ◽  
Hormone Release ◽  
Beta Hydroxybutyrate ◽  
Pancreatic Hormone ◽  
Syringe Injection ◽  
Stimulation Of

A procedure was developed for the isolation of intact islets of Langerhans from sheep pancreas. The pancreas was disrupted by syringe injection of Hanks solution followed by collagenase incubation and islet separation by sedimentation. The islets were incubated in varying concentrations of glucose and butyrate. The rate of insulin release was approximately linear while the glucose and butyrate concentrations were increased. In additional studies at 2.5 and 5.0 mM levels of substrate concentration, the stimulation of insulin had the following pattern: octanoate greater than hexanoate greater than butyrate, whereas beta-hydroxybutyrate, lactate, acetate, and propionate had only slight stimulatory effects that were not statistically significant. Decanoate did not alter insulin release from isolated islets. These data confirm earlier in vivo reports that fatty acids stimulate pancreatic hormone release in sheep and that the stimulus is related to chain length of the fatty acid through C-8 but that C-10 has no effect. A hypothesis was suggested to explain these results based on chain length, solubility, and plasma membrane alterations.

Stimulation of insulin secretion and potentiation of glibenclamide-induced insulin release by the dimethyl ester of glutamic acid in anaesthetized rats

1995 ◽  
Vol 27 (1) ◽  
pp. 27-30 ◽  
Author(s):  
David Vicent ◽  
Juan A. Garcia-Martinez ◽  
Marisa L. Villanueva-Peñacarrillo ◽  
Isabel Valverde ◽  
Willy J. Malaisse
Keyword(s):  
Insulin Secretion ◽  
Glutamic Acid ◽  
Insulin Release ◽  
Dimethyl Ester ◽  
Anaesthetized Rats ◽  
Stimulation Of

In Vivo Stimulation of Insulin Secretion by Novel Esters of Succinic Acid

1995 ◽  
Vol 27 (05) ◽  
pp. 251-252 ◽  
Author(s):  
T.-M. Zhang ◽  
F. Björkling ◽  
W. Malaisse
Keyword(s):  
Insulin Secretion ◽  
Succinic Acid ◽  
Stimulation Of

scholarly journals Proteomic exploration of pancreatic islets in mice null for the α2A adrenergic receptor

2005 ◽  
Vol 35 (1) ◽  
pp. 73-88 ◽  
Author(s):  
Xinran Hu ◽  
David Friedman ◽  
Salisha Hill ◽  
Richard Caprioli ◽  
Wendell Nicholson ◽  
...  
Keyword(s):  
Insulin Release ◽  
Adrenergic Receptor ◽  
Ex Vivo ◽  
Wild Type ◽  
Downstream Signaling ◽  
Glucose Levels ◽  
Endogenous Catecholamines ◽  
Stimulation Of

The present studies extend recent findings that mice null for the α2A adrenergic receptor (α2A AR KO mice) lack suppression of exogenous secretagogue-stimulated insulin secretion in response to α2 AR agonists by evaluating the endogenous secretagogue, glucose, ex vivo, and providing in vivo data that baseline insulin levels are elevated and baseline glucose levels are decreased in α2A AR KO mice. These latter findings reveal that the α2A AR subtype regulates glucose-stimulated insulin release in response to endogenous catecholamines in vivo. The changes in α2A AR responsiveness and resultant changes in insulin/glucose homeostasis encouraged us to utilize proteomics strategies to identify possible α2A AR downstream signaling molecules or other resultant changes due to perturbation of α2A AR expression. Although agonist stimulation of islets from wild type (WT) mice did not significantly alter islet protein profiles, several proteins were enriched in islets from α2A AR KO mice when compared with those from WT mice, including an enzyme participating in insulin protein processing. The present studies document the important role of the α2A AR subtype in tonic suppression of insulin release in response to endogenous catecholamines as well as exogenous α2 agonists and provide insights into pleiotropic changes that result from loss of α2A AR expression and tonic suppression of insulin release.

Heterogeneous secretion of individual B cells in response to D-glucose and to nonglucidic nutrient secretagogues

1995 ◽  
Vol 268 (3) ◽  
pp. C611-C618 ◽  
Author(s):  
D. Bosco ◽  
P. Meda ◽  
B. Thorens ◽  
W. J. Malaisse
Keyword(s):  
B Cells ◽  
Carboxylic Acid ◽  
Glutamic Acid ◽  
Succinic Acid ◽  
Insulin Release ◽  
Dimethyl Ester ◽  
Plaque Assay ◽  
Incubation Periods ◽  
Pancreatic B Cells ◽  
Monomethyl Ester

We used a hemolytic plaque assay for insulin to determine whether the same pancreatic B cells respond to D-glucose, 2-amino-bicyclo[2,2,1]heptane-2-carboxylic acid (BCH) and the association of this nonmetabolized analogue of L-leucine with either the monomethyl ester of succinic acid (SME) or the dimethyl ester of L-glutamic acid (GME). During a 30-min incubation in the absence of D-glucose, BCH alone (5 mM) had no effect on insulin release. In contrast, the combination of BCH with either SME (10 mM) or GME (3 mM) stimulated insulin release to the same extent observed in the sole presence of 16.7 mM D-glucose. The effects of BCH plus SME and BCH plus GME on both percentage of secreting B cells and total insulin output were little affected in the presence of D-glucose concentrations ranging from 0 to 16.7 mM. Varying the concentration of SME from 2 to 10 mM also did not influence these effects. In other experiments, the very same B cells were first exposed 45 min to 16.7 mM D-glucose, then incubated 45 min in the presence of only BCH and SME. Under these conditions, most (80.3 +/- 2.5%) of the cells contributing to insulin release did so during both incubation periods. Furthermore, virtually all cells responding to BCH and SME during the second incubation corresponded to cells also responsive to D-glucose during the first incubation. Similar observations were made when the sequence of the two incubations was reversed.(ABSTRACT TRUNCATED AT 250 WORDS)

Mass fragmentographic determination of endogenous glycine and glutamic acid released in vivo from the pigeon optic tectum. Effect of electric stimulation of a midbrain nucleus

1981 ◽  
Vol 224 (2) ◽  
pp. 327-336 ◽  
Author(s):  
M. Wolfensberger ◽  
J.C. Reubi ◽  
V. <Canzˇek ◽  
U. Redweik ◽  
H.Ch. Curtius ◽  
...  
Keyword(s):  
Glutamic Acid ◽  
Optic Tectum ◽  
Electric Stimulation ◽  
Stimulation Of
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